Milestones in Cancer Research and Discovery

During the past 250 years, we have witnessed many landmark discoveries in our efforts to make progress against cancer, an affliction known to humanity for thousands of years. This timeline shows a few key milestones in the history of cancer research.

1775: Chimney Soot & Squamous Cell Carcinoma

Percivall Pott identifies a relationship between exposure to chimney soot and the incidence of squamous cell carcinoma of the scrotum among chimney sweeps. His report is the first to clearly link an environmental exposure to the development of cancer.

1863: Inflammation & Cancer

Rudolph Virchow identifies white blood cells (leukocytes) in cancerous tissue, making the first connection between inflammation and cancer. Virchow also coins the term "leukemia" and is the first person to describe the excess number of white blood cells in the blood of patients with this disease.

1882: The First Radical Mastectomy to Treat Breast Cancer

William Halsted performs the first radical mastectomy to treat breast cancer. This surgical procedure remains the standard operation for breast cancer until the latter half of the 20th century.

1886: Inheritance of Cancer Risk

Brazilian ophthalmologist Hilário de Gouvêa provides the first documented evidence that a susceptibility to cancer can be passed on from a parent to a child. He reports that two of seven children born to a father who was successfully treated for childhood retinoblastoma, a malignant tumor of the eye, also developed the disease.

1895: The First X-Ray

Wilhelm Roentgen discovers x-rays. The first x-ray picture is an image of his wife's hand.

1898: Radium & Polonium

Marie and Pierre Curie discover the radioactive elements radium and polonium. Within a few years, the use of radium in cancer treatment begins.

1899: The First Use of Radiation Therapy to Cure Cancer

Swedish physicians Tor Stenbeck and Tage Sjogren describe the first cases of basal cell carcinoma of the skin and squamous cell carcinoma of the skin cured by X-ray therapy.

1902: Cancer Tumors & Single Cells with Chromosome Damage

Theodor Boveri proposes that cancerous tumors arise from single cells that have experienced chromosome damage and suggests that chromosome alterations cause the cells to divide uncontrollably.

1909: Immune Surveillance

Paul Ehrlich proposes that the immune system usually suppresses tumor formation, a concept that becomes known as the "immune surveillance" hypothesis. This proposal prompts research, which continues today, to harness the power of the immune system to fight cancer.

1911: Cancer in Chickens

Peyton Rous discovers a virus that causes cancer in chickens (Rous sarcoma virus), establishing that some cancers are caused by infectious agents.

1915: Cancer in Rabbits

Katsusaburo Yamagiwa and Koichi Ichikawa induce cancer in rabbits by applying coal tar to their skin, providing experimental proof that chemicals can cause cancer.

1928: The Pap Smear

George Papanicolaou discovers that cervical cancer can be detected by examining cells from the vagina under a microscope. This breakthrough leads to the development of the Pap test, which allows abnormal cervical cells to be detected and removed before they become cancerous.

1932: The Modified Radical Mastectomy for Breast Cancer

David H. Patey develops the modified radical mastectomy for breast cancer. This surgical procedure is less disfiguring than the radical mastectomy and eventually replaces it as the standard surgical treatment for breast cancer.

1937: The National Cancer Institute (NCI)

Legislation signed by President Franklin D. Roosevelt establishes the National Cancer Institute (NCI).

1937: Breast-Sparing Surgery Followed by Radiation

Sir Geoffrey Keynes describes the treatment of breast cancer with breast-sparing surgery followed by radiation therapy. After surgery to remove the tumor, long needles containing radium are inserted throughout the affected breast and near the adjacent axillary lymph nodes.

1941: Hormonal Therapy

Charles Huggins discovers that removing the testicles to lower testosterone production or administering estrogens causes prostate tumors to regress. Such hormonal manipulation—more commonly known as hormonal therapy—continues to be a mainstay of prostate cancer treatment.

1947: Antimetabolites

Sidney Farber shows that treatment with the antimetabolite drug aminopterin, a derivative of folic acid, induces temporary remissions in children with acute leukemia. Antimetabolite drugs are structurally similar to chemicals needed for important cellular processes, such as DNA synthesis, and cause cell death by blocking those processes.

1949: Nitrogen Mustard

The Food and Drug Administration (FDA) approves nitrogen mustard (mechlorethamine) for the treatment of cancer. Nitrogen mustard belongs to a class of drugs called alkylating agents, which kill cells by chemically modifying their DNA.

1950: Cigarette Smoking & Lung Cancer

Ernst Wynder, Evarts Graham, and Richard Doll identify cigarette smoking as an important factor in the development of lung cancer.

1953: The First Complete Cure of a Human Solid Tumor

Roy Hertz and Min Chiu Li achieve the first complete cure of a human solid tumor by chemotherapy when they use the drug methotrexate to treat a patient with choriocarcinoma, a rare cancer of the reproductive tissue that mainly affects women.

1958: Combination Chemotherapy

NCI researchers Emil Frei, Emil Freireich, and James Holland and their colleagues demonstrate that combination chemotherapy with the drugs 6-mercaptopurine and methotrexate can induce partial and complete remissions and prolong survival in children and adults with acute leukemia.

1960: The Philadelphia Chromosome

Peter Nowell and David Hungerford describe an unusually small chromosome in the cancer cells of patients with chronic myelogenous leukemia (CML). This chromosome, which becomes known as the Philadelphia chromosome, is found in the leukemia cells of 95% of patients with CML.

1964: A Focus on Cigarette Smoking

The U.S. Surgeon General issues a report stating that cigarette smoking is an important health hazard in the United States and that action is required to reduce its harmful effects.

1964: The Epstein-Barr virus

For the first time, a virus—the Epstein-Barr virus (EBV)—is linked to a human cancer (Burkitt lymphoma). EBV is later shown to cause several other cancers, including nasopharyngeal carcinoma, Hodgkin lymphoma, and some gastric (stomach) cancers.

1971: The National Cancer Act

On December 23, President Richard M. Nixon signs the National Cancer Act, which authorizes the NCI Director to coordinate all activities of the National Cancer Program, establish national cancer research centers, and establish national cancer control programs.

1976: The DNA of Normal Chicken Cells

Dominique Stehelin, Harold Varmus, J. Michael Bishop, and Peter Vogt discover that the DNA of normal chicken cells contains a gene related to the oncogene (cancer-causing gene) of avian sarcoma virus, which causes cancer in chickens. This finding eventually leads to the discovery of human oncogenes.

1978: Tamoxifen

FDA approves tamoxifen, an antiestrogen drug originally developed as a birth control treatment, for the treatment of breast cancer. Tamoxifen represents the first of a class of drugs known as selective estrogen receptor modulators, or SERMs, to be approved for cancer therapy.

1979: The TP53 Gene

The TP53 gene (also called p53), the most commonly mutated gene in human cancer, is discovered. It is a tumor suppressor gene, meaning its protein product (p53 protein) helps control cell proliferation and suppress tumor growth.

1984: HER2 Gene Discovered

Researchers discover a new oncogene in rat cells that they call “neu.” The human version of this gene, called HER2 (and ErbB2), is overexpressed in about 20% to 25% of breast cancers (known as HER2-positive breast cancers) and is associated with more aggressive disease and a poor prognosis.

1984: HPV 16 & 18

DNA from human papillomavirus (HPV) types 16 and 18 is identified in a large percentage of cervical cancers, establishing a link between infection with these HPV types and cervical carcinogenesis.

1985: Breast-Conserving Surgery

Results from an NCI-supported clinical trial show that women with early-stage breast cancer who were treated with breast-conserving surgery (lumpectomy) followed by whole-breast radiation therapy had similar rates of overall survival and disease-free survival as women who were treated with mastectomy alone.

1986: HER2 Oncogene Cloning

The human oncogene HER2 (also called neu and erbB2) is cloned. Overexpression of the protein product of this gene, which occurs in about 20% to 25% of breast cancers (known as HER2-positive breast cancers), is associated with more aggressive disease and a poor prognosis.

1993: Guaiac Fecal Occult Blood Testing (FOBT)

Results from an NCI-supported clinical trial show that annual screening with guaiac fecal occult blood testing (FOBT) can reduce colorectal cancer mortality by about 33%.

1994: BRCA1 Tumor Suppressor Gene Cloning

The tumor suppressor gene BRCA1 is cloned. Specific inherited mutations in this gene greatly increase the risks of breast and ovarian cancer in women and the risks of several other cancers in both men and women.

1995: BRCA2 Tumor Suppressor Gene Cloning

The tumor suppressor gene BRCA2 is cloned. Similar to BRCA1, inheriting specific BRCA2 gene mutations greatly increases the risks of breast and ovarian cancer in women and the risks of several other cancers in both men and women.

1996: Anastrozole

FDA approves anastrozole for the treatment of estrogen receptor-positive advanced breast cancer in postmenopausal women. Anastrozole is the first aromatase inhibitor (a drug that blocks the production of estrogen in the body) to be approved for cancer therapy.

1997: Rituximab

FDA approves rituximab, a monoclonal antibody, for use in patients with treatment-resistant, low-grade or follicular B-cell non-Hodgkin lymphoma (NHL). Rituximab is the first monoclonal antibody approved for use in cancer therapy. It is later approved as an initial treatment for these types of NHL, for another type of NHL called diffuse large B-cell lymphoma, and for chronic lymphocytic leukemia.

1998: NCI-Sponsored Breast Cancer Prevention Trial

Results of the NCI-sponsored Breast Cancer Prevention Trial show that the antiestrogen drug tamoxifen can reduce the incidence of breast cancer among women who are at increased risk of the disease by about 50%. FDA approves tamoxifen to reduce the incidence of breast cancer in women at increased risk.

1998: Trastuzumab

FDA approves trastuzumab, a monoclonal antibody that targets cancer cells that overexpress the HER2 gene, for the treatment of women with HER2-positive metastatic breast cancer. Trastuzumab is later approved for the adjuvant (post-operative) treatment of women with HER2-positive early-stage breast cancer.

2001: Imatinib Mesylate

Results of a clinical trial show that the drug imatinib mesylate, which targets a unique protein produced by the Philadelphia chromosome, is effective against chronic myelogenous leukemia (CML). Imatinib treatment changes the usually fatal disease into a manageable condition. Later, it is also shown to be effective in the treatment of gastrointestinal stromal tumors (GIST).

2003: NCI-Sponsored Prostate Cancer Prevention Trial (PCPT)

Results of the NCI-sponsored Prostate Cancer Prevention Trial (PCPT) show that the drug finasteride, which reduces the production of male hormones in the body, lowers a man's risk of prostate cancer by about 25%.

2006: NCI's Study of Tamoxifen and Raloxifene (STAR)

Results of NCI's Study of Tamoxifen and Raloxifene (STAR) show that postmenopausal women at increased risk of breast cancer can reduce their risk of developing the disease if they take the antiestrogen drug raloxifene. The risk of serious side effects is lower with raloxifene than with tamoxifen.

2006: Gardasil

FDA approves the human papillomavirus (HPV) vaccine Gardasil, which protects against infection by the two HPV types (HPV 16 and 18) that cause approximately 70% of all cases of cervical cancer and two additional HPV types (HPV 6 and 11) that cause 90% of genital warts. Gardasil is the first vaccine approved to prevent cervical cancer. NCI scientists made technological advances that enabled development of Gardasil and subsequent HPV vaccines.

2009: Cervarix

FDA approves Cervarix, a second vaccine that protects against infection by the two HPV types that cause approximately 70% of all cases of cervical cancer worldwide. 

2010: The First Human Cancer Treatment Vaccine

FDA approves sipuleucel-T, a cancer treatment vaccine that is made using a patient's own immune system cells (dendritic cells), for the treatment of metastatic prostate cancer that no longer responds to hormonal therapy. It is the first (and so far only) human cancer treatment vaccine to be approved.

2010: NCI-Sponsored Lung Cancer Screening Trial (NLST)

Initial results of the NCI-sponsored Lung Cancer Screening Trial (NLST) show that screening with low-dose helical computerized tomography (CT) reduced lung cancer deaths by about 20% in a large group of current and former heavy smokers.

2011: Ipilimumab

FDA approves the use of ipilimumab, a monoclonal antibody, for the treatment of inoperable or metastatic melanoma. Ipilimumab stimulates the immune system to attack cancer cells by removing a "brake" that normally controls the intensity of immune responses.

2012: NCI-Sponsored PLCO Cancer Screening Trial

Results of the NCI-sponsored PLCO Cancer Screening Trial confirm that screening people 55 years of age and older for colorectal cancer using flexible sigmoidoscopy reduces colorectal cancer incidence and mortality. In the PLCO trial, screened individuals had a 21% lower risk of developing colorectal cancer and a 26% lower risk of dying from the disease than the control subjects.

2013: Ado-Trastuzumab Emtansine (T-DM1)

FDA approves ado-trastuzumab emtansine (T-DM1) for the treatment of patients with HER2-positive breast cancer who were previously treated with trastuzumab and/or a taxane drug. T-DM1 is an immunotoxin (an antibody-drug conjugate) that is made by chemically linking the monoclonal antibody trastuzumab to the cytotoxic agent mertansine, which inhibits cell proliferation by blocking the formation of microtubules.

2014: Analyzing DNA in Cancer

Researchers from The Cancer Genome Atlas (TCGA) project, a joint effort by NCI and the National Human Genome Research Institute to analyze the DNA and other molecular changes in more than 30 types of human cancer, find that gastric (stomach) cancer is actually four different diseases, not just one, based on differing tumor characteristics. This finding from TCGA and other related projects may potentially lead to a new classification system for cancer, in which cancers are classified by their molecular abnormalities as well as their organ or tissue site of origin.

2014: Pembrolizumab

FDA approves pembrolizumab for the treatment of advanced melanoma. This monoclonal antibody blocks the activity of a protein called PD1 on immune cells, which increases the strength of immune responses against cancer.

2014: Gardasil 9

FDA approves Gardasil 9, a vaccine that protects against infection with the same four HPV types as Gardasil plus five more cancer-causing HPV types that together account for nearly 90% of cervical cancers. It is now the only HPV vaccine available in the United States.

2015: NCI-MATCH Clinical Trial

NCI and the ECOG-ACRIN Cancer Research Group launch the NCI-MATCH (Molecular Analysis for Therapy Choice) clinical trial to test more than 20 drugs and drug combinations based on molecular analysis of tumors in people with cancer. The study is designed to determine whether targeted therapies for people whose tumors have specific gene mutations will be effective regardless of their cancer type.

2015: Talimogene Laherparepvec

FDA approves talimogene laherparepvec (T-VEC) for the treatment of some patients with metastatic melanoma that cannot be surgically removed. T-VEC, the first oncolytic virus approved for clinical use, works by infecting and killing tumor cells and stimulating an immune response against cancer cells throughout the body. 

2016: Cancer Moonshot℠

Congress passes the 21st Century Cures Act, which provides funding for the Cancer Moonshot, a broad program to accelerate cancer research by investing in specific research initiatives that have the potential to transform cancer care, detection, and prevention.

2017: Pediatric MATCH

NCI and the Children’s Oncology Group launch Pediatric MATCH, an effort to extend molecular analysis and targeted treatment to children and adolescents with cancer. Like NCI-MATCH, Pediatric MATCH seeks to determine if treating tumors with molecularly targeted drugs based on the tumor’s genetic characteristics rather than the type of cancer or cancer site will be effective.

2017: CAR T-Cell Therapies

FDA approves tisagenlecleucel to treat a form of acute lymphoblastic leukemia in certain children and young adults. FDA subsequently approves axicabtagene ciloleucel for patients with large B-cell lymphomas whose cancer has progressed after receiving at least two prior treatment regimens. Both treatments are chimeric antigen receptor (CAR) T-cell therapies that are personalized for each patient. To create these therapies, T cells are removed from the patient, genetically altered to recognize cancer-specific antigens, grown to large numbers in the lab, and then infused back into the patient to stimulate their immune system to attack cancer cells.

2017: Tumor-Agnostic Approval for Pembrolizumab

FDA extends approval of pembrolizumab to treat metastatic and inoperable solid tumors that have certain genetic changes, wherever they occur in the body , that have progressed following prior treatment and that have no alternative treatment options. With this tissue-agnostic approval, pembrolizumab becomes the first cancer treatment based solely on the presence of a genetic feature in a tumor, rather than a person’s cancer type.

2017: Genomic Profiling Tests

FDA clears two products to test tumors for genetic changes that may make the tumors susceptible to treatment with FDA-approved molecularly targeted drugs. In November, FDA authorizes the MSK-IMPACT test developed and used by Memorial Sloan Kettering Cancer Center to analyze tumors for potentially actionable changes in 468 cancer-related genes. In December, FDA approves the FoundationOne CDx test, which evaluates genetic changes in 324 genes known to fuel cancer growth. The FoundationOne test serves as a companion diagnostic for several FDA-approved drugs targeting five common types of cancer.

2018: TCGA PanCancer Atlas

NIH-funded researchers with TCGA complete an in-depth genomic analysis of 33 cancer types. The PanCancer Atlas provides a detailed genomic analysis of molecular and clinical data from more than 10,000 tumors that gives cancer researchers an unprecedented understanding of how, where, and why tumors arise in humans. 

2018: NCI-Sponsored TAILORx Clinical Trial

Results from the NCI-sponsored Trial Assigning IndividuaLized Options for Treatment (Rx), or TAILORx, clinical trial show that most women with early-stage breast cancer do not benefit from having chemotherapy after surgery. The trial used a molecular test that assesses the expression of 21 genes associated with breast cancer recurrence to assign women with early-stage, hormone receptor–positive, HER2-negative breast cancer that hasn’t spread to the lymph nodes to the most appropriate and effective post-operative treatment. It is one of the first trials to examine a way to personalize cancer treatment

2018: Larotrectinib

FDA approves larotrectinib, the first drug that targets tumors with NTRK gene fusions. The approval is for pediatric or adult patients with metastatic or inoperable solid tumors that have worsened after previous treatment anywhere in the body driven by an NTRK gene fusion without a known acquired resistance mutation. Larotrectinib is the second drug approved to treat cancer with specific molecular features regardless of where the cancer is located.

2020: International Pan-Cancer Analysis of Whole Genomes

A consortium of international researchers analyzes more than 2,600 whole genomes from 38 types of cancer and matching normal tissues to identify common patterns of molecular changes. The Pan-Cancer Analysis of Whole Genomes study, which used data collected by the International Cancer Genome Consortium and TCGA, uncovers the complex role that changes throughout the genome play in cancer development, growth, and spread. The study also extends genomic analyses of cancer beyond the protein-coding regions to the complete genetic composition of cells.  

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  • Published: 05 February 2020

The evolutionary history of 2,658 cancers

  • Moritz Gerstung 1 , 2 , 3   na1 ,
  • Clemency Jolly 4   na1 ,
  • Ignaty Leshchiner 5   na1 ,
  • Stefan C. Dentro 3 , 4 , 6   na1 ,
  • Santiago Gonzalez 1   na1 ,
  • Daniel Rosebrock 5 ,
  • Thomas J. Mitchell 3 , 7 ,
  • Yulia Rubanova 8 , 9 ,
  • Pavana Anur 10 ,
  • Kaixian Yu 11 ,
  • Maxime Tarabichi 3 , 4 ,
  • Amit Deshwar 8 , 9 ,
  • Jeff Wintersinger 8 , 9 ,
  • Kortine Kleinheinz 12 , 13 ,
  • Ignacio Vázquez-García 3 , 7 ,
  • Kerstin Haase 4 ,
  • Lara Jerman 1 , 14 ,
  • Subhajit Sengupta 15 ,
  • Geoff Macintyre 16 ,
  • Salem Malikic 17 , 18 ,
  • Nilgun Donmez 17 , 18 ,
  • Dimitri G. Livitz 5 ,
  • Marek Cmero 19 , 20 ,
  • Jonas Demeulemeester 4 , 21 ,
  • Steven Schumacher 5 ,
  • Yu Fan 11 ,
  • Xiaotong Yao 22 , 23 ,
  • Juhee Lee 24 ,
  • Matthias Schlesner 12 ,
  • Paul C. Boutros 8 , 25 , 26 ,
  • David D. Bowtell 27 ,
  • Hongtu Zhu 11 ,
  • Gad Getz 5 , 28 , 29 , 30 ,
  • Marcin Imielinski 22 , 23 ,
  • Rameen Beroukhim 5 , 31 ,
  • S. Cenk Sahinalp 18 , 32 ,
  • Yuan Ji 15 , 33 ,
  • Martin Peifer 34 ,
  • Florian Markowetz 16 ,
  • Ville Mustonen 35 ,
  • Ke Yuan 16 , 36 ,
  • Wenyi Wang 11 ,
  • Quaid D. Morris 8 , 9 ,
  • PCAWG Evolution & Heterogeneity Working Group ,
  • Paul T. Spellman 10   na2 ,
  • David C. Wedge 6 , 37   na2 ,
  • Peter Van Loo 4 , 21   na2 &

PCAWG Consortium

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  • Cancer genomics
  • Computational biology and bioinformatics
  • Molecular evolution

An Author Correction to this article was published on 25 January 2023

This article has been updated

Cancer develops through a process of somatic evolution 1 , 2 . Sequencing data from a single biopsy represent a snapshot of this process that can reveal the timing of specific genomic aberrations and the changing influence of mutational processes 3 . Here, by whole-genome sequencing analysis of 2,658 cancers as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA) 4 , we reconstruct the life history and evolution of mutational processes and driver mutation sequences of 38 types of cancer. Early oncogenesis is characterized by mutations in a constrained set of driver genes, and specific copy number gains, such as trisomy 7 in glioblastoma and isochromosome 17q in medulloblastoma. The mutational spectrum changes significantly throughout tumour evolution in 40% of samples. A nearly fourfold diversification of driver genes and increased genomic instability are features of later stages. Copy number alterations often occur in mitotic crises, and lead to simultaneous gains of chromosomal segments. Timing analyses suggest that driver mutations often precede diagnosis by many years, if not decades. Together, these results determine the evolutionary trajectories of cancer, and highlight opportunities for early cancer detection.

Similar to the evolution in species, the approximately 10 14 cells in the human body are subject to the forces of mutation and selection 1 . This process of somatic evolution begins in the zygote and only comes to rest at death, as cells are constantly exposed to mutagenic stresses, introducing 1–10 mutations per cell division 2 . These mutagenic forces lead to a gradual accumulation of point mutations throughout life, observed in a range of healthy tissues 5 , 6 , 7 , 8 , 9 , 10 , 11 and cancers 12 . Although these mutations are predominantly selectively neutral passenger mutations, some are proliferatively advantageous driver mutations 13 . The types of mutation in cancer genomes are well studied, but little is known about the times when these lesions arise during somatic evolution and where the boundary between normal evolution and cancer progression should be drawn.

Sequencing of bulk tumour samples enables partial reconstruction of the evolutionary history of individual tumours, based on the catalogue of somatic mutations they have accumulated 3 , 14 , 15 . These inferences include timing of chromosomal gains during early somatic evolution 16 , phylogenetic analysis of late cancer evolution using matched primary and metastatic tumour samples from individual patients 17 , 18 , 19 , 20 , and temporal ordering of driver mutations across many samples 21 , 22 .

The PCAWG Consortium has aggregated whole-genome sequencing data from 2,658 cancers 4 , generated by the ICGC and TCGA, and produced high-accuracy somatic variant calls, driver mutations, and mutational signatures 4 , 23 , 24 (Methods and Supplementary Information ).

Here, we leverage the PCAWG dataset to characterize the evolutionary history of 2,778 cancer samples from 2,658 unique donors across 38 cancer types. We infer timing and patterns of chromosomal evolution and learn typical sequences of mutations across samples of each cancer type. We then define broad periods of tumour evolution and examine how drivers and mutational signatures vary between these epochs. Using clock-like mutational processes, we map mutation timing estimates into approximate real time. Combined, these analyses allow us to sketch out the typical evolutionary trajectories of cancer, and map them in real time relative to the point of diagnosis.

Reconstructing the life history of tumours

The genome of a cancer cell is shaped by the cumulative somatic aberrations that have arisen during its evolutionary past, and part of this history can be reconstructed from whole-genome sequencing data 3 (Fig. 1a ). Initially, each point mutation occurs on a single chromosome in a single cell, which gives rise to a lineage of cells bearing the same mutation. If that chromosomal locus is subsequently duplicated, any point mutation on this allele preceding the gain will subsequently be present on the two resulting allelic copies, unlike mutations succeeding the gain, or mutations on the other allele. As sequencing data enable the measurement of the number of allelic copies, one can define categories of early and late clonal variants, preceding or succeeding copy number gains, as well as unspecified clonal variants, which are common to all cancer cells, but cannot be timed further. Lastly, we identify subclonal mutations, which are present in only a subset of cells and have occurred after the most recent common ancestor (MRCA) of all cancer cells in the tumour sample ( Supplementary Information ).

figure 1

a , Principles of timing mutations and copy number gains based on whole-genome sequencing. The number of sequencing reads reporting point mutations can be used to discriminate variants as early or late clonal (green or purple, respectively) in cases of specific copy number gains, as well as clonal (blue) or subclonal (red) in cases without. b , Annotated point mutations in one sample based on VAF (top), copy number (CN) state and structural variants (middle), and resulting timing estimates (bottom). LOH, loss of heterozygosity. c , Overview of the molecular timing distribution of copy number gains across cancer types. Pie charts depict the distribution of the inferred mutation time for a given copy number gain in a cancer type. Green denotes early clonal gains, with a gradient to purple for late gains. The size of each chart is proportional to the recurrence of this event. Abbreviations for each cancer type are defined in  Supplementary Table 1 . d , Heat maps representing molecular timing estimates of gains on different chromosome arms ( x axis) for individual samples ( y axis) for selected tumour types. e , Temporal patterns of two near-diploid cases illustrating synchronous gains (top) and asynchronous gains (bottom). f , Left, distribution of synchronous and asynchronous gain patterns across samples, split by WGD status. Uninformative samples have too few or too small gains for accurate timing. Right, the enrichment of synchronous gains in near-diploid samples is shown by systematic permutation tests. g , Proportion of copy number segments ( n  = 90,387) with secondary gains. Error bars denote 95% credible intervals. ND, near diploid. h , Distribution of the relative latency of n  = 824 secondary gains with available timing information, scaled to the time after the first gain and aggregated per chromosome.

Source data

The ratio of duplicated to non-duplicated mutations within a gained region can be used to estimate the time point when the gain happened during clonal evolution, referred to here as molecular time, which measures the time of occurrence relative to the total number of (clonal) mutations. For example, there would be few, if any, co-amplified early clonal mutations if the gain had occurred right after fertilization, whereas a gain that happened towards the end of clonal tumour evolution would contain many duplicated mutations 14 (Fig. 1a , Methods).

These analyses are illustrated in Fig. 1b . As expected, the variant allele frequencies (VAFs) of somatic point mutations cluster around the values imposed by the purity of the sample, local copy number configuration and identified subclonal populations. The depicted clear cell renal cell carcinoma has gained chromosome arm 5q at an early molecular time as part of an unbalanced translocation t(3p;5q), which confirms the notion that this lesion often occurs in adolescence in this cancer type 16 . At a later time point, the sample underwent a whole genome duplication (WGD) event, duplicating all alleles, including the derivative chromosome, in a single event, as evidenced by the mutation time estimates of all copy number gains clustering around a single time point, independently of the exact copy number state.

Timing patterns of copy number gains

To systematically examine the mutational timing of chromosomal gains throughout the evolution of tumours in the PCAWG dataset, we applied this analysis to the 2,116 samples with copy number gains suitable for timing ( Supplementary Information ). We find that chromosomal gains occur across a wide range of molecular times (median molecular time 0.60, interquartile range (IQR) 0.10–0.87), with systematic differences between tumour types, whereas within tumour types, different chromosomes typically show similar distributions (Fig. 1c , Extended Data Figs. 1 , 2 , Supplementary Information ). In glioblastoma and medulloblastoma, a substantial fraction of gains occurs early in molecular time. By contrast, in lung cancers, melanomas and papillary kidney cancers, gains arise towards the end of the molecular timescale. Most tumour types, including breast, ovarian and colorectal cancers, show relatively broad periods of chromosomal instability, indicating a very variable timing of gains across samples.

There are, however, certain tumour types with consistently early or late gains of specific chromosomal regions. Most pronounced is glioblastoma, in which 90% of tumours contain single copy gains of chromosome 7, 19 or 20 (Fig. 1c, d ). Notably, these gains are consistently timed within the first 10% of molecular time, which suggests that they arise very early in a patient’s lifetime. In the case of trisomy 7, typically less than 3 out of 600 single nucleotide variants (SNVs) on the whole chromosome precede the gain (Extended Data Fig. 3a, b ). On the basis of a mutation rate of µ  = 4.8 × 10 −10 to 3.0 × 10 −9 SNVs per base pair per division 25 , this indicates that the trisomy occurs within the first 6–39 cell divisions, suggesting a possible early developmental origin, in agreement with somatic mosaicisms observed in the healthy brain 26 . Similarly, the duplications leading to isochromosome 17q in medulloblastoma are timed exceptionally early (Extended Data Fig. 3c, d ).

Notably, we observed that gains in the same tumour often appear to occur at a similar molecular time, pointing towards punctuated bursts of copy number gains involving most gained segments (Fig. 1e ). Although this is expected in tumours with WGD (Fig. 1b ), it may seem surprising to observe synchronous gains in near-diploid tumours, particularly as only 6% of co-amplified chromosomal segments were linked by a direct inter-chromosomal structural variant. Still, synchronous gains are frequent, occurring in 57% (468 out of 815) of informative near-diploid tumours, 61% more frequently than expected by chance ( P  < 0.01, permutation test; Fig. 1f ). Because most arm-level gains increment the allele-specific copy number by 1 (80–90%; Fig. 1g ), it seems that these gains arise through mis-segregation of single copies during anaphase. This notion is further supported by the observation that in about 85% of segments with two gains of the same allele, the second gain appears with noticeable latency after the first (Fig. 1h ). Therefore, the extensive chromosome-scale copy number aberrations observed in many cancer genomes are seemingly caused by a limited number of events—possibly by merotelic attachments of chromosomes to multipolar mitotic spindles 27 , or as a consequence of negative selection of individual aneuploidies 28 —offering an explanation for observations of punctuated evolution in breast and colorectal cancer 29 , 30 .

Timing of point mutations in driver genes

As outlined above, point mutations (SNVs and insertions and deletions (indels)) can be qualitatively assigned to different epochs, allowing the timing of driver mutations. Out of the 47 million point mutations in 2,583 unique samples, 22% were early clonal, 7% late clonal, 53% unspecified clonal and 17% subclonal (Fig. 2a ). Among a panel of 453 cancer driver genes, 5,913 oncogenic point mutations were identified 4 , of which 29% were early clonal, 5% late clonal, 56% unspecified clonal and 8% subclonal. It thus emerges that common drivers are enriched in the early clonal and unspecified clonal categories and depleted in the late clonal and subclonal ones, indicating a preferential early timing (Fig. 2b ). For example, driver mutations in TP53 and KRAS are 12 and 8 times enriched in early clonal stages, respectively. For TP53 , this trend is independent of tumour type (Fig. 2c ). Mutations in PIK3CA are two times more frequently clonal than expected, and non-coding changes near the TERT gene are three times more frequently early clonal.

figure 2

a , Top, distribution of point mutations over different mutation periods in n  = 2,778 samples. Middle, timing distribution of driver mutations in the 50 most recurrent lesions across n  = 2,583 white listed samples from unique donors. Bottom, distribution of driver mutations across cancer types; colour as defined in the inset. b , Relative timing of the 50 most recurrent driver lesions, calculated as the odds ratio of early versus late clonal driver mutations versus background, or clonal versus subclonal. Error bars denote 95% confidence intervals derived from bootstrap resampling. Odds ratios overlapping 1 in less than 5% of bootstrap samples are considered significant (coloured). The underlying number of samples with a given mutation is shown in a . c , Relative timing of TP53 mutations across cancer types, as in b . The number of samples is defined in the x -axis labels. d , Estimated number of unique lesions (genes) contributing 50% of all driver mutations in different timing epochs across n  = 2,583 unique samples, containing n  = 5,756 driver mutations with available timing information. Error bars denote the range between 0 and 1 pseudocounts; bars denote the average of the two values. NA, not applicable; NS, not significant.

Aggregating the clonal status of all driver point mutations over time reveals an increased diversity of driver genes mutated at later stages of tumour development: 50% of all early clonal driver mutations occur in just 9 genes, whereas 50% of late and subclonal mutations occur in approximately 35 different genes each, a nearly fourfold increase (Fig. 2d ). Consistent with previous studies of individual tumour types 31 , 32 , 33 , 34 , these results suggest that, in general, the very early events in cancer evolution occur in a constrained set of common drivers, and a more diverse array of drivers is involved in late tumour development.

Relative timing of somatic driver events

Although timing estimates of individual events reflect evolutionary periods that differ from one sample to another, they define in part the order in which driver mutations and copy number alterations have occurred in each sample (Fig. 3a–d ). As confirmed by simulations, aggregating these orderings across samples defines a probabilistic ranking of lesions (Fig. 3a ), recapitulating whether each mutation occurs preferentially early or late during tumour evolution (Extended Data Figs. 4 , 5 , Supplementary Information ).

figure 3

a , Schematic representation of the ordering process. b – d , Examples of individual patient trajectories (partial ordering relationships), the constituent data for the ordering model process. e – g , Preferential ordering diagrams for colorectal adenocarcinoma (ColoRect–AdenoCA) ( e ), pancreatic neuroendocrine cancer (Panc–Endocrine) ( f ) and glioblastoma (CNS–GBM) ( g ). Probability distributions show the uncertainty of timing for specific events in the cohort. Events with odds above 10 (either earlier or later) are highlighted. The prevalence of the event type in the cohort is displayed as a bar plot on the right.

In colorectal adenocarcinoma, for example, we find APC mutations to have the highest odds of occurring early, followed by KRAS , loss of 17p and TP53 , and SMAD4 (Fig. 3b , e). Whole-genome duplications occur after tumours have accumulated several driver mutations, and many chromosomal gains and losses are typically late. These results are in agreement with the classical APC-KRAS-TP53 progression model of Fearon and Vogelstein 35 , but add considerable detail.

In many cancer types, the sequence of events during cancer progression has not previously been determined in detail. For example, in pancreatic neuroendocrine cancers, we find that many chromosomal losses, including those of chromosomes 2, 6, 11 and 16, are among the earliest events, followed by driver mutations in MEN1 and DAXX (Fig. 3c, f ). WGD events occur later, after many of these tumours have reached a pseudo-haploid state due to widespread chromosomal losses. In glioblastoma, we find that the loss of chromosome 10, and driver mutations in TP53 and EGFR are very early, often preceding early gains of chromosomes 7, 19 and 20 (Fig. 3d, g ). Mutations in the TERT promoter tend to occur at early to intermediate time points, whereas other driver mutations and copy number changes tend to be later events.

Across cancer types, we typically find TP53 mutations among the earliest events, as well as losses of chromosome 17 ( Supplementary Information ). WGD events usually have an intermediate ranking, and most copy number changes occur later. Losses typically precede gains, and consistent with the results above, common drivers typically occur before rare drivers.

Timing of mutational signatures

The cancer genome is shaped by various mutational processes over its lifetime, stemming from exogenous and cell-intrinsic DNA damage, and error-prone DNA replication, leaving behind characteristic mutational spectra, termed mutational signatures 24 , 36 . Stratifying mutations by their clonal allelic status, we find evidence for a changing mutational spectrum between early and late clonal time points in 29% (530 out of 1,852) of informative samples ( P  < 0.05, Bonferroni-adjusted likelihood-ratio test), typically changing the spectrum by 19% (median absolute difference; range 4–66%) (Fig. 4a, b , Extended Data Fig. 6 ). Similarly, 30% of informative samples (729 out of 2,387) displayed changes of their mutation spectrum between the clonal and subclonal state, with median difference of 21% (range 3–72%). Combined, the mutation spectrum changes throughout tumour evolution in 40% of samples (1,069 out of 2,688).

figure 4

a , Example of tumours with substantial changes between mutation spectra of early (left) and late (right) clonal time points. The attribution of mutations to the most characteristic signatures are shown. b , Example of clonal-to-subclonal mutation spectrum change. c , Fold changes between relative proportions of early and late clonal mutations attributed to individual mutational signatures. Points are coloured by tissue type. Data are shown for samples ( n  = 530) with measurable changes in their overall mutation spectra and restricted to signatures active in at least 10 samples. Box plots demarcate the first and third quartiles of the distribution, with the median shown in the centre and whiskers covering data within 1.5× the IQR from the box. d , Fold changes between clonal and subclonal periods in samples ( n  = 729) with measurable changes in their mutation spectra, analogous to c .

To quantify whether the observed temporal changes can be attributed to known and suspected mutational processes, we decomposed the mutational spectra at each time point into a catalogue of 57 mutational signatures, including double base substitution and indel signatures 24 (Methods).

In general, these mutational signatures display a predominantly undirected temporal variability over several orders of magnitude (Fig. 4c, d , Extended Data Fig. 7 ). In addition, several signatures demonstrate distinct temporal trends. As one may expect, signatures of exogenous mutagens are predominantly active in the early clonal stages of tumorigenesis. These include tobacco smoking in lung adenocarcinoma (signature SBS4, median fold change 0.43, IQR 0.31–0.72), consistent with previous reports 37 , 38 , and ultraviolet light exposure in melanoma (SBS7; median fold change 0.16, IQR 0.09–0.43). Another strong decrease over time is found for a signature of unknown aetiology, SBS12, which acts mostly in liver cancers (median fold change 0.22, IQR 0.06–0.41). In chronic lymphoid leukaemia, there was a 20-fold relative decrease in mutations associated with somatic hypermutation (SBS9; median fold change 0.05, IQR 0.02–0.43) from clonal to subclonal stages.

Some mutational processes tend to increase throughout cancer evolution. For example, we see that APOBEC mutagenesis (SBS2 and SBS13) increases in many cancer types from the early to late clonal stages (median fold change 2.0, IQR 0.8–3.6), as does a newly described signature SBS38 (median fold 3.6, IQR 1.8–11). Signatures of defective mismatch repair (SBS6, 14, 15, 20, 21, 26 and 44) increase from clonal to subclonal stages (median fold 1.8, IQR 1.2–3.0).

Chronological time estimates

The molecular timing data presented above do not measure the occurrence of events in chronological time. If the rate at which mutations are acquired per year in each sample was constant, the chronological time would simply be the product of the estimated molecular timing and age at diagnosis. However, this relation will be nonlinear if the mutation rate changes over time, and is inflated by acquired mutational processes, as suggested by the analysis in the previous section. Some of these issues can be mitigated by counting only mutations contributed by endogenous and less variable mutational processes, such as CpG-to-TpG mutations (hereafter CpG>TpG) caused by spontaneous deamination of 5-methyl-cytosine to thymine at CpG dinucleotides, which have been proposed as a molecular clock 12 . Our supplementary analysis suggests that, although the baseline CpG>TpG mutation rate in cancers is very close to that in normal cells, there appears to be a moderate increase (1–10 times, adding between 20 and 40% of mutations) in cancers (Extended Data Fig. 8 ). As this shifts chronological timing estimates, we model different scenarios of the evolution of the CpG>TpG mutation rate (Fig. 5a ).

figure 5

a , Mapping of molecular timing estimates to chronological time under different scenarios of increases in the CpG>TpG mutation rate. A greater increase before diagnosis indicates an inflation of the mutation timescale. b , Median latency between WGDs and the last detectable subclone before diagnosis under different scenarios of CpG>TpG mutation rate increases for n  = 569 non-hypermutant cancers with at least 100 informative SNVs, low tumour in normal contamination and at least five samples per tumour histology. c , Median latency between the MRCA and the last detectable subclone before diagnosis for different CpG>TpG mutation rate changes in n  = 1,921 non-hypermutant samples with low tumour in normal contamination and at least 5 cases per cancer type.

Applying this logic to time WGDs, which yield sufficient numbers of CpG>TpG mutations, demonstrates that they occur several years and possibly even a decade or more before diagnosis in some cancer types, under a range of scenarios of mutation rate increase (Fig. 5b , Extended Data Fig. 9 ). A notable example is ovarian adenocarcinoma, which appears to have a median latency of more than 10 years. This holds true even under a scenario of a CpG>TpG rate increase of 20-fold, which would be far beyond the 7.5-fold rate increase observed in matched primary and relapse samples 39 (Extended Data Fig. 8f ). Notably, these results suggest WGD may occur throughout the entire female reproductive life (Extended Data Fig. 9b ). The latency between the MRCA and the last detectable subclone is shorter, typically several months to years (Fig. 5c ).

These timescales of cancer evolution are further supported by the fact that progression of most known precancerous lesions to carcinomas usually spans many years, if not decades 40 , 41 , 42 , 43 , 44 , 45 . Our data corroborate these timescales and extend them to cancer types without detectable premalignant conditions, raising the hope that these tumours could also be detected in less malignant stages.

To our knowledge, our study presents the first large-scale genome-wide reconstruction of the evolutionary history of cancers, reconstructing both early (pre-cancer) and later stages of 38 cancer types. This is facilitated by the timing of copy number gains relative to all other events in the genome, through multiplicity and clonal status of co-amplified point mutations. However, several limitations exist ( Supplementary Information ). Perhaps most importantly, molecular timing is based on point mutations and is therefore subject to changes in mutation rate. Notably, healthy tissues acquire point mutations at rates not too dissimilar from those seen in cancers, particularly when considering only endogenous mutational processes, and furthermore, some tissues are riddled with microscopic clonal expansions of driver gene mutations 5 , 6 , 7 , 8 , 9 , 11 . This is direct evidence that the life history of almost every cell in the human body, including those that develop into cancer, is driven by somatic evolution.

Together, the data presented here enable us to draw approximate timelines summarizing the typical evolutionary history of each cancer type (Fig. 6 , Supplementary Information for all other cancer types). These make use of the qualitative timing of point mutations and copy number alterations, as well as signature activities, which can be interleaved with the chronological estimates of WGD and the appearance of the MRCA.

figure 6

a – d , Timelines representing the length of time, in years, between the fertilized egg and the median age of diagnosis for colorectal adenocarcinoma ( a ), squamous cell lung cancer ( b ), ovarian adenocarcinoma ( c ) and pancreatic adenocarcinoma ( d ). Real-time estimates for major events, such as WGD and the emergence of the MRCA, are used to define early, variable, late and subclonal stages of tumour evolution approximately in chronological time. The range of chronological time estimates according to varying clock mutation acceleration rates is shown as well, with tick marks corresponding to 1×, 2.5×, 5×, 7.5×, 10× and 20×. Driver mutations and copy number alterations (CNA) are shown in each stage according to their preferential timing, as defined by relative ordering. Mutational signatures (Sigs) that, on average, change over the course of tumour evolution, or are substantially active but not changing, are shown in the epoch in which their activity is greatest. DBS, double base substitution; SBS, single base substitutions. Where applicable, lesions with a known timing from the literature are annotated; dagger symbols denotes events that were found to have a different timing; asterisk symbol denotes events that agree with our timing.

It is remarkable that the evolution of practically all cancers displays some level of order, which agrees very well with, and adds much detail to, established models of cancer progression 35 , 46 . For example, TP53 with accompanying 17p deletion is one of the most frequent initiating mutations in a variety of cancers, including ovarian cancer, in which it is the hallmark of its precancerous precursor lesions 47 . Furthermore, the list of typically early drivers includes most other highly recurrent cancer genes, such as KRAS , TERT and CDKN2A , indicating a preferred role in early and possibly even pre-cancer evolution. This initially constrained set of genes broadens at later stages of cancer development, suggesting an epistatic fitness landscape canalizing the first steps of cancer evolution. Over time, as tumours evolve, they follow increasingly diverse paths driven by individually rare driver mutations, and by copy number alternations. However, none of these trends is absolute, and the evolutionary paths of individual tumours are highly variable, showing that cancer evolution follows trends, but is far from deterministic.

Our study sheds light on the typical timescales of in vivo tumour development, with initial driver events seemingly occurring up to decades before diagnosis, demonstrating how cancer genomes are shaped by a lifelong process of somatic evolution, with fluid boundaries between normal ageing processes 5 , 6 , 7 , 8 , 9 , 10 , 11 and cancer evolution. Nevertheless, the presence of genetic aberrations with such long latency raises hopes that aberrant clones could be detected early, before reaching their full malignant potential.

The PCAWG series consists of 2,778 tumour samples (2,703 white listed, 75 grey listed) from 2,658 donors. All samples in this dataset underwent whole-genome sequencing (minimum average coverage 30× in the tumour, 25× in the matched normal samples), and were processed with a set of project-specific pipelines for alignment, variant calling, and quality control 4 . Copy number calls were established by combining the output of six individual callers into a consensus using a multi-tier approach, resulting in a copy number profile, a purity and ploidy value and whether the tumour has undergone a WGD ( Supplementary Information ). Consensus subclonal architectures have been obtained by integrating the output of 11 subclonal reconstruction callers, after which all SNVs, indels and structural variants are assigned to a mutation cluster using the MutationTimer.R approach ( Supplementary Information ). Driver calls have been defined by the PCAWG Driver Working Group 4 , and mutational signatures are defined by the PCAWG Signatures Working Group 24 . A more detailed description can be found in  Supplementary Information, section 1 .

Data accrual was based on sequencing experiments performed by individual member groups of the ICGC and TCGA, as described in an associated study 4 . As this is a meta-analysis of existing data, power calculations were not performed and the investigators were not blinded to cancer diagnoses.

Timing of gains

We used three related approaches to calculate the timing of copy number gains (see  Supplementary Information, section 2 ). In brief, the common feature is that the expected VAF of a mutation ( E ) is related to the underlying number of alleles carrying a mutation according to the formula: E [ X ] =  nmfρ /[ N (1 −  ρ ) +  Cρ ], in which X is the number of reads, n denotes the coverage of the locus, the mutation copy number m is the number of alleles carrying the mutation (which is usually inferred), f is the frequency of the clone carrying the given mutation ( f  = 1 for clonal mutations). N is the normal copy number (2 on autosomes, 1 or 2 for chromosome X and 0 or 1 for chromosome Y), C is the total copy number of the tumour, and ρ is the purity of the sample.

The number of mutations n m  at each allelic copy number m  then informs about the time when the gain has occurred. The basic formulae for timing each gain are, depending on the copy number configuration:

in which 2 + 1 refers to major and minor copy number of 2 and 1, respectively. Methods differ slightly in how the number of mutations present on each allele are calculated and how uncertainty is handled ( Supplementary Information ).

Timing of mutations

The mutation copy number m and the clonal frequency f is calculated according to the principles indicated above. Details can be found in  Supplementary Information, section 2 . Mutations with f  = 1 are denoted as ‘clonal’, and mutations with f < 1 as ‘subclonal’. Mutations with f  = 1 and m > 1 are denoted as ‘early clonal’ (co-amplified). In cases with f  = 1, m  = 1 and C > 2, mutations were annotated as ‘late clonal’, if the minor copy number was 0, otherwise ‘clonal’ (unspecified).

Timing of driver mutations

A catalogue of driver point mutations (SNVs and indels) was provided by the PCAWG Drivers and Functional Interpretation Group 4 . The timing category was calculated as above. From the four timing categories, the odds ratios of early/late clonal and clonal (early, late or unspecified clonal)/subclonal were calculated for driver mutations against the distribution of all other mutations present in fragments with the same copy number composition in the samples with each particular driver. The background distribution of these odds ratios was assessed with 1,000 bootstraps ( Supplementary Information, section 4.1 ).

Integrative timing

For each pair of driver point mutations and recurrent copy number alterations, an ordering was established (earlier, later or unspecified). The information underlying this decision was derived from the timing of each driver point mutation, as well as from the timing status of clonal and subclonal copy number segments. These tables were aggregated across all samples and a sports statistics model was employed to calculate the overall ranking of driver mutations. A full description is given in  Supplementary Information, section 4.2 .

Mutational trinucleotide substitution signatures, as defined by the PCAWG Mutational Signatures Working Group 24 , were fit to samples with observed signature activity, after splitting point mutations into either of the four epochs. A likelihood ratio test based on the multinomial distribution was used to test for differences in the mutation spectra between time points. Time-resolved exposures were calculated using non-negative linear least squares. Full details are given in Supplementary Information, section 5 .

Real-time estimation of WGD and MRCA

CpG>TpG mutations were counted in an NpCpG context, except for skin–melanoma, in which CpCpG and TpCpG were excluded owing to the overlapping UV mutation spectrum. For visual comparison, the number of mutations was scaled to the effective genome size, defined as the 1/mean( m i / C i ), in which m i is the estimated number of allelic copies of each mutation, and C i is the total copy number at that locus, thereby scaling to the final copy number and the time of change.

A hierarchical Bayesian linear regression was fit to relate the age at diagnosis to the scaled number of mutations, ensuring positive slope and intercept through a shared gamma distribution across cancer types.

For tumours with several time points, the set of mutations shared between diagnosis and relapse ( n D ) and those specific to the relapse ( n R ) was calculated. The rate acceleration was calculated as: a  =  n R / n D  ×  t D / t R . This analysis was performed separately for all substitutions and for CpG>TpG mutations.

On the basis of these analyses, a typical increase of 5× for most cancer types was chosen, with a lower value of 2.5× for brain cancers and a value of 7.5× for ovarian cancer.

The correction for transforming an estimate of a copy number gain in mutation time into chronological time depends not only on the rate acceleration, but also on the time at which this acceleration occurred. As this is generally unknown, we performed Monte Carlo simulations of rate accelerations spanning an interval of 15 years before diagnosis, corresponding roughly to 25% of time for a diagnosis at 60 years of age, noting that a 5× rate increase over this duration yields an offset of about 33% of mutations, compatible with our data. Subclonal mutations were assumed to occur at full acceleration. The proportion of subclonal mutations was divided by the number of identified subclones, thus conservatively assuming branching evolution. Full details are given in  Supplementary Information, section 6 .

Cancer timelines

The results from each of the different timing analyses are combined in timelines of cancer evolution for each tumour type (Fig. 6 and Supplementary Information ). Each timeline begins at the fertilized egg, and spans up to the median age of diagnosis within each cohort. Real-time estimates for WGD and the MRCA act as anchor points, allowing us to roughly map the four broadly defined time periods (early clonal, intermediate, late clonal and subclonal) to chronological time during a patient’s lifespan. Specific driver mutations or copy number alterations can be placed within each of these time frames based on their ordering from the league model analysis. Signatures are shown if they typically change over time (95% confidence intervals of mean change not overlapping 0), and if they are strongly active (contributing at least 10% mutations to one time point). Signatures are shown on the timeline in the epoch of their greatest activity. Where an event found in our study has a known timing in the literature, the agreement is annotated on the timeline; with an asterisk denoting an agreed timing, and dagger symbol denoting a timing that is different to our results. Full details are given in  Supplementary Information, section 7 .

Reporting summary

Further information on research design is available in the  Nature Research Reporting Summary linked to this paper.

Data availability

Somatic and germline variant calls, mutational signatures, subclonal reconstructions, transcript abundance, splice calls and other core data generated by the ICGC/TCGA PCAWG Consortium are described elsewhere 4 and available for download at https://dcc.icgc.org/releases/PCAWG . Further information on accessing the data, including raw read files, can be found at https://docs.icgc.org/pcawg/data/ . In accordance with the data access policies of the ICGC and TCGA projects, most molecular, clinical and specimen data are in an open tier that does not require access approval. To access information that could potentially identify participants, such as germline alleles and underlying sequencing data, researchers will need to apply to the TCGA Data Access Committee (DAC) via dbGaP ( https://dbgap.ncbi.nlm.nih.gov/aa/wga.cgi?page=login ) for access to the TCGA portion of the dataset, and to the ICGC Data Access Compliance Office (DACO; http://icgc.org/daco ) for the ICGC portion. In addition, to access somatic SNVs derived from TCGA donors, researchers will also need to obtain dbGaP authorization. Datasets used and results presented in this study, including timing estimates for copy number gains, chronological estimates of WGD and MRCA, as well as mutation signature changes, are described in  Supplementary Note 3 and are available at https://dcc.icgc.org/releases/PCAWG/evolution-heterogeneity .

Code availability

The core computational pipelines used by the PCAWG Consortium for alignment, quality control and variant calling are available to the public at https://dockstore.org/search?search=pcawg under the GNU General Public License v3.0, which allows for reuse and distribution. Analysis code presented in this study is available through the GitHub repository https://github.com/PCAWG-11/Evolution . This archive contains relevant software and analysis workflows as submodules, which include code for timing copy number gains, point mutations and mutation signatures, real-time timing and evolutionary league model analysis, as well as scripts to generate the figures presented: CancerTiming (v.3.1.8), MutationTimeR (v.0.1), PhylogicNDT (v.1.1) and a series of custom scripts (v. 1.0), with detailed versions of other packages used.

Change history

25 january 2023.

A Correction to this paper has been published: https://doi.org/10.1038/s41586-022-05601-4

Cairns, J. Mutation selection and the natural history of cancer. Nature 255 , 197–200 (1975).

Article   ADS   CAS   Google Scholar  

Martincorena, I. & Campbell, P. J. Somatic mutation in cancer and normal cells. Science 349 , 1483–1489 (2015).

Nik-Zainal, S. et al. The life history of 21 breast cancers. Cell 149 , 994–1007 (2012).

Article   CAS   Google Scholar  

The ICGC/TCGA Pan-Cancer Analysis of Whole Genomes Consortium. Pan-cancer analysis of whole genomes. Nature https://doi.org/10.1038/s41586-020-1969-6 (2020).

Moore, L. et al. The mutational landscape of normal human endometrial epithelium. Preprint at bioRxiv https://doi.org/10.1101/505685 (2018).

Lee-Six, H. et al. The landscape of somatic mutation in normal colorectal epithelial cells. Nature 574 , 532–537 (2019).

Lee-Six, H. et al. Population dynamics of normal human blood inferred from somatic mutations. Nature 561 , 473–478 (2018).

Martincorena, I. et al. Somatic mutant clones colonize the human esophagus with age. Science 362 , 911–917 (2018).

Martincorena, I. et al. High burden and pervasive positive selection of somatic mutations in normal human skin. Science 348 , 880–886 (2015).

Welch, J. S. et al. The origin and evolution of mutations in acute myeloid leukemia. Cell 150 , 264–278 (2012).

Yokoyama, A. et al. Age-related remodelling of oesophageal epithelia by mutated cancer drivers. Nature 565 , 312–317 (2019).

Alexandrov, L. B. et al. Clock-like mutational processes in human somatic cells. Nat. Genet . 47 , 1402–1407 (2015).

Nowell, P. C. The clonal evolution of tumor cell populations. Science 194 , 23–28 (1976).

Durinck, S. et al. Temporal dissection of tumorigenesis in primary cancers. Cancer Discov . 1 , 137–143 (2011).

Jolly, C. & Van Loo, P. Timing somatic events in the evolution of cancer. Genome Biol . 19 , 95 (2018).

Article   Google Scholar  

Mitchell, T. J. et al. Timing the landmark events in the evolution of clear cell renal cell cancer: TRACERx Renal. Cell 173 , 611–623 (2018).

Gerlinger, M. et al. Intratumor heterogeneity and branched evolution revealed by multiregion sequencing. N. Engl. J. Med . 366 , 883–892 (2012).

Gundem, G. et al. The evolutionary history of lethal metastatic prostate cancer. Nature 520 , 353–357 (2015).

Yates, L. R. et al. Subclonal diversification of primary breast cancer revealed by multiregion sequencing. Nat. Med . 21 , 751–759 (2015).

Brastianos, P. K. et al. Genomic characterization of brain metastases reveals branched evolution and potential therapeutic targets. Cancer Discov . 5 , 1164–1177 (2015).

Papaemmanuil, E. et al. Clinical and biological implications of driver mutations in myelodysplastic syndromes. Blood 122 , 3616–3627 (2013).

Landau, D. A. et al. Mutations driving CLL and their evolution in progression and relapse. Nature 526 , 525–530 (2015).

Rheinbay, E. et al. Analyses of non-coding somatic drivers in 2,658 cancer whole genomes. Nature https://doi.org/10.1038/s41586-020-1965-x (2020).

Alexandrov, L. B. The repertoire of mutational signatures in human cancer. Nature https://doi.org/10.1038/s41586-020-1943-3 (2020).

Keogh, M. J. et al. High prevalence of focal and multi-focal somatic genetic variants in the human brain. Nat. Commun . 9 , 4257 (2018).

Article   ADS   Google Scholar  

Heim, S. et al. Trisomy 7 and sex chromosome loss in human brain tissue. Cytogenet. Cell Genet . 52 , 136–138 (1989).

Ganem, N. J., Godinho, S. A. & Pellman, D. A mechanism linking extra centrosomes to chromosomal instability. Nature 460 , 278–282 (2009).

Sheltzer, J. M. et al. Single-chromosome gains commonly function as tumor suppressors. Cancer Cell 31 , 240–255 (2017).

Gao, R. et al. Punctuated copy number evolution and clonal stasis in triple-negative breast cancer. Nat. Genet . 48 , 1119–1130 (2016).

Cross, W. et al. The evolutionary landscape of colorectal tumorigenesis. Nat. Ecol. Evol. 2 , 1661–1672 (2018).

Gerlinger, M. et al. Genomic architecture and evolution of clear cell renal cell carcinomas defined by multiregion sequencing. Nat. Genet . 46 , 225–233 (2014).

Gibson, W. J. et al. The genomic landscape and evolution of endometrial carcinoma progression and abdominopelvic metastasis. Nat. Genet . 48 , 848–855 (2016).

Yates, L. R. et al. Genomic evolution of breast cancer metastasis and relapse. Cancer Cell 32 , 169–184 (2017).

Jamal-Hanjani, M. et al. Tracking the evolution of non-small-cell lung cancer. N. Engl. J. Med . 376 , 2109–2121 (2017).

Fearon, E. R. & Vogelstein, B. A genetic model for colorectal tumorigenesis. Cell 61 , 759–767 (1990).

Alexandrov, L. B. et al. Signatures of mutational processes in human cancer. Nature 500 , 415–421 (2013).

McGranahan, N. et al. Clonal status of actionable driver events and the timing of mutational processes in cancer evolution. Sci. Transl. Med . 7 , 283ra54 (2015).

Rosenthal, R., McGranahan, N., Herrero, J., Taylor, B. S. & Swanton, C. DeconstructSigs: delineating mutational processes in single tumors distinguishes DNA repair deficiencies and patterns of carcinoma evolution. Genome Biol . 17 , 31 (2016).

Patch, A.-M. et al. Whole-genome characterization of chemoresistant ovarian cancer. Nature 521 , 489–494 (2015).

Bostwick, D. G. & Qian, J. High-grade prostatic intraepithelial neoplasia. Mod. Pathol . 17 , 360–379 (2004).

Brenner, H. et al. Risk of progression of advanced adenomas to colorectal cancer by age and sex: estimates based on 840,149 screening colonoscopies. Gut 56 , 1585–1589 (2007).

Gazdar, A. F. & Brambilla, E. Preneoplasia of lung cancer. Cancer Biomark . 9 , 385–396 (2010).

Sanders, M. E., Schuyler, P. A., Dupont, W. D. & Page, D. L. The natural history of low-grade ductal carcinoma in situ of the breast in women treated by biopsy only revealed over 30 years of long-term follow-up. Cancer 103 , 2481–2484 (2005).

Schlecht, N. F. et al. Human papillomavirus infection and time to progression and regression of cervical intraepithelial neoplasia. J. Natl. Cancer Inst . 95 , 1336–1343 (2003).

Whitson, M. J. & Falk, G. W. Predictors of progression to high-grade dysplasia or adenocarcinoma in Barrett’s esophagus. Gastroenterol. Clin. North Am . 44 , 299–315 (2015).

Bardeesy, N. & DePinho, R. A. Pancreatic cancer biology and genetics. Nat. Rev. Cancer 2 , 897–909 (2002).

Folkins, A. K. et al. A candidate precursor to pelvic serous cancer (p53 signature) and its prevalence in ovaries and fallopian tubes from women with BRCA mutations. Gynecol. Oncol . 109 , 168–173 (2008).

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Acknowledgements

We thank H. Lee-Six and L. Moore for sharing data on mutation burden in normal tissues. This work was supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK (FC001202), the UK Medical Research Council (FC001202) and the Wellcome Trust (FC001202). This project was enabled through the Crick Scientific Computing STP and through access to the MRC eMedLab Medical Bioinformatics infrastructure, supported by the Medical Research Council (grant number MR/L016311/1). M.T. and J.D. are postdoctoral fellows supported by the European Union’s Horizon 2020 research and innovation program (Marie Skłodowska-Curie grant agreement number 747852-SIOMICS and 703594-DECODE). J.D. is a postdoctoral fellow of the FWO. F.M., G.M. and K. Yuan acknowledge the support of the University of Cambridge, Cancer Research UK and Hutchison Whampoa Limited. G.M., K. Yuan and F.M. were funded by CRUK core grants C14303/A17197 and A19274. S. Sengupta and Y.J. are supported by NIH R01 CA132897. S.M. is supported by the Vanier Canada Graduate Scholarship. S.C.S. is supported by the NSERC Discovery Frontiers Project, “The Cancer Genome Collaboratory” and NIH Grant GM108308. H.Z. is supported by grant NIMH086633 and an endowed Bao-Shan Jing Professorship in Diagnostic Imaging. W.W. is supported by the US National Cancer Institute (1R01 CA183793 and P30 CA016672). P.T.S. was supported by U24CA210957 and 1U24CA143799. D.C.W. is funded by the Li Ka Shing foundation. P.V.L. is a Winton Group Leader in recognition of the Winton Charitable Foundation’s support towards the establishment of The Francis Crick Institute. We acknowledge the contributions of the many clinical networks across ICGC and TCGA who provided samples and data to the PCAWG Consortium, and the contributions of the Technical Working Group and the Germline Working Group of the PCAWG Consortium for collation, realignment and harmonized variant calling of the cancer genomes used in this study. We thank the patients and their families for their participation in the individual ICGC and TCGA projects.

Author information

These authors contributed equally: Moritz Gerstung, Clemency Jolly, Ignaty Leshchiner, Stefan C. Dentro, Santiago Gonzalez

These authors jointly supervised this work: Paul T. Spellman, David C. Wedge, Peter Van Loo

A list of members and their affiliations appears at the end of the paper

A list of members and their affiliations appears online

Authors and Affiliations

European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Cambridge, UK

Moritz Gerstung, Santiago Gonzalez, Lara Jerman, Moritz Gerstung, Santiago Gonzalez & Lara Jerman

European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany

Moritz Gerstung & Moritz Gerstung

Wellcome Sanger Institute, Cambridge, UK

Moritz Gerstung, Stefan C. Dentro, Thomas J. Mitchell, Maxime Tarabichi, Ignacio Vázquez-García, Stefan C. Dentro, Moritz Gerstung, Maxime Tarabichi, David J. Adams, Peter J. Campbell, Kevin J. Dawson, Henry Lee-Six, Inigo Martincorena, Thomas J. Mitchell & Ignacio Vázquez-García

The Francis Crick Institute, London, UK

Clemency Jolly, Stefan C. Dentro, Maxime Tarabichi, Kerstin Haase, Jonas Demeulemeester, Stefan C. Dentro, Clemency Jolly, Kerstin Haase, Maxime Tarabichi, Jonas Demeulemeester, Matthew Fittall, Peter Van Loo & Peter Van Loo

Broad Institute of MIT and Harvard, Cambridge, MA, USA

Ignaty Leshchiner, Daniel Rosebrock, Dimitri G. Livitz, Steven Schumacher, Gad Getz, Rameen Beroukhim, Ignaty Leshchiner, Rameen Beroukhim, Gad Getz, Gavin Ha, Dimitri G. Livitz, Daniel Rosebrock, Steven Schumacher & Oliver Spiro

Big Data Institute, University of Oxford, Oxford, UK

Stefan C. Dentro, Stefan C. Dentro, David C. Wedge & David C. Wedge

University of Cambridge, Cambridge, UK

Thomas J. Mitchell, Ignacio Vázquez-García, Thomas J. Mitchell & Ignacio Vázquez-García

University of Toronto, Toronto, Ontario, Canada

Yulia Rubanova, Amit Deshwar, Jeff Wintersinger, Paul C. Boutros, Quaid D. Morris, Jeff Wintersinger, Amit G. Deshwar, Yulia Rubanova, Paul C. Boutros, Ruian Shi, Shankar Vembu & Quaid D. Morris

Vector Institute, Toronto, Ontario, Canada

Yulia Rubanova, Amit Deshwar, Jeff Wintersinger, Quaid D. Morris, Jeff Wintersinger, Amit G. Deshwar, Yulia Rubanova & Quaid D. Morris

Molecular and Medical Genetics, Oregon Health & Science University, Portland, OR, USA

Pavana Anur, Pavana Anur, Myron Peto, Paul T. Spellman & Paul T. Spellman

The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Kaixian Yu, Yu Fan, Hongtu Zhu, Wenyi Wang, Kaixian Yu, Shaolong Cao, Yu Fan, Seung Jun Shin, Hongtu Zhu & Wenyi Wang

German Cancer Research Center (DKFZ), Heidelberg, Germany

Kortine Kleinheinz, Matthias Schlesner, Roland Eils, Kortine Kleinheinz & Matthias Schlesner

Heidelberg University, Heidelberg, Germany

Kortine Kleinheinz, Roland Eils & Kortine Kleinheinz

University of Ljubljana, Ljubljana, Slovenia

Lara Jerman & Lara Jerman

NorthShore University HealthSystem, Evanston, IL, USA

Subhajit Sengupta, Yuan Ji, Yuan Ji & Subhajit Sengupta

Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK

Geoff Macintyre, Florian Markowetz, Ke Yuan, Geoff Macintyre, Ruben M. Drews, Florian Markowetz & Ke Yuan

Simon Fraser University, Burnaby, British Columbia, Canada

Salem Malikic, Nilgun Donmez, Nilgun Donmez & Salem Malikic

Vancouver Prostate Centre, Vancouver, British Columbia, Canada

Salem Malikic, Nilgun Donmez, S. Cenk Sahinalp, Nilgun Donmez, Salem Malikic & S. Cenk Sahinalp

University of Melbourne, Melbourne, Victoria, Australia

Marek Cmero, Elizabeth L. Christie, Marek Cmero & Dale W. Garsed

Walter and Eliza Hall Institute, Melbourne, Victoria, Australia

Marek Cmero & Marek Cmero

University of Leuven, Leuven, Belgium

Jonas Demeulemeester, Jonas Demeulemeester, Peter Van Loo & Peter Van Loo

Weill Cornell Medicine, New York, NY, USA

Xiaotong Yao, Marcin Imielinski, Marcin Imielinski & Xiaotong Yao

New York Genome Center, New York, NY, USA

University of California Santa Cruz, Santa Cruz, CA, USA

Juhee Lee & Juhee Lee

Ontario Institute for Cancer Research, Toronto, Ontario, Canada

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University of California, Los Angeles, CA, USA

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Indiana University, Bloomington, IN, USA

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The University of Chicago, Chicago, IL, USA

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University of Cologne, Cologne, Germany

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University of Helsinki, Helsinki, Finland

Ville Mustonen & Ville Mustonen

University of Glasgow, Glasgow, UK

Ke Yuan & Ke Yuan

Oxford NIHR Biomedical Research Centre, Oxford, UK

David C. Wedge & David C. Wedge

Department of Computer Science, Carleton College, Northfield, MN, USA

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Department of Computer Science, Princeton University, Princeton, NJ, USA

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Korea University, Seoul, South Korea

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Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX, USA

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Applied Tumor Genomics Research Program, Research Programs Unit, University of Helsinki, Helsinki, Finland

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The McDonnell Genome Institute at Washington University, St. Louis, MO, USA

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Department of Veterinary Medicine, Transmissible Cancer Group, University of Cambridge, Cambridge, UK

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Stephan H. Bernhart, Hans Binder, Steve Hoffmann & Peter F. Stadler

Interdisciplinary Center for Bioinformatics, University of Leipzig, Leipzig, Germany

Stephan H. Bernhart, Hans Binder, Steve Hoffmann, Helene Kretzmer & Peter F. Stadler

Transcriptome Bioinformatics, LIFE Research Center for Civilization Diseases, University of Leipzig, Leipzig, Germany

Stephan H. Bernhart, Steve Hoffmann, Helene Kretzmer & Peter F. Stadler

Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA

Rameen Beroukhim, Angela N. Brooks, Susan Bullman, Andrew D. Cherniack, Levi Garraway, Matthew Meyerson, Chandra Sekhar Pedamallu, Steven E. Schumacher, Juliann Shih & Jeremiah A. Wala

Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA

Rameen Beroukhim, Aquila Fatima, Andrea L. Richardson, Steven E. Schumacher, Ofer Shapira, Andrew Tutt & Jeremiah A. Wala

Rameen Beroukhim, Gad Getz, Kirsten Kübler, Matthew Meyerson, Chandra Sekhar Pedamallu, Paz Polak, Esther Rheinbay & Jeremiah A. Wala

USC Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA

Mario Berrios, Moiz S. Bootwalla, Andrea Holbrook, Phillip H. Lai, Dennis T. Maglinte, David J. Van Den Berg & Daniel J. Weisenberger

Department of Diagnostics and Public Health, University and Hospital Trust of Verona, Verona, Italy

Samantha Bersani, Ivana Cataldo, Claudio Luchini & Maria Scardoni

Department of Mathematics, Aarhus University, Aarhus, Denmark

Johanna Bertl & Asger Hobolth

Department of Molecular Medicine (MOMA), Aarhus University Hospital, Aarhus N, Denmark

Johanna Bertl, Henrik Hornshøj, Malene Juul, Randi Istrup Juul, Tobias Madsen, Morten Muhlig Nielsen & Jakob Skou Pedersen

Instituto Carlos Slim de la Salud, Mexico City, Mexico

Miguel Betancourt

Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada

Vinayak Bhandari, Paul C. Boutros, Robert G. Bristow, Keren Isaev, Constance H. Li, Jüri Reimand, Michael H. A. Roehrl & Bradly G. Wouters

Cancer Division, Garvan Institute of Medical Research, Kinghorn Cancer Centre, University of New South Wales (UNSW Sydney), Sydney, NSW, Australia

Andrew V. Biankin, David K. Chang, Lorraine A. Chantrill, Angela Chou, Anthony J. Gill, Amber L. Johns, James G. Kench, David K. Miller, Adnan M. Nagrial, Marina Pajic, Mark Pinese, Ilse Rooman, Christopher J. Scarlett, Christopher W. Toon & Jianmin Wu

South Western Sydney Clinical School, Faculty of Medicine, University of New South Wales (UNSW Sydney), Liverpool, NSW, Australia

Andrew V. Biankin

West of Scotland Pancreatic Unit, Glasgow Royal Infirmary, Glasgow, UK

Andrew V. Biankin & Nigel B. Jamieson

Center for Digital Health, Berlin Institute of Health and Charitè - Universitätsmedizin Berlin, Berlin, Germany

Matthias Bieg

Heidelberg Center for Personalized Oncology (DKFZ-HIPO), German Cancer Research Center (DKFZ), Heidelberg, Germany

Matthias Bieg, Ivo Buchhalter, Barbara Hutter & Nagarajan Paramasivam

The Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, NC, USA

Darell Bigner

Massachusetts General Hospital, Boston, MA, USA

Michael Birrer, Vikram Deshpande, William C. Faquin, Nicholas J. Haradhvala, Kirsten Kübler, Michael S. Lawrence, David N. Louis, Yosef E. Maruvka, G. Petur Nielsen, Esther Rheinbay, Mara Rosenberg, Dennis C. Sgroi & Chin-Lee Wu

National Institute of Biomedical Genomics, Kalyani, West Bengal, India

Nidhan K. Biswas, Arindam Maitra & Partha P. Majumder

Institute of Clinical Medicine and Institute of Oral Biology, University of Oslo, Oslo, Norway

Bodil Bjerkehagen

University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Lori Boice, Mei Huang, Sonia Puig & Leigh B. Thorne

ARC-Net Centre for Applied Research on Cancer, University and Hospital Trust of Verona, Verona, Italy

Giada Bonizzato, Cinzia Cantù, Ivana Cataldo, Vincenzo Corbo, Sonia Grimaldi, Rita T. Lawlor, Andrea Mafficini, Borislav C. Rusev, Aldo Scarpa, Katarzyna O. Sikora, Nicola Sperandio, Alain Viari & Caterina Vicentini

The Institute of Cancer Research, London, UK

Johann S. De Bono, Niedzica Camacho, Colin S. Cooper, Sandra E. Edwards, Rosalind A. Eeles, Zsofia Kote-Jarai, Daniel A. Leongamornlert, Lucy Matthews & Sue Merson

Centre for Computational Biology, Duke-NUS Medical School, Singapore, Singapore

Arnoud Boot, Ioana Cutcutache, Mi Ni Huang, John R. McPherson, Steven G. Rozen & Yang Wu

Programme in Cancer and Stem Cell Biology, Duke-NUS Medical School, Singapore, Singapore

Arnoud Boot, Ioana Cutcutache, Mi Ni Huang, John R. McPherson, Steven G. Rozen, Patrick Tan, Bin Tean Teh & Yang Wu

Division of Oncology and Pathology, Department of Clinical Sciences Lund, Lund University, Lund, Sweden

Ake Borg, Markus Ringnér & Johan Staaf

Department of Pediatric Oncology, Hematology and Clinical Immunology, Heinrich-Heine-University, Düsseldorf, Germany

Arndt Borkhardt & Jessica I. Hoell

Laboratory for Medical Science Mathematics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan

Keith A. Boroevich, Todd A. Johnson, Michael S. Lawrence & Tatsuhiko Tsunoda

RIKEN Center for Integrative Medical Sciences, Yokohama, Japan

Keith A. Boroevich, Akihiro Fujimoto, Masashi Fujita, Mayuko Furuta, Kazuhiro Maejima, Hidewaki Nakagawa, Kaoru Nakano & Aya Sasaki-Oku

Department of Internal Medicine/Hematology, Friedrich-Ebert-Hospital, Neumünster, Germany

Christoph Borst & Siegfried Haas

Departments of Dermatology and Pathology, Yale University, New Haven, CT, USA

Marcus Bosenberg

Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain

Mattia Bosio, German M. Demidov, Oliver Drechsel, Georgia Escaramis, Xavier Estivill, Aliaksei Z. Holik, Francesc Muyas, Stephan Ossowski, Raquel Rabionet & Hana Susak

Radcliffe Department of Medicine, University of Oxford, Oxford, UK

Jacqueline Boultwood

Canadian Center for Computational Genomics, McGill University, Montreal, QC, Canada

Guillaume Bourque

Department of Human Genetics, McGill University, Montreal, QC, Canada

Guillaume Bourque, Mark Lathrop & Yasser Riazalhosseini

Department of Human Genetics, University of California Los Angeles, Los Angeles, CA, USA

Paul C. Boutros

Department of Pharmacology, University of Toronto, Toronto, ON, Canada

Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland

G. Steven Bova & Tapio Visakorpi

Haematology, Leeds Teaching Hospitals NHS Trust, Leeds, UK

David T. Bowen

Translational Research and Innovation, Centre Léon Bérard, Lyon, France

Sandrine Boyault

Fox Chase Cancer Center, Philadelphia, PA, USA

Jeffrey Boyd & Elaine R. Mardis

International Agency for Research on Cancer, World Health Organization, Lyon, France

Paul Brennan & Ghislaine Scelo

Earlham Institute, Norwich, UK

Daniel S. Brewer & Colin S. Cooper

Norwich Medical School, University of East Anglia, Norwich, UK

Department of Molecular Biology, Faculty of Science, Radboud Institute for Molecular Life Sciences, Radboud University, Nijmegen, HB, The Netherlands

Arie B. Brinkman

CRUK Manchester Institute and Centre, Manchester, UK

Robert G. Bristow

Department of Radiation Oncology, University of Toronto, Toronto, ON, Canada

Division of Cancer Sciences, Manchester Cancer Research Centre, University of Manchester, Manchester, UK

Radiation Medicine Program, Princess Margaret Cancer Centre, Toronto, ON, Canada

Robert G. Bristow & Fei-Fei Fei Liu

Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

Jane E. Brock & Sabina Signoretti

Department of Surgery, Division of Thoracic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA

Malcolm Brock

Division of Molecular Pathology, The Netherlands Cancer Institute, Oncode Institute, Amsterdam, CX, The Netherlands

Annegien Broeks & Jos Jonkers

Department of Biomolecular Engineering, University of California Santa Cruz, Santa Cruz, CA, USA

Angela N. Brooks, David Haan, Maximillian G. Marin, Thomas J. Matthew, Yulia Newton, Cameron M. Soulette & Joshua M. Stuart

UC Santa Cruz Genomics Institute, University of California Santa Cruz, Santa Cruz, CA, USA

Angela N. Brooks, Brian Craft, Mary J. Goldman, David Haussler, Joshua M. Stuart & Jingchun Zhu

Division of Applied Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany

Benedikt Brors, Lars Feuerbach, Chen Hong, Charles David Imbusch & Lina Sieverling

German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany

Benedikt Brors, Barbara Hutter, Peter Lichter, Dirk Schadendorf & Holger Sültmann

National Center for Tumor Diseases (NCT) Heidelberg, Heidelberg, Germany

Benedikt Brors, Barbara Hutter, Holger Sültmann & Thorsten Zenz

Center for Biological Sequence Analysis, Department of Bio and Health Informatics, Technical University of Denmark, Lyngby, Denmark

Søren Brunak

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, Copenhagen, Denmark

Institute for Molecular Bioscience, University of Queensland, St. Lucia, Brisbane, QLD, Australia

Timothy J. C. Bruxner, Oliver Holmes, Stephen H. Kazakoff, Conrad R. Leonard, Felicity Newell, Katia Nones, Ann-Marie Patch, John V. Pearson, Michael C. Quinn, Nick M. Waddell, Nicola Waddell, Scott Wood & Qinying Xu

Biomedical Engineering, Oregon Health and Science University, Portland, OR, USA

Alex Buchanan & Kyle Ellrott

Division of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany

Ivo Buchhalter, Calvin Wing Yiu Chan, Roland Eils, Michael C. Heinold, Carl Herrmann, Natalie Jäger, Rolf Kabbe, Jules N. A. Kerssemakers, Kortine Kleinheinz, Nagarajan Paramasivam, Manuel Prinz, Matthias Schlesner & Johannes Werner

Institute of Pharmacy and Molecular Biotechnology and BioQuant, Heidelberg University, Heidelberg, Germany

Ivo Buchhalter, Roland Eils, Michael C. Heinold, Carl Herrmann, Daniel Hübschmann, Kortine Kleinheinz & Umut H. Toprak

Federal Ministry of Education and Research, Berlin, Germany

Christiane Buchholz

Melanoma Institute Australia, University of Sydney, Sydney, NSW, Australia

Hazel Burke, Ricardo De Paoli-Iseppi, Nicholas K. Hayward, Peter Hersey, Valerie Jakrot, Hojabr Kakavand, Georgina V. Long, Graham J. Mann, Robyn P. M. Saw, Richard A. Scolyer, Ping Shang, Andrew J. Spillane, Jonathan R. Stretch, John F. F. Thompson & James S. Wilmott

Pediatric Hematology and Oncology, University Hospital Muenster, Muenster, Germany

Birgit Burkhardt

Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

Kathleen H. Burns & Christopher Umbricht

McKusick-Nathans Institute of Genetic Medicine, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University School of Medicine, Baltimore, MD, USA

Kathleen H. Burns

Foundation Medicine, Inc, Cambridge, MA, USA

John Busanovich

Department of Biomedical Data Science, Stanford University School of Medicine, Stanford, CA, USA

Carlos D. Bustamante & Francisco M. De La Vega

Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA

Carlos D. Bustamante, Francisco M. De La Vega, Suyash S. Shringarpure, Nasa Sinnott-Armstrong & Mark H. Wright

Bakar Computational Health Sciences Institute and Department of Pediatrics, University of California, San Francisco, CA, USA

Atul J. Butte & Jieming Chen

Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway

Anne-Lise Børresen-Dale

National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Samantha J. Caesar-Johnson, John A. Demchok, Ina Felau, Roy Tarnuzzer, Zhining Wang, Liming Yang, Jean C. Zenklusen & Jiashan Zhang

Royal Marsden NHS Foundation Trust, London and Sutton, UK

Declan Cahill, Nening M. Dennis, Tim Dudderidge, Rosalind A. Eeles, Cyril Fisher, Steven Hazell, Vincent Khoo, Pardeep Kumar, Naomi Livni, Erik Mayer, David Nicol, Christopher Ogden, Edward W. Rowe, Sarah Thomas, Alan Thompson & Nicholas van As

Genome Biology Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany

Claudia Calabrese, Serap Erkek, Moritz Gerstung, Santiago Gonzalez, Nina Habermann, Wolfgang Huber, Lara Jerman, Jan O. Korbel, Esa Pitkänen, Benjamin Raeder, Tobias Rausch, Vasilisa A. Rudneva, Oliver Stegle, Stephanie Sungalee, Lara Urban, Sebastian M. Waszak, Joachim Weischenfeldt & Sergei Yakneen

Department of Oncology, University of Cambridge, Cambridge, UK

Carlos Caldas & Suet-Feung Chin

Li Ka Shing Centre, Cancer Research UK Cambridge Institute, University of Cambridge, Cambridge, UK

Carlos Caldas, Suet-Feung Chin, Ruben M. Drews, Paul A. Edwards, Matthew Eldridge, Steve Hawkins, Andy G. Lynch, Geoff Macintyre, Florian Markowetz, Charlie E. Massie, David E. Neal, Simon Tavaré & Ke Yuan

Institut Gustave Roussy, Villejuif, France

Fabien Calvo

Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

Peter J. Campbell, Vincent J. Gnanapragasam, William Howat, Thomas J. Mitchell, David E. Neal, Nimish C. Shah & Anne Y. Warren

Department of Haematology, University of Cambridge, Cambridge, UK

Peter J. Campbell

Anatomia Patológica, Hospital Clinic, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain

Elias Campo

Spanish Ministry of Science and Innovation, Madrid, Spain

University of Michigan Comprehensive Cancer Center, Ann Arbor, MI, USA

Thomas E. Carey

Department for BioMedical Research, University of Bern, Bern, Switzerland

Joana Carlevaro-Fita

Department of Medical Oncology, Inselspital, University Hospital and University of Bern, Bern, Switzerland

Joana Carlevaro-Fita, Rory Johnson & Andrés Lanzós

Graduate School for Cellular and Biomedical Sciences, University of Bern, Bern, Switzerland

Joana Carlevaro-Fita & Andrés Lanzós

University of Pavia, Pavia, Italy

Mario Cazzola & Luca Malcovati

University of Alabama at Birmingham, Birmingham, AL, USA

Robert Cerfolio

UHN Program in BioSpecimen Sciences, Toronto General Hospital, Toronto, ON, Canada

Dianne E. Chadwick, Sheng-Ben Liang, Michael H. A. Roehrl & Sagedeh Shahabi

Department of Urology, Icahn School of Medicine at Mount Sinai, New York, NY, USA

Dimple Chakravarty

Centre for Law and Genetics, University of Tasmania, Sandy Bay Campus, Hobart, TAS, Australia

Don Chalmers

Faculty of Biosciences, Heidelberg University, Heidelberg, Germany

Calvin Wing Yiu Chan, Chen Hong & Lina Sieverling

Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada

Division of Anatomic Pathology, Mayo Clinic, Rochester, MN, USA

Vishal S. Chandan

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Stephen J. Chanock, Xing Hua, Lisa Mirabello, Lei Song & Bin Zhu

Illawarra Shoalhaven Local Health District L3 Illawarra Cancer Care Centre, Wollongong Hospital, Wollongong, NSW, Australia

Lorraine A. Chantrill

BioForA, French National Institute for Agriculture, Food, and Environment (INRAE), ONF, Orléans, France

Aurélien Chateigner

Department of Biostatistics, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA

Nilanjan Chatterjee

University of California San Diego, San Diego, CA, USA

Zhaohong Chen, Michelle T. Dow, Claudiu Farcas, S. M. Ashiqul Islam, Antonios Koures, Lucila Ohno-Machado, Christos Sotiriou & Ashley Williams

Division of Experimental Pathology, Mayo Clinic, Rochester, MN, USA

Jeremy Chien

Centre for Cancer Research, The Westmead Institute for Medical Research, University of Sydney, Sydney, NSW, Australia

Yoke-Eng Chiew, Angela Chou, Jillian A. Hung, Catherine J. Kennedy, Graham J. Mann, Gulietta M. Pupo, Sarah-Jane Schramm, Varsha Tembe & Anna deFazio

Department of Gynaecological Oncology, Westmead Hospital, Sydney, NSW, Australia

Yoke-Eng Chiew, Jillian A. Hung, Catherine J. Kennedy & Anna deFazio

PDXen Biosystems Inc, Seoul, South Korea

Sunghoon Cho

Korea Advanced Institute of Science and Technology, Daejeon, South Korea

Jung Kyoon Choi, Young Seok Ju & Christopher J. Yoon

Electronics and Telecommunications Research Institute, Daejeon, South Korea

Wan Choi, Seung-Hyup Jeon, Hyunghwan Kim & Youngchoon Woo

Institut National du Cancer (INCA), Boulogne-Billancourt, France

Christine Chomienne & Iris Pauporté

Department of Genetics, Informatics Institute, University of Alabama at Birmingham, Birmingham, AL, USA

Zechen Chong

Division of Medical Oncology, National Cancer Centre, Singapore, Singapore

Su Pin Choo

Medical Oncology, University and Hospital Trust of Verona, Verona, Italy

Sara Cingarlini & Michele Milella

Department of Pediatrics, University Hospital Schleswig-Holstein, Kiel, Germany

Alexander Claviez

Hepatobiliary/Pancreatic Surgical Oncology Program, University Health Network, Toronto, ON, Canada

Sean Cleary, Ashton A. Connor & Steven Gallinger

School of Biological Sciences, University of Auckland, Auckland, New Zealand

Nicole Cloonan

Department of Surgery, University of Melbourne, Parkville, VIC, Australia

Marek Cmero

The Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, VIC, Australia

Walter and Eliza Hall Institute, Parkville, VIC, Australia

Vancouver Prostate Centre, Vancouver, Canada

Colin C. Collins, Nilgun Donmez, Faraz Hach, Salem Malikic, S. Cenk Sahinalp, Iman Sarrafi & Raunak Shrestha

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada

Ashton A. Connor, Steven Gallinger, Robert C. Grant, Treasa A. McPherson & Iris Selander

University of East Anglia, Norwich, UK

Colin S. Cooper

Norfolk and Norwich University Hospital NHS Trust, Norwich, UK

Matthew G. Cordes, Catrina C. Fronick & Tom Roques

Victorian Institute of Forensic Medicine, Southbank, VIC, Australia

Stephen M. Cordner

Department of Biomedical Informatics, Harvard Medical School, Boston, MA, USA

Isidro Cortés-Ciriano, Jake June-Koo Lee & Peter J. Park

Department of Chemistry, Centre for Molecular Science Informatics, University of Cambridge, Cambridge, UK

Isidro Cortés-Ciriano

Ludwig Center at Harvard Medical School, Boston, MA, USA

Kyle Covington, HarshaVardhan Doddapaneni, Richard A. Gibbs, Jianhong Hu, Joy C. Jayaseelan, Viktoriya Korchina, Lora Lewis, Donna M. Muzny, Linghua Wang, David A. Wheeler & Liu Xi

Peter MacCallum Cancer Centre, University of Melbourne, Melbourne, VIC, Australia

Prue A. Cowin, Anne Hamilton, Gisela Mir Arnau & Ravikiran Vedururu

Physics Division, Optimization and Systems Biology Lab, Massachusetts General Hospital, Boston, MA, USA

David Craft

Department of Medicine, Baylor College of Medicine, Houston, TX, USA

Chad J. Creighton

Yupeng Cun, Martin Peifer & Tsun-Po Yang

International Genomics Consortium, Phoenix, AZ, USA

Erin Curley & Troy Shelton

Genomics Research Program, Ontario Institute for Cancer Research, Toronto, ON, Canada

Karolina Czajka, Jenna Eagles, Thomas J. Hudson, Jeremy Johns, Faridah Mbabaali, John D. McPherson, Jessica K. Miller, Danielle Pasternack, Michelle Sam & Lee E. Timms

Barking Havering and Redbridge University Hospitals NHS Trust, Romford, UK

Bogdan Czerniak, Adel El-Naggar & David Khoo

Children’s Hospital at Westmead, University of Sydney, Sydney, NSW, Australia

Rebecca A. Dagg

Department of Medicine, Section of Endocrinology, University and Hospital Trust of Verona, Verona, Italy

Maria Vittoria Davi

Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, NY, USA

Natalie R. Davidson, Andre Kahles, Kjong-Van Lehmann, Alessandro Pastore, Gunnar Rätsch, Chris Sander, Yasin Senbabaoglu & Nicholas D. Socci

Department of Biology, ETH Zurich, Zürich, Switzerland

Natalie R. Davidson, Andre Kahles, Kjong-Van Lehmann, Gunnar Rätsch & Stefan G. Stark

Department of Computer Science, ETH Zurich, Zurich, Switzerland

Natalie R. Davidson, Andre Kahles, Kjong-Van Lehmann & Gunnar Rätsch

SIB Swiss Institute of Bioinformatics, Lausanne, Switzerland

Weill Cornell Medical College, New York, NY, USA

Natalie R. Davidson, Bishoy M. Faltas & Gunnar Rätsch

Academic Department of Medical Genetics, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK

Helen Davies & Serena Nik-Zainal

MRC Cancer Unit, University of Cambridge, Cambridge, UK

Helen Davies, Rebecca C. Fitzgerald, Nicola Grehan, Serena Nik-Zainal & Maria O’Donovan

Departments of Pediatrics and Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Ian J. Davis

Seven Bridges Genomics, Charlestown, MA, USA

Brandi N. Davis-Dusenbery, Sinisa Ivkovic, Milena Kovacevic, Ana Mijalkovic Lazic, Sanja Mijalkovic, Mia Nastic, Petar Radovic & Nebojsa Tijanic

Annai Systems, Inc, Carlsbad, CA, USA

Francisco M. De La Vega, Tal Shmaya & Dai-Ying Wu

Department of Pathology, General Hospital of Treviso, Department of Medicine, University of Padua, Treviso, Italy

Angelo P. Dei Tos

Department of Computational Biology, University of Lausanne, Lausanne, Switzerland

Olivier Delaneau

Department of Genetic Medicine and Development, University of Geneva Medical School, Geneva, CH, Switzerland

Swiss Institute of Bioinformatics, University of Geneva, Geneva, CH, Switzerland

Jonas Demeulemeester, Stefan C. Dentro, Matthew W. Fittall, Kerstin Haase, Clemency Jolly, Maxime Tarabichi & Peter Van Loo

Jonas Demeulemeester & Peter Van Loo

Institute of Medical Genetics and Applied Genomics, University of Tübingen, Tübingen, Germany

German M. Demidov, Francesc Muyas & Stephan Ossowski

Computational and Systems Biology, Genome Institute of Singapore, Singapore, Singapore

Deniz Demircioğlu & Jonathan Göke

School of Computing, National University of Singapore, Singapore, Singapore

Deniz Demircioğlu

Big Data Institute, Li Ka Shing Centre, University of Oxford, Oxford, UK

Stefan C. Dentro & David C. Wedge

Biomedical Data Science Laboratory, Francis Crick Institute, London, UK

Nikita Desai

Bioinformatics Group, Department of Computer Science, University College London, London, UK

The Edward S. Rogers Sr. Department of Electrical and Computer Engineering, University of Toronto, Toronto, ON, Canada

Amit G. Deshwar

Breast Cancer Translational Research Laboratory JC Heuson, Institut Jules Bordet, Brussels, Belgium

Christine Desmedt

Department of Oncology, Laboratory for Translational Breast Cancer Research, KU Leuven, Leuven, Belgium

Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain

Jordi Deu-Pons, Joan Frigola, Abel Gonzalez-Perez, Ferran Muiños, Loris Mularoni, Oriol Pich, Iker Reyes-Salazar, Carlota Rubio-Perez, Radhakrishnan Sabarinathan & David Tamborero

Research Program on Biomedical Informatics, Universitat Pompeu Fabra, Barcelona, Spain

Jordi Deu-Pons, Abel Gonzalez-Perez, Ferran Muiños, Loris Mularoni, Oriol Pich, Carlota Rubio-Perez, Radhakrishnan Sabarinathan & David Tamborero

Division of Medical Oncology, Princess Margaret Cancer Centre, Toronto, ON, Canada

Neesha C. Dhani, David Hedley & Malcolm J. Moore

Department of Physiology and Biophysics, Weill Cornell Medicine, New York, NY, USA

Priyanka Dhingra, Ekta Khurana, Eric Minwei Liu & Alexander Martinez-Fundichely

Institute for Computational Biomedicine, Weill Cornell Medicine, New York, NY, USA

Department of Pathology, UPMC Shadyside, Pittsburgh, PA, USA

Independent Consultant, Wellesley, USA

Anthony DiBiase

Department of Cell and Molecular Biology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden

Klev Diamanti, Jan Komorowski & Husen M. Umer

Department of Medicine and Department of Genetics, Washington University School of Medicine, St. Louis, St. Louis, MO, USA

Li Ding, Robert S. Fulton, Michael D. McLellan, Michael C. Wendl & Venkata D. Yellapantula

Hefei University of Technology, Anhui, China

Shuai Ding & Shanlin Yang

Translational Cancer Research Unit, GZA Hospitals St.-Augustinus, Center for Oncological Research, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium

Luc Dirix, Steven Van Laere, Gert G. Van den Eynden & Peter Vermeulen

Simon Fraser University, Burnaby, BC, Canada

Nilgun Donmez, Ermin Hodzic, Salem Malikic, S. Cenk Sahinalp & Iman Sarrafi

University of Pennsylvania, Philadelphia, PA, USA

Ronny Drapkin

Faculty of Science and Technology, University of Vic—Central University of Catalonia (UVic-UCC), Vic, Spain

Ana Dueso-Barroso

The Wellcome Trust, London, UK

Michael Dunn

The Hospital for Sick Children, Toronto, ON, Canada

Lewis Jonathan Dursi

Department of Pathology, Queen Elizabeth University Hospital, Glasgow, UK

Fraser R. Duthie

Department of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia

Ken Dutton-Regester, Nicholas K. Hayward, Oliver Holmes, Peter A. Johansson, Stephen H. Kazakoff, Conrad R. Leonard, Felicity Newell, Katia Nones, Ann-Marie Patch, John V. Pearson, Antonia L. Pritchard, Michael C. Quinn, Paresh Vyas, Nicola Waddell, Scott Wood & Qinying Xu

Department of Oncology, Centre for Cancer Genetic Epidemiology, University of Cambridge, Cambridge, UK

Douglas F. Easton

Department of Public Health and Primary Care, Centre for Cancer Genetic Epidemiology, University of Cambridge, Cambridge, UK

Prostate Cancer Canada, Toronto, ON, Canada

Stuart Edmonds

Paul A. Edwards, Anthony R. Green, Andy G. Lynch, Florian Markowetz & Thomas J. Mitchell

Department of Laboratory Medicine, Translational Cancer Research, Lund University Cancer Center at Medicon Village, Lund University, Lund, Sweden

Anna Ehinger

Juergen Eils, Roland Eils & Daniel Hübschmann

New BIH Digital Health Center, Berlin Institute of Health (BIH) and Charité - Universitätsmedizin Berlin, Berlin, Germany

Juergen Eils, Roland Eils & Chris Lawerenz

CIBER Epidemiología y Salud Pública (CIBERESP), Madrid, Spain

Georgia Escaramis

Research Group on Statistics, Econometrics and Health (GRECS), UdG, Barcelona, Spain

Quantitative Genomics Laboratories (qGenomics), Barcelona, Spain

Xavier Estivill

Icelandic Cancer Registry, Icelandic Cancer Society, Reykjavik, Iceland

Jorunn E. Eyfjord, Holmfridur Hilmarsdottir & Jon G. Jonasson

State Key Laboratory of Cancer Biology, and Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Shaanxi, China

Daiming Fan & Yongzhan Nie

Department of Medicine (DIMED), Surgical Pathology Unit, University of Padua, Padua, Italy

Matteo Fassan

Rigshospitalet, Copenhagen, Denmark

Francesco Favero

Center for Cancer Genomics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Martin L. Ferguson

Department of Biochemistry and Molecular Medicine, University of Montreal, Montreal, QC, Canada

Vincent Ferretti

Australian Institute of Tropical Health and Medicine, James Cook University, Douglas, QLD, Australia

Matthew A. Field

Department of Neuro-Oncology, Istituto Neurologico Besta, Milano, Italy

Gaetano Finocchiaro

Bioplatforms Australia, North Ryde, NSW, Australia

Anna Fitzgerald & Catherine A. Shang

Department of Pathology (Research), University College London Cancer Institute, London, UK

Adrienne M. Flanagan

Department of Surgical Oncology, Princess Margaret Cancer Centre, Toronto, ON, Canada

Neil E. Fleshner

Department of Medical Oncology, Josephine Nefkens Institute and Cancer Genomics Centre, Erasmus Medical Center, Rotterdam, CN, The Netherlands

John A. Foekens, John W. M. Martens, F. Germán Rodríguez-González, Anieta M. Sieuwerts & Marcel Smid

The University of Queensland Thoracic Research Centre, The Prince Charles Hospital, Brisbane, QLD, Australia

Kwun M. Fong

CIBIO/InBIO - Research Center in Biodiversity and Genetic Resources, Universidade do Porto, Vairão, Portugal

Nuno A. Fonseca

HCA Laboratories, London, UK

Christopher S. Foster

University of Liverpool, Liverpool, UK

The Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel

Milana Frenkel-Morgenstern

Department of Neurosurgery, University of Florida, Gainesville, FL, USA

William Friedman

Department of Pathology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan

Masashi Fukayama & Tetsuo Ushiku

University of Milano Bicocca, Monza, Italy

Carlo Gambacorti-Passerini

BGI-Shenzhen, Shenzhen, China

Shengjie Gao, Yong Hou, Chang Li, Lin Li, Siliang Li, Xiaobo Li, Xinyue Li, Dongbing Liu, Xingmin Liu, Qiang Pan-Hammarström, Hong Su, Jian Wang, Kui Wu, Heng Xiong, Huanming Yang, Chen Ye, Xiuqing Zhang, Yong Zhou & Shida Zhu

Department of Pathology, Oslo University Hospital Ulleval, Oslo, Norway

Øystein Garred

Center for Biomedical Informatics, Harvard Medical School, Boston, MA, USA

Nils Gehlenborg

Department Biochemistry and Molecular Biomedicine, University of Barcelona, Barcelona, Spain

Josep L. L. Gelpi

Office of Cancer Genomics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Daniela S. Gerhard

Cancer Epigenomics, German Cancer Research Center (DKFZ), Heidelberg, Germany

Clarissa Gerhauser, Christoph Plass & Dieter Weichenhan

Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Jeffrey E. Gershenwald

Department of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Department of Computer Science, Yale University, New Haven, CT, USA

Mark Gerstein & Fabio C. P. Navarro

Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA

Mark Gerstein, Sushant Kumar, Lucas Lochovsky, Shaoke Lou, Patrick D. McGillivray, Fabio C. P. Navarro, Leonidas Salichos & Jonathan Warrell

Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT, USA

Mark Gerstein, Arif O. Harmanci, Sushant Kumar, Donghoon Lee, Shantao Li, Xiaotong Li, Lucas Lochovsky, Shaoke Lou, William Meyerson, Leonidas Salichos, Jonathan Warrell, Jing Zhang & Yan Zhang

Center for Cancer Research, Massachusetts General Hospital, Boston, MA, USA

Gad Getz & Paz Polak

Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA

Ronald Ghossein, Dilip D. Giri, Christine A. Iacobuzio-Donahue, Jorge Reis-Filho & Victor Reuter

Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA

Nasra H. Giama, Catherine D. Moser & Lewis R. Roberts

University of Sydney, Sydney, NSW, Australia

Anthony J. Gill & James G. Kench

University of Oxford, Oxford, UK

Pelvender Gill, Freddie C. Hamdy, Katalin Karaszi, Adam Lambert, Luke Marsden, Clare Verrill & Paresh Vyas

Department of Surgery, Academic Urology Group, University of Cambridge, Cambridge, UK

Vincent J. Gnanapragasam

Department of Medicine II, University of Würzburg, Wuerzburg, Germany

Maria Elisabeth Goebler

Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL, USA

Carmen Gomez

Institut Hospital del Mar d’Investigacions Mèdiques (IMIM), Barcelona, Spain

Abel Gonzalez-Perez

Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences (NIEHS), Durham, NC, USA

Dmitry A. Gordenin & Natalie Saini

St. Thomas’s Hospital, London, UK

James Gossage

Osaka International Cancer Center, Osaka, Japan

Kunihito Gotoh

Department of Pathology, Skåne University Hospital, Lund University, Lund, Sweden

Dorthe Grabau

Department of Medical Oncology, Beatson West of Scotland Cancer Centre, Glasgow, UK

Janet S. Graham

National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA

Eric Green, Carolyn M. Hutter & Heidi J. Sofia

Centre for Cancer Research, Victorian Comprehensive Cancer Centre, University of Melbourne, Melbourne, VIC, Australia

Sean M. Grimmond

Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL, USA

Robert L. Grossman

German Center for Infection Research (DZIF), Partner Site Hamburg-Borstel-Lübeck-Riems, Hamburg, Germany

Adam Grundhoff

Bioinformatics Research Centre (BiRC), Aarhus University, Aarhus, Denmark

Qianyun Guo, Asger Hobolth & Jakob Skou Pedersen

Department of Biotechnology, Ministry of Science and Technology, Government of India, New Delhi, Delhi, India

Shailja Gupta & K. VijayRaghavan

National Cancer Centre Singapore, Singapore, Singapore

Jonathan Göke

Brandeis University, Waltham, MA, USA

James E. Haber

Department of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada

Department of Internal Medicine, Stanford University, Stanford, CA, USA

Mark P. Hamilton

The University of Texas Health Science Center at Houston, Houston, TX, USA

Leng Han, Yang Yang & Xuanping Zhang

Imperial College NHS Trust, Imperial College, London, INY, UK

George B. Hanna

Senckenberg Institute of Pathology, University of Frankfurt Medical School, Frankfurt, Germany

Martin Hansmann

Department of Medicine, Division of Biomedical Informatics, UC San Diego School of Medicine, San Diego, CA, USA

Olivier Harismendy

Center for Precision Health, School of Biomedical Informatics, The University of Texas Health Science Center, Houston, TX, USA

Arif O. Harmanci

Oxford Nanopore Technologies, New York, NY, USA

Eoghan Harrington & Sissel Juul

Institute of Medical Science, University of Tokyo, Tokyo, Japan

Takanori Hasegawa, Shuto Hayashi, Seiya Imoto, Mitsuhiro Komura, Satoru Miyano, Naoki Miyoshi, Kazuhiro Ohi, Eigo Shimizu, Yuichi Shiraishi, Hiroko Tanaka & Rui Yamaguchi

Howard Hughes Medical Institute, University of California Santa Cruz, Santa Cruz, CA, USA

David Haussler

Wakayama Medical University, Wakayama, Japan

Shinya Hayami, Masaki Ueno & Hiroki Yamaue

Department of Internal Medicine, Division of Medical Oncology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

D. Neil Hayes

University of Tennessee Health Science Center for Cancer Research, Memphis, TN, USA

Department of Histopathology, Salford Royal NHS Foundation Trust, Salford, UK

Stephen J. Hayes

Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK

BIOPIC, ICG and College of Life Sciences, Peking University, Beijing, China

Yao He & Zemin Zhang

Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, China

Children’s Hospital of Philadelphia, Philadelphia, PA, USA

Allison P. Heath

Department of Bioinformatics and Computational Biology and Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Apurva M. Hegde, Yiling Lu & John N. Weinstein

Karolinska Institute, Stockholm, Sweden

Eva Hellstrom-Lindberg & Jesper Lagergren

The Donnelly Centre, University of Toronto, Toronto, ON, Canada

Mohamed Helmy & Jeffrey A. Wintersinger

Department of Medical Genetics, College of Medicine, Hallym University, Chuncheon, South Korea

Seong Gu Heo, Eun Pyo Hong & Ji Wan Park

Department of Experimental and Health Sciences, Institute of Evolutionary Biology (UPF-CSIC), Universitat Pompeu Fabra, Barcelona, Spain

José María Heredia-Genestar, Tomas Marques-Bonet & Arcadi Navarro

Health Data Science Unit, University Clinics, Heidelberg, Germany

Carl Herrmann

Massachusetts General Hospital Center for Cancer Research, Charlestown, MA, USA

Julian M. Hess & Yosef E. Maruvka

Hokkaido University, Sapporo, Japan

Satoshi Hirano & Toru Nakamura

Department of Pathology and Clinical Laboratory, National Cancer Center Hospital, Tokyo, Japan

Nobuyoshi Hiraoka

Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Katherine A. Hoadley & Tara J. Skelly

Computational Biology, Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany

Steve Hoffmann

University of Melbourne Centre for Cancer Research, Melbourne, VIC, Australia

Oliver Hofmann

University of Nebraska Medical Center, Omaha, NE, USA

Michael A. Hollingsworth & Sarah P. Thayer

Syntekabio Inc, Daejeon, South Korea

Jongwhi H. Hong

Department of Pathology, Academic Medical Center, Amsterdam, AZ, The Netherlands

Gerrit K. Hooijer

China National GeneBank-Shenzhen, Shenzhen, China

Yong Hou, Chang Li, Siliang Li, Xiaobo Li, Dongbing Liu, Xingmin Liu, Henk G. Stunnenberg, Hong Su, Kui Wu, Heng Xiong, Chen Ye & Shida Zhu

Division of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany

Volker Hovestadt, Murat Iskar, Peter Lichter, Bernhard Radlwimmer & Marc Zapatka

Division of Life Science and Applied Genomics Center, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China

Taobo Hu, Yogesh Kumar, Eric Z. Ma, Zhenggang Wu & Hong Xue

Icahn School of Medicine at Mount Sinai, New York, NY, USA

Kuan-lin Huang

Geneplus-Shenzhen, Shenzhen, China

School of Computer Science and Technology, Xi’an Jiaotong University, Xi’an, China

Yi Huang, Jiayin Wang, Xiao Xiao & Xuanping Zhang

AbbVie, North Chicago, IL, USA

Thomas J. Hudson

Institute of Pathology, Charité – University Medicine Berlin, Berlin, Germany

Michael Hummel & Dido Lenze

Centre for Translational and Applied Genomics, British Columbia Cancer Agency, Vancouver, BC, Canada

David Huntsman

Edinburgh Royal Infirmary, Edinburgh, UK

Ted R. Hupp

Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Berlin, Germany

Matthew R. Huska, Julia Markowski & Roland F. Schwarz

Department of Pediatric Immunology, Hematology and Oncology, University Hospital, Heidelberg, Germany

Daniel Hübschmann

Daniel Hübschmann, Christof von Kalle & Roland F. Schwarz

Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM), Heidelberg, Germany

Institute for Computational Biomedicine, Weill Cornell Medical College, New York, NY, USA

Marcin Imielinski

Marcin Imielinski & Xiaotong Yao

Department of Urology, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA

William B. Isaacs

Department of Preventive Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

Shumpei Ishikawa, Hiroto Katoh & Daisuke Komura

Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA

Michael Ittmann

Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX, USA

Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA

Technical University of Denmark, Lyngby, Denmark

Jose M. G. Izarzugaza

Department of Pathology, College of Medicine, Hanyang University, Seoul, South Korea

Jocelyne Jacquemier, Hyung-Yong Kim & Gu Kong

Academic Unit of Surgery, School of Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow Royal Infirmary, Glasgow, UK

Nigel B. Jamieson

Department of Pathology, Asan Medical Center, College of Medicine, Ulsan University, Songpa-gu, Seoul, South Korea

Se Jin Jang & Hee Jin Lee

Science Writer, Garrett Park, MD, USA

Karine Jegalian

International Cancer Genome Consortium (ICGC)/ICGC Accelerating Research in Genomic Oncology (ARGO) Secretariat, Ontario Institute for Cancer Research, Toronto, ON, Canada

Jennifer L. Jennings

Lara Jerman

Department of Public Health Sciences, University of Chicago, Chicago, IL, USA

Research Institute, NorthShore University HealthSystem, Evanston, IL, USA

Department for Biomedical Research, University of Bern, Bern, Switzerland

Rory Johnson, Andrés Lanzós & Mark A. Rubin

Centre of Genomics and Policy, McGill University and Génome Québec Innovation Centre, Montreal, QC, Canada

Yann Joly, Bartha M. Knoppers, Mark Phillips & Adrian Thorogood

Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Corbin D. Jones

Hopp Children’s Cancer Center (KiTZ), Heidelberg, Germany

David T. W. Jones, Marcel Kool & Stefan M. Pfister

Pediatric Glioma Research Group, German Cancer Research Center (DKFZ), Heidelberg, Germany

David T. W. Jones

Cancer Research UK, London, UK

Nic Jones & David Scott

Indivumed GmbH, Hamburg, Germany

Hartmut Juhl

Genome Integration Data Center, Syntekabio, Inc, Daejeon, South Korea

Jongsun Jung

University Hospital Zurich, Zurich, Switzerland

Andre Kahles, Kjong-Van Lehmann & Gunnar Rätsch

Clinical Bioinformatics, Swiss Institute of Bioinformatics, Geneva, Switzerland

Abdullah Kahraman

Institute for Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland

Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland

Abdullah Kahraman & Christian von Mering

MRC Human Genetics Unit, MRC IGMM, University of Edinburgh, Edinburgh, UK

Vera B. Kaiser & Colin A. Semple

Women’s Cancer Program at the Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA

Beth Karlan

Department of Biology, Bioinformatics Group, Division of Molecular Biology, Faculty of Science, University of Zagreb, Zagreb, Croatia

Rosa Karlić

Department for Internal Medicine II, University Hospital Schleswig-Holstein, Kiel, Germany

Dennis Karsch & Michael Kneba

Genetics and Molecular Pathology, SA Pathology, Adelaide, SA, Australia

Karin S. Kassahn

Department of Gastric Surgery, National Cancer Center Hospital, Tokyo, Japan

Hitoshi Katai

Department of Bioinformatics, Division of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan

Mamoru Kato, Hirofumi Rokutan & Mihoko Saito-Adachi

A.A. Kharkevich Institute of Information Transmission Problems, Moscow, Russia

Marat D. Kazanov

Oncology and Immunology, Dmitry Rogachev National Research Center of Pediatric Hematology, Moscow, Russia

Skolkovo Institute of Science and Technology, Moscow, Russia

Department of Surgery, The George Washington University, School of Medicine and Health Science, Washington, DC, USA

Electron Kebebew

Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

Melanoma Institute Australia, Macquarie University, Sydney, NSW, Australia

Richard F. Kefford

MIT Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA, USA

Manolis Kellis

Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Sydney, NSW, Australia

James G. Kench & Richard A. Scolyer

Cholangiocarcinoma Screening and Care Program and Liver Fluke and Cholangiocarcinoma Research Centre, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand

Narong Khuntikeo

Controlled Department and Institution, New York, NY, USA

Ekta Khurana

Englander Institute for Precision Medicine, Weill Cornell Medicine, New York, NY, USA

Ekta Khurana & Alexander Martinez-Fundichely

National Cancer Center, Gyeonggi, South Korea

Hark Kyun Kim

Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul, South Korea

Hyung-Lae Kim

Health Sciences Department of Biomedical Informatics, University of California San Diego, La Jolla, CA, USA

Research Core Center, National Cancer Centre Korea, Goyang-si, South Korea

Jong K. Kim

Department of Health Sciences and Technology, Sungkyunkwan University School of Medicine, Seoul, South Korea

Youngwook Kim

Samsung Genome Institute, Seoul, South Korea

Breast Oncology Program, Dana-Farber/Brigham and Women’s Cancer Center, Boston, MA, USA

Tari A. King

Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY, USA

Tari A. King & Samuel Singer

Division of Breast Surgery, Brigham and Women’s Hospital, Boston, MA, USA

Integrative Bioinformatics Support Group, National Institute of Environmental Health Sciences (NIEHS), Durham, NC, USA

Leszek J. Klimczak

Department of Clinical Science, University of Bergen, Bergen, Norway

Stian Knappskog & Ola Myklebost

Center For Medical Innovation, Seoul National University Hospital, Seoul, South Korea

Youngil Koh

Department of Internal Medicine, Seoul National University Hospital, Seoul, South Korea

Youngil Koh & Sung-Soo Yoon

Institute of Computer Science, Polish Academy of Sciences, Warsawa, Poland

Jan Komorowski

Functional and Structural Genomics, German Cancer Research Center (DKFZ), Heidelberg, Germany

Marcel Kool, Andrey Korshunov, Michael Koscher, Stefan M. Pfister & Qi Wang

Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, , National Institutes of Health, Bethesda, MD, USA

Roelof Koster

Institute for Medical Informatics Statistics and Epidemiology, University of Leipzig, Leipzig, Germany

Markus Kreuz & Markus Loeffler

Morgan Welch Inflammatory Breast Cancer Research Program and Clinic, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Savitri Krishnamurthy

Department of Hematology and Oncology, Georg-Augusts-University of Göttingen, Göttingen, Germany

Dieter Kube & Lorenz H. P. Trümper

Institute of Cell Biology (Cancer Research), University of Duisburg-Essen, Essen, Germany

Ralf Küppers

King’s College London and Guy’s and St. Thomas’ NHS Foundation Trust, London, UK

Jesper Lagergren

Center for Epigenetics, Van Andel Research Institute, Grand Rapids, MI, USA

Peter W. Laird

The University of Queensland Centre for Clinical Research, Royal Brisbane and Women’s Hospital, Herston, QLD, Australia

Sunil R. Lakhani & Peter T. Simpson

Department of Pediatric Oncology and Hematology, University of Cologne, Cologne, Germany

Pablo Landgraf

University of Düsseldorf, Düsseldorf, Germany

Pablo Landgraf & Guido Reifenberger

Department of Pathology, Institut Jules Bordet, Brussels, Belgium

Denis Larsimont

Institute of Biomedicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

Erik Larsson

Children’s Medical Research Institute, Sydney, NSW, Australia

Loretta M. S. Lau & Hilda A. Pickett

ILSbio, LLC Biobank, Chestertown, MD, USA

Division of Genetics and Genomics, Boston Children’s Hospital, Harvard Medical School, Boston, MA, USA

Eunjung Alice Lee

Institute for Bioengineering and Biopharmaceutical Research (IBBR), Hanyang University, Seoul, South Korea

Jeong-Yeon Lee

Department of Statistics, University of California Santa Cruz, Santa Cruz, CA, USA

National Genotyping Center, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan

Ming Ta Michael Lee

Department of Vertebrate Genomics/Otto Warburg Laboratory Gene Regulation and Systems Biology of Cancer, Max Planck Institute for Molecular Genetics, Berlin, Germany

Hans Lehrach, Hans-Jörg Warnatz & Marie-Laure Yaspo

McGill University and Genome Quebec Innovation Centre, Montreal, QC, Canada

Louis Letourneau

biobyte solutions GmbH, Heidelberg, Germany

Ivica Letunic

Gynecologic Oncology, NYU Laura and Isaac Perlmutter Cancer Center, New York University, New York, NY, USA

Douglas A. Levine

Division of Oncology, Stem Cell Biology Section, Washington University School of Medicine, St. Louis, MO, USA

Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Harvard University, Cambridge, MA, USA

Urologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

W. M. Linehan

University of Oslo, Oslo, Norway

Ole Christian Lingjærde & Torill Sauer

University of Toronto, Toronto, ON, Canada

Fei-Fei Fei Liu, Quaid D. Morris, Ruian Shi, Shankar Vembu & Fan Yang

Peking University, Beijing, China

Fenglin Liu, Fan Zhang, Liangtao Zheng & Xiuqing Zheng

School of Life Sciences, Peking University, Beijing, China

Fenglin Liu

Leidos Biomedical Research, Inc, McLean, VA, USA

Hematology, Hospital Clinic, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain

Armando Lopez-Guillermo

Second Military Medical University, Shanghai, China

Yong-Jie Lu & Hongwei Zhang

Chinese Cancer Genome Consortium, Shenzhen, China

Department of Medical Oncology, Beijing Hospital, Beijing, China

Laboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing, China

Youyong Lu & Rui Xing

School of Medicine/School of Mathematics and Statistics, University of St. Andrews, St, Andrews, Fife, UK

Andy G. Lynch

Institute for Systems Biology, Seattle, WA, USA

Lisa Lype, Sheila M. Reynolds & Ilya Shmulevich

Department of Biochemistry and Molecular Biology, Faculty of Medicine, University Institute of Oncology-IUOPA, Oviedo, Spain

Carlos López-Otín & Xose S. Puente

Institut Bergonié, Bordeaux, France

Gaetan MacGrogan

Cancer Unit, MRC University of Cambridge, Cambridge, UK

Shona MacRae

Department of Pathology and Laboratory Medicine, Center for Personalized Medicine, Children’s Hospital Los Angeles, Los Angeles, CA, USA

Dennis T. Maglinte

John Curtin School of Medical Research, Canberra, ACT, Australia

Graham J. Mann

MVZ Department of Oncology, PraxisClinic am Johannisplatz, Leipzig, Germany

Luisa Mantovani-Löffler

Department of Information Technology, Ghent University, Ghent, Belgium

Kathleen Marchal & Sergio Pulido-Tamayo

Department of Plant Biotechnology and Bioinformatics, Ghent University, Ghent, Belgium

Kathleen Marchal, Sergio Pulido-Tamayo & Lieven P. C. Verbeke

Institute for Genomic Medicine, Nationwide Children’s Hospital, Columbus, OH, USA

Elaine R. Mardis

Computational Biology Program, School of Medicine, Oregon Health and Science University, Portland, OR, USA

Adam A. Margolin & Adam J. Struck

Department of Surgery, Duke University, Durham, NC, USA

Jeffrey Marks

Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, Spain

Tomas Marques-Bonet, Jose I. Martin-Subero, Arcadi Navarro, David Torrents & Alfonso Valencia

Institut Català de Paleontologia Miquel Crusafont, Universitat Autònoma de Barcelona, Barcelona, Spain

Tomas Marques-Bonet

Sancha Martin & Ke Yuan

Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain

Jose I. Martin-Subero

Division of Oncology, Washington University School of Medicine, St. Louis, MO, USA

R. Jay Mashl

Department of Surgery and Cancer, Imperial College, London, INY, UK

Applications Department, Oxford Nanopore Technologies, Oxford, UK

Simon Mayes & Daniel J. Turner

Department of Obstetrics, Gynecology and Reproductive Services, University of California San Francisco, San Francisco, CA, USA

Karen McCune & Karen Smith-McCune

Department of Biochemistry and Molecular Medicine, University California at Davis, Sacramento, CA, USA

John D. McPherson

STTARR Innovation Facility, Princess Margaret Cancer Centre, Toronto, ON, Canada

Discipline of Surgery, Western Sydney University, Penrith, NSW, Australia

Neil D. Merrett

Yale School of Medicine, Yale University, New Haven, CT, USA

William Meyerson

Department of Genetics, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Piotr A. Mieczkowski, Joel S. Parker, Charles M. Perou, Donghui Tan, Umadevi Veluvolu & Matthew D. Wilkerson

Departments of Neurology and Neurosurgery, Henry Ford Hospital, Detroit, MI, USA

Tom Mikkelsen

Precision Oncology, OHSU Knight Cancer Institute, Oregon Health and Science University, Portland, OR, USA

Gordon B. Mills

Institute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany

Sarah Minner, Guido Sauter & Ronald Simon

Department of Health Sciences, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan

Shinichi Mizuno

Heidelberg Academy of Sciences and Humanities, Heidelberg, Germany

Fruzsina Molnár-Gábor

Department of Clinical Pathology, University of Melbourne, Melbourne, VIC, Australia

Carl Morrison, Karin A. Oien, Chawalit Pairojkul, Paul M. Waring & Marc J. van de Vijver

Department of Pathology, Roswell Park Cancer Institute, Buffalo, NY, USA

Carl Morrison

Department of Computer Science, University of Helsinki, Helsinki, Finland

Ville Mustonen

Institute of Biotechnology, University of Helsinki, Helsinki, Finland

Organismal and Evolutionary Biology Research Programme, University of Helsinki, Helsinki, Finland

Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Washington University School of Medicine, St. Louis, MO, USA

David Mutch

Penrose St. Francis Health Services, Colorado Springs, CO, USA

Jerome Myers

Institute of Pathology, Ulm University and University Hospital of Ulm, Ulm, Germany

Peter Möller

National Cancer Center, Tokyo, Japan

Hitoshi Nakagama

Genome Institute of Singapore, Singapore, Singapore

Tannistha Nandi & Patrick Tan

32Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT, USA

Fabio C. P. Navarro

German Cancer Aid, Bonn, Germany

Gerd Nettekoven & Laura Planko

Programme in Cancer and Stem Cell Biology, Centre for Computational Biology, Duke-NUS Medical School, Singapore, Singapore

Alvin Wei Tian Ng

The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China

Fourth Military Medical University, Shaanxi, China

Yongzhan Nie

The University of Cambridge School of Clinical Medicine, Cambridge, UK

Serena Nik-Zainal

St. Jude Children’s Research Hospital, Memphis, TN, USA

Paul A. Northcott

University Health Network, Princess Margaret Cancer Centre, Toronto, ON, Canada

Faiyaz Notta & Ming Tsao

Center for Biomolecular Science and Engineering, University of California Santa Cruz, Santa Cruz, CA, USA

Brian D. O’Connor

Department of Medicine, University of Chicago, Chicago, IL, USA

Peter O’Donnell

Department of Neurology, Mayo Clinic, Rochester, MN, USA

Brian Patrick O’Neill

Cambridge Oesophagogastric Centre, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

J. Robert O’Neill

Institute of Cancer Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, UK

Karin A. Oien

Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA

Akinyemi I. Ojesina

HudsonAlpha Institute for Biotechnology, Huntsville, AL, USA

O’Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USA

Department of Pathology, Keio University School of Medicine, Tokyo, Japan

Hidenori Ojima

Department of Hepatobiliary and Pancreatic Oncology, National Cancer Center Hospital, Tokyo, Japan

Takuji Okusaka

Sage Bionetworks, Seattle, WA, USA

Larsson Omberg

Lymphoma Genomic Translational Research Laboratory, National Cancer Centre, Singapore, Singapore

Choon Kiat Ong

Department of Clinical Pathology, Robert-Bosch-Hospital, Stuttgart, Germany

Department of Cell and Systems Biology, University of Toronto, Toronto, ON, Canada

B. F. Francis Ouellette

Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden

Qiang Pan-Hammarström

Center for Liver Cancer, Research Institute and Hospital, National Cancer Center, Gyeonggi, South Korea

Joong-Won Park

Division of Hematology-Oncology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea

Keunchil Park

Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University School of Medicine, Seoul, South Korea

Cheonan Industry-Academic Collaboration Foundation, Sangmyung University, Cheonan, South Korea

Kiejung Park

NYU Langone Medical Center, New York, NY, USA

Harvey Pass

Department of Hematology and Medical Oncology, Cleveland Clinic, Cleveland, OH, USA

Nathan A. Pennell

Department of Radiation Oncology, University of California San Francisco, San Francisco, CA, USA

Marc D. Perry

Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA

Gloria M. Petersen

Helen F. Graham Cancer Center at Christiana Care Health Systems, Newark, DE, USA

Nicholas Petrelli

Heidelberg University Hospital, Heidelberg, Germany

Stefan M. Pfister

CSRA Incorporated, Fairfax, VA, USA

Todd D. Pihl

Research Department of Pathology, University College London Cancer Institute, London, UK

Nischalan Pillay

Department of Research Oncology, Guy’s Hospital, King’s Health Partners AHSC, King’s College London School of Medicine, London, UK

Sarah Pinder

Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia

Andreia V. Pinho

University Hospital of Minjoz, INSERM UMR 1098, Besançon, France

Xavier Pivot

Spanish National Cancer Research Centre, Madrid, Spain

Center of Digestive Diseases and Liver Transplantation, Fundeni Clinical Institute, Bucharest, Romania

Irinel Popescu

Cureline, Inc, South San Francisco, CA, USA

Olga Potapova

St. Luke’s Cancer Centre, Royal Surrey County Hospital NHS Foundation Trust, Guildford, UK

Shaun R. Preston

Cambridge Breast Unit, Addenbrooke’s Hospital, Cambridge University Hospital NHS Foundation Trust and NIHR Cambridge Biomedical Research Centre, Cambridge, UK

Elena Provenzano

East of Scotland Breast Service, Ninewells Hospital, Aberdeen, UK

Colin A. Purdie

Department of Genetics, Microbiology and Statistics, University of Barcelona, IRSJD, IBUB, Barcelona, Spain

Raquel Rabionet

Department of Obstetrics and Gynecology, Medical College of Wisconsin, Milwaukee, WI, USA

Janet S. Rader

Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA, USA

Suresh Ramalingam

Benjamin J. Raphael & Matthew A. Reyna

Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA

W. Kimryn Rathmell

Ohio State University College of Medicine and Arthur G. James Comprehensive Cancer Center, Columbus, OH, USA

Matthew Ringel

Department of Surgery, Yokohama City University Graduate School of Medicine, Kanagawa, Japan

Yasushi Rino

Division of Chromatin Networks, German Cancer Research Center (DKFZ) and BioQuant, Heidelberg, Germany

Karsten Rippe

Research Computing Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Jeffrey Roach

School of Molecular Biosciences and Center for Reproductive Biology, Washington State University, Pullman, WA, USA

Steven A. Roberts

Finsen Laboratory and Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark

F. Germán Rodríguez-González, Nikos Sidiropoulos & Joachim Weischenfeldt

Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada

Michael H. A. Roehrl & Stefano Serra

Department of Pathology, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA

Michael H. A. Roehrl

University Hospital Giessen, Pediatric Hematology and Oncology, Giessen, Germany

Marius Rohde

Oncologie Sénologie, ICM Institut Régional du Cancer, Montpellier, France

Gilles Romieu

Institute of Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany

Philip C. Rosenstiel & Markus B. Schilhabel

Institute of Pathology, University of Wuerzburg, Wuerzburg, Germany

Andreas Rosenwald

Department of Urology, North Bristol NHS Trust, Bristol, UK

Edward W. Rowe

SingHealth, Duke-NUS Institute of Precision Medicine, National Heart Centre Singapore, Singapore, Singapore

Steven G. Rozen, Patrick Tan & Bin Tean Teh

Department of Computer Science, University of Toronto, Toronto, ON, Canada

Yulia Rubanova, Jared T. Simpson & Jeffrey A. Wintersinger

Bern Center for Precision Medicine, University Hospital of Bern, University of Bern, Bern, Switzerland

Mark A. Rubin

Englander Institute for Precision Medicine, Weill Cornell Medicine and New York Presbyterian Hospital, New York, NY, USA

Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA

Pathology and Laboratory, Weill Cornell Medical College, New York, NY, USA

Vall d’Hebron Institute of Oncology: VHIO, Barcelona, Spain

Carlota Rubio-Perez

General and Hepatobiliary-Biliary Surgery, Pancreas Institute, University and Hospital Trust of Verona, Verona, Italy

Andrea Ruzzenente

National Centre for Biological Sciences, Tata Institute of Fundamental Research, Bangalore, India

Radhakrishnan Sabarinathan

S. Cenk Sahinalp

Department of Pathology, GZA-ZNA Hospitals, Antwerp, Belgium

Roberto Salgado

Analytical Biological Services, Inc, Wilmington, DE, USA

Charles Saller

Sydney Medical School, University of Sydney, Sydney, NSW, Australia

Jaswinder S. Samra & Richard A. Scolyer

cBio Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA

Chris Sander & Ciyue Shen

Department of Cell Biology, Harvard Medical School, Boston, MA, USA

Advanced Centre for Treatment Research and Education in Cancer, Tata Memorial Centre, Navi Mumbai, Maharashtra, India

Rajiv Sarin

School of Environmental and Life Sciences, Faculty of Science, The University of Newcastle, Ourimbah, NSW, Australia

Christopher J. Scarlett

Department of Dermatology, University Hospital of Essen, Essen, Germany

Dirk Schadendorf

Bioinformatics and Omics Data Analytics, German Cancer Research Center (DKFZ), Heidelberg, Germany

Matthias Schlesner

Department of Urology, Charité Universitätsmedizin Berlin, Berlin, Germany

Thorsten Schlomm & Joachim Weischenfeldt

Martini-Clinic, Prostate Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany

Thorsten Schlomm

Department of General Internal Medicine, University of Kiel, Kiel, Germany

Stefan Schreiber

German Cancer Consortium (DKTK), Partner site Berlin, Berlin, Germany

Roland F. Schwarz

Cancer Research Institute, Beth Israel Deaconess Medical Center, Boston, MA, USA

Ralph Scully

University of Pittsburgh, Pittsburgh, PA, USA

Raja Seethala

Department of Ophthalmology and Ocular Genomics Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA

Ayellet V. Segre

Center for Psychiatric Genetics, NorthShore University HealthSystem, Evanston, IL, USA

Subhajit Sengupta

Van Andel Research Institute, Grand Rapids, MI, USA

Hui Shen & Wanding Zhou

Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan

Tatsuhiro Shibata, Hirokazu Taniguchi & Tomoko Urushidate

Japan Agency for Medical Research and Development, Tokyo, Japan

Kiyo Shimizu & Takashi Yugawa

Seung Jun Shin & Stefan G. Stark

Murtha Cancer Center, Walter Reed National Military Medical Center, Bethesda, MD, USA

Craig Shriver

Human Genetics, University of Kiel, Kiel, Germany

Reiner Siebert

Department of Oncologic Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA

Sabina Signoretti

Oregon Health and Science University, Portland, OR, USA

Jaclyn Smith

Center for RNA Interference and Noncoding RNA, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Anil K. Sood

Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

Sharmila Sothi

Department of Radiation Oncology, Radboud University Nijmegen Medical Centre, Nijmegen, GA, The Netherlands

Paul N. Span

Institute for Genomics and Systems Biology, University of Chicago, Chicago, IL, USA

Jonathan Spring

Clinic for Hematology and Oncology, St.-Antonius-Hospital, Eschweiler, Germany

Peter Staib

Computational and Systems Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA

Stefan G. Stark

University of Iceland, Reykjavik, Iceland

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Division of Computational Genomics and Systems Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany

Oliver Stegle

Dundee Cancer Centre, Ninewells Hospital, Dundee, UK

Alasdair Stenhouse & Alastair M. Thompson

Department for Internal Medicine III, University of Ulm and University Hospital of Ulm, Ulm, Germany

Stephan Stilgenbauer

Institut Curie, INSERM Unit 830, Paris, France

Henk G. Stunnenberg & Anne Vincent-Salomon

Department of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Kanagawa, Japan

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Department of Laboratory Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, GA, The Netherlands

Division of Cancer Genome Research, German Cancer Research Center (DKFZ), Heidelberg, Germany

Holger Sültmann

Department of General Surgery, Singapore General Hospital, Singapore, Singapore

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Cancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore

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Department of Medical and Clinical Genetics, Genome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland

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East Anglian Medical Genetics Service, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

Patrick Tarpey

Irving Institute for Cancer Dynamics, Columbia University, New York, NY, USA

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Institute of Molecular and Cell Biology, Singapore, Singapore

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Laboratory of Cancer Epigenome, Division of Medical Science, National Cancer Centre Singapore, Singapore, Singapore

Universite Lyon, INCa-Synergie, Centre Léon Bérard, Lyon, France

Gilles Thomas

Department of Urology, Mayo Clinic, Rochester, MN, USA

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Royal National Orthopaedic Hospital - Stanmore, Stanmore, Middlesex, UK

Roberto Tirabosco

Department of Biochemistry, Genetics and Immunology, University of Vigo, Vigo, Spain

Giovanni Paolo II / I.R.C.C.S. Cancer Institute, Bari, BA, Italy

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Neuroblastoma Genomics, German Cancer Research Center (DKFZ), Heidelberg, Germany

Umut H. Toprak

Fondazione Policlinico Universitario Gemelli IRCCS, Rome, Italy, Rome, Italy

Giampaolo Tortora

University of Verona, Verona, Italy

Centre National de Génotypage, CEA - Institute de Génomique, Evry, France

CAPHRI Research School, Maastricht University, Maastricht, ER, The Netherlands

David Townend

Department of Biopathology, Centre Léon Bérard, Lyon, France

Isabelle Treilleux

Université Claude Bernard Lyon 1, Villeurbanne, France

Core Research for Evolutional Science and Technology (CREST), JST, Tokyo, Japan

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Department of Biological Sciences, Laboratory for Medical Science Mathematics, Graduate School of Science, University of Tokyo, Yokohama, Japan

Department of Medical Science Mathematics, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan

Cancer Ageing and Somatic Mutation Programme, Wellcome Sanger Institute, Hinxton, UK

Jose M. C. Tubio

University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK

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Centre for Cancer Research and Cell Biology, Queen’s University, Belfast, UK

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Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Naoto T. Ueno

Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA

Christopher Umbricht

Department of Oncology-Pathology, Science for Life Laboratory, Karolinska Institute, Stockholm, Sweden

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School of Cancer Sciences, Faculty of Medicine, University of Southampton, Southampton, UK

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Department of Gene Technology, Tallinn University of Technology, Tallinn, Estonia

Liis Uusküla-Reimand

Genetics and Genome Biology Program, SickKids Research Institute, The Hospital for Sick Children, Toronto, ON, Canada

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Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway

Miguel Vazquez

Argmix Consulting, North Vancouver, BC, Canada

Shankar Vembu

Department of Information Technology, Ghent University, Interuniversitair Micro-Electronica Centrum (IMEC), Ghent, Belgium

Lieven P. C. Verbeke

Nuffield Department of Surgical Sciences, John Radcliffe Hospital, University of Oxford, Oxford, UK

Clare Verrill

Institute of Mathematics and Computer Science, University of Latvia, Riga, LV, Latvia

Juris Viksna

Discipline of Pathology, Sydney Medical School, University of Sydney, Sydney, NSW, Australia

Ricardo E. Vilain

Department of Applied Mathematics and Theoretical Physics, Centre for Mathematical Sciences, University of Cambridge, Cambridge, UK

Ignacio Vázquez-García

Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA

Ignacio Vázquez-García & Venkata D. Yellapantula

Department of Statistics, Columbia University, New York, NY, USA

Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden

Claes Wadelius

School of Electronic and Information Engineering, Xi’an Jiaotong University, Xi’an, China

Jiayin Wang & Kai Ye

Department of Histopathology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

Anne Y. Warren

Oxford NIHR Biomedical Research Centre, University of Oxford, Oxford, UK

David C. Wedge

Georgia Regents University Cancer Center, Augusta, GA, USA

Paul Weinberger

Wythenshawe Hospital, Manchester, UK

Department of Genetics, Washington University School of Medicine, St.Louis, MO, USA

Michael C. Wendl

Department of Biological Oceanography, Leibniz Institute of Baltic Sea Research, Rostock, Germany

Johannes Werner

Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK

Justin P. Whalley

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA

Thoracic Oncology Laboratory, Mayo Clinic, Rochester, MN, USA

Dennis Wigle

Richard K. Wilson

Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, Mayo Clinic, Rochester, MN, USA

Boris Winterhoff

International Institute for Molecular Oncology, Poznań, Poland

Maciej Wiznerowicz

Poznan University of Medical Sciences, Poznań, Poland

Genomics and Proteomics Core Facility High Throughput Sequencing Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany

Stephan Wolf

NCCS-VARI Translational Research Laboratory, National Cancer Centre Singapore, Singapore, Singapore

Bernice H. Wong

Edison Family Center for Genome Sciences and Systems Biology, Washington University, St. Louis, MO, USA

Winghing Wong

MRC-University of Glasgow Centre for Virus Research, Glasgow, UK

Derek W. Wright

Department of Medical Informatics and Clinical Epidemiology, Division of Bioinformatics and Computational Biology, OHSU Knight Cancer Institute, Oregon Health and Science University, Portland, OR, USA

Guanming Wu

School of Electronic Information and Communications, Huazhong University of Science and Technology, Wuhan, China

Department of Applied Mathematics and Statistics, Johns Hopkins University, Baltimore, MD, USA

Department of Cancer Genome Informatics, Graduate School of Medicine, Osaka University, Osaka, Japan

Shinichi Yachida

Institute of Computer Science, Heidelberg University, Heidelberg, Germany

Sergei Yakneen

School of Mathematics and Statistics, University of Sydney, Sydney, NSW, Australia

Jean Y. Yang

Ben May Department for Cancer Research, University of Chicago, Chicago, IL, USA

Lixing Yang

Department of Human Genetics, University of Chicago, Chicago, IL, USA

Tri-Institutional PhD Program in Computational Biology and Medicine, Weill Cornell Medicine, New York, NY, USA

Xiaotong Yao

The First Affiliated Hospital, Xi’an Jiaotong University, Xi’an, China

Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China

Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX, USA

Kaixian Yu & Hongtu Zhu

Duke-NUS Medical School, Singapore, Singapore

Department of Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China

School of Computing Science, University of Glasgow, Glasgow, UK

Division of Orthopaedic Surgery, Oslo University Hospital, Oslo, Norway

Olga Zaikova

Eastern Clinical School, Monash University, Melbourne, VIC, Australia

Nikolajs Zeps

Epworth HealthCare, Richmond, VIC, Australia

Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA

Cheng-Zhong Zhang

Department of Biomedical Informatics, College of Medicine, The Ohio State University, Columbus, OH, USA

The Ohio State University Comprehensive Cancer Center (OSUCCC – James), Columbus, OH, USA

The University of Texas School of Biomedical Informatics (SBMI) at Houston, Houston, TX, USA

Zhongming Zhao

Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Department of Biochemistry and Molecular Genetics, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA

Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia

Anna deFazio

Department of Pathology, Erasmus Medical Center Rotterdam, Rotterdam, GD, The Netherlands

Carolien H. M. van Deurzen

Division of Molecular Carcinogenesis, The Netherlands Cancer Institute, Amsterdam, CX, The Netherlands

L. van’t Veer

Institute of Molecular Life Sciences and Swiss Institute of Bioinformatics, University of Zurich, Zurich, Switzerland

Christian von Mering

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  • , Sean Cleary
  • , Nicole Cloonan
  • , Colin C. Collins
  • , Ashton A. Connor
  • , Susanna L. Cooke
  • , Colin S. Cooper
  • , Leslie Cope
  • , Vincenzo Corbo
  • , Matthew G. Cordes
  • , Stephen M. Cordner
  • , Isidro Cortés-Ciriano
  • , Kyle Covington
  • , Prue A. Cowin
  • , Brian Craft
  • , David Craft
  • , Chad J. Creighton
  • , Erin Curley
  • , Ioana Cutcutache
  • , Karolina Czajka
  • , Bogdan Czerniak
  • , Rebecca A. Dagg
  • , Ludmila Danilova
  • , Maria Vittoria Davi
  • , Natalie R. Davidson
  • , Helen Davies
  • , Ian J. Davis
  • , Brandi N. Davis-Dusenbery
  • , Francisco M. De La Vega
  • , Ricardo De Paoli-Iseppi
  • , Timothy Defreitas
  • , Angelo P. Dei Tos
  • , Olivier Delaneau
  • , John A. Demchok
  • , German M. Demidov
  • , Deniz Demircioğlu
  • , Nening M. Dennis
  • , Robert E. Denroche
  • , Stefan C. Dentro
  • , Nikita Desai
  • , Vikram Deshpande
  • , Christine Desmedt
  • , Jordi Deu-Pons
  • , Noreen Dhalla
  • , Neesha C. Dhani
  • , Priyanka Dhingra
  • , Rajiv Dhir
  • , Anthony DiBiase
  • , Klev Diamanti
  • , Shuai Ding
  • , Huy Q. Dinh
  • , Luc Dirix
  • , HarshaVardhan Doddapaneni
  • , Michelle T. Dow
  • , Ronny Drapkin
  • , Oliver Drechsel
  • , Serge Serge
  • , Tim Dudderidge
  • , Ana Dueso-Barroso
  • , Andrew J. Dunford
  • , Michael Dunn
  • , Lewis Jonathan Dursi
  • , Fraser R. Duthie
  • , Ken Dutton-Regester
  • , Jenna Eagles
  • , Douglas F. Easton
  • , Stuart Edmonds
  • , Paul A. Edwards
  • , Sandra E. Edwards
  • , Rosalind A. Eeles
  • , Anna Ehinger
  • , Juergen Eils
  • , Adel El-Naggar
  • , Matthew Eldridge
  • , Kyle Ellrott
  • , Serap Erkek
  • , Georgia Escaramis
  • , Shadrielle M. G. Espiritu
  • , Xavier Estivill
  • , Dariush Etemadmoghadam
  • , Jorunn E. Eyfjord
  • , Bishoy M. Faltas
  • , Daiming Fan
  • , William C. Faquin
  • , Claudiu Farcas
  • , Matteo Fassan
  • , Aquila Fatima
  • , Francesco Favero
  • , Nodirjon Fayzullaev
  • , Ina Felau
  • , Sian Fereday
  • , Martin L. Ferguson
  • , Vincent Ferretti
  • , Lars Feuerbach
  • , Matthew A. Field
  • , J. Lynn Fink
  • , Gaetano Finocchiaro
  • , Cyril Fisher
  • , Matthew W. Fittall
  • , Anna Fitzgerald
  • , Rebecca C. Fitzgerald
  • , Adrienne M. Flanagan
  • , Neil E. Fleshner
  • , Paul Flicek
  • , John A. Foekens
  • , Kwun M. Fong
  • , Nuno A. Fonseca
  • , Christopher S. Foster
  • , Natalie S. Fox
  • , Michael Fraser
  • , Scott Frazer
  • , Milana Frenkel-Morgenstern
  • , William Friedman
  • , Joan Frigola
  • , Catrina C. Fronick
  • , Akihiro Fujimoto
  • , Masashi Fujita
  • , Masashi Fukayama
  • , Lucinda A. Fulton
  • , Robert S. Fulton
  • , Mayuko Furuta
  • , P. Andrew Futreal
  • , Anja Füllgrabe
  • , Stacey B. Gabriel
  • , Steven Gallinger
  • , Carlo Gambacorti-Passerini
  • , Jianjiong Gao
  • , Shengjie Gao
  • , Levi Garraway
  • , Øystein Garred
  • , Erik Garrison
  • , Nils Gehlenborg
  • , Josep L. L. Gelpi
  • , Joshy George
  • , Daniela S. Gerhard
  • , Clarissa Gerhauser
  • , Jeffrey E. Gershenwald
  • , Mark Gerstein
  • , Mohammed Ghori
  • , Ronald Ghossein
  • , Nasra H. Giama
  • , Richard A. Gibbs
  • , Bob Gibson
  • , Anthony J. Gill
  • , Pelvender Gill
  • , Dilip D. Giri
  • , Dominik Glodzik
  • , Vincent J. Gnanapragasam
  • , Maria Elisabeth Goebler
  • , Mary J. Goldman
  • , Carmen Gomez
  • , Abel Gonzalez-Perez
  • , Dmitry A. Gordenin
  • , James Gossage
  • , Kunihito Gotoh
  • , Ramaswamy Govindan
  • , Dorthe Grabau
  • , Janet S. Graham
  • , Robert C. Grant
  • , Anthony R. Green
  • , Eric Green
  • , Liliana Greger
  • , Nicola Grehan
  • , Sonia Grimaldi
  • , Sean M. Grimmond
  • , Robert L. Grossman
  • , Adam Grundhoff
  • , Gunes Gundem
  • , Qianyun Guo
  • , Manaswi Gupta
  • , Shailja Gupta
  • , Ivo G. Gut
  • , Marta Gut
  • , Jonathan Göke
  • , Andrea Haake
  • , David Haan
  • , Siegfried Haas
  • , James E. Haber
  • , Nina Habermann
  • , Faraz Hach
  • , Syed Haider
  • , Natsuko Hama
  • , Freddie C. Hamdy
  • , Anne Hamilton
  • , Mark P. Hamilton
  • , George B. Hanna
  • , Martin Hansmann
  • , Nicholas J. Haradhvala
  • , Olivier Harismendy
  • , Ivon Harliwong
  • , Arif O. Harmanci
  • , Eoghan Harrington
  • , Takanori Hasegawa
  • , David Haussler
  • , Steve Hawkins
  • , Shinya Hayami
  • , Shuto Hayashi
  • , D. Neil Hayes
  • , Stephen J. Hayes
  • , Nicholas K. Hayward
  • , Steven Hazell
  • , Allison P. Heath
  • , Simon C. Heath
  • , David Hedley
  • , Apurva M. Hegde
  • , David I. Heiman
  • , Michael C. Heinold
  • , Zachary Heins
  • , Lawrence E. Heisler
  • , Eva Hellstrom-Lindberg
  • , Mohamed Helmy
  • , Seong Gu Heo
  • , Austin J. Hepperla
  • , José María Heredia-Genestar
  • , Carl Herrmann
  • , Peter Hersey
  • , Julian M. Hess
  • , Holmfridur Hilmarsdottir
  • , Jonathan Hinton
  • , Satoshi Hirano
  • , Nobuyoshi Hiraoka
  • , Katherine A. Hoadley
  • , Asger Hobolth
  • , Ermin Hodzic
  • , Jessica I. Hoell
  • , Steve Hoffmann
  • , Oliver Hofmann
  • , Andrea Holbrook
  • , Aliaksei Z. Holik
  • , Michael A. Hollingsworth
  • , Oliver Holmes
  • , Robert A. Holt
  • , Chen Hong
  • , Eun Pyo Hong
  • , Jongwhi H. Hong
  • , Gerrit K. Hooijer
  • , Henrik Hornshøj
  • , Fumie Hosoda
  • , Volker Hovestadt
  • , William Howat
  • , Alan P. Hoyle
  • , Ralph H. Hruban
  • , Jianhong Hu
  • , Kuan-lin Huang
  • , Mei Huang
  • , Mi Ni Huang
  • , Vincent Huang
  • , Wolfgang Huber
  • , Thomas J. Hudson
  • , Michael Hummel
  • , Jillian A. Hung
  • , David Huntsman
  • , Ted R. Hupp
  • , Jason Huse
  • , Matthew R. Huska
  • , Barbara Hutter
  • , Carolyn M. Hutter
  • , Daniel Hübschmann
  • , Christine A. Iacobuzio-Donahue
  • , Charles David Imbusch
  • , Seiya Imoto
  • , William B. Isaacs
  • , Keren Isaev
  • , Shumpei Ishikawa
  • , Murat Iskar
  • , S. M. Ashiqul Islam
  • , Michael Ittmann
  • , Sinisa Ivkovic
  • , Jose M. G. Izarzugaza
  • , Jocelyne Jacquemier
  • , Valerie Jakrot
  • , Nigel B. Jamieson
  • , Gun Ho Jang
  • , Se Jin Jang
  • , Joy C. Jayaseelan
  • , Reyka Jayasinghe
  • , Stuart R. Jefferys
  • , Karine Jegalian
  • , Jennifer L. Jennings
  • , Seung-Hyup Jeon
  • , Peter A. Johansson
  • , Amber L. Johns
  • , Jeremy Johns
  • , Rory Johnson
  • , Todd A. Johnson
  • , Yann Joly
  • , Jon G. Jonasson
  • , Corbin D. Jones
  • , David R. Jones
  • , David T. W. Jones
  • , Nic Jones
  • , Steven J. M. Jones
  • , Jos Jonkers
  • , Young Seok Ju
  • , Hartmut Juhl
  • , Jongsun Jung
  • , Malene Juul
  • , Randi Istrup Juul
  • , Sissel Juul
  • , Natalie Jäger
  • , Rolf Kabbe
  • , Andre Kahles
  • , Abdullah Kahraman
  • , Vera B. Kaiser
  • , Hojabr Kakavand
  • , Sangeetha Kalimuthu
  • , Christof von Kalle
  • , Koo Jeong Kang
  • , Katalin Karaszi
  • , Beth Karlan
  • , Rosa Karlić
  • , Dennis Karsch
  • , Katayoon Kasaian
  • , Karin S. Kassahn
  • , Hitoshi Katai
  • , Mamoru Kato
  • , Hiroto Katoh
  • , Yoshiiku Kawakami
  • , Jonathan D. Kay
  • , Stephen H. Kazakoff
  • , Marat D. Kazanov
  • , Maria Keays
  • , Electron Kebebew
  • , Richard F. Kefford
  • , Manolis Kellis
  • , James G. Kench
  • , Catherine J. Kennedy
  • , Jules N. A. Kerssemakers
  • , David Khoo
  • , Vincent Khoo
  • , Narong Khuntikeo
  • , Ekta Khurana
  • , Helena Kilpinen
  • , Hark Kyun Kim
  • , Hyung-Lae Kim
  • , Hyung-Yong Kim
  • , Hyunghwan Kim
  • , Jaegil Kim
  • , Jihoon Kim
  • , Jong K. Kim
  • , Youngwook Kim
  • , Tari A. King
  • , Wolfram Klapper
  • , Leszek J. Klimczak
  • , Stian Knappskog
  • , Michael Kneba
  • , Bartha M. Knoppers
  • , Youngil Koh
  • , Jan Komorowski
  • , Daisuke Komura
  • , Mitsuhiro Komura
  • , Marcel Kool
  • , Jan O. Korbel
  • , Viktoriya Korchina
  • , Andrey Korshunov
  • , Michael Koscher
  • , Roelof Koster
  • , Zsofia Kote-Jarai
  • , Antonios Koures
  • , Milena Kovacevic
  • , Barbara Kremeyer
  • , Helene Kretzmer
  • , Markus Kreuz
  • , Savitri Krishnamurthy
  • , Dieter Kube
  • , Kiran Kumar
  • , Pardeep Kumar
  • , Sushant Kumar
  • , Yogesh Kumar
  • , Ritika Kundra
  • , Kirsten Kübler
  • , Ralf Küppers
  • , Jesper Lagergren
  • , Phillip H. Lai
  • , Peter W. Laird
  • , Sunil R. Lakhani
  • , Christopher M. Lalansingh
  • , Emilie Lalonde
  • , Fabien C. Lamaze
  • , Adam Lambert
  • , Eric Lander
  • , Pablo Landgraf
  • , Luca Landoni
  • , Anita Langerød
  • , Andrés Lanzós
  • , Denis Larsimont
  • , Erik Larsson
  • , Mark Lathrop
  • , Loretta M. S. Lau
  • , Chris Lawerenz
  • , Rita T. Lawlor
  • , Michael S. Lawrence
  • , Alexander J. Lazar
  • , Ana Mijalkovic Lazic
  • , Darlene Lee
  • , Donghoon Lee
  • , Eunjung Alice Lee
  • , Hee Jin Lee
  • , Jake June-Koo Lee
  • , Jeong-Yeon Lee
  • , Ming Ta Michael Lee
  • , Kjong-Van Lehmann
  • , Hans Lehrach
  • , Dido Lenze
  • , Conrad R. Leonard
  • , Daniel A. Leongamornlert
  • , Louis Letourneau
  • , Ivica Letunic
  • , Douglas A. Levine
  • , Lora Lewis
  • , Constance H. Li
  • , Haiyan Irene Li
  • , Shantao Li
  • , Siliang Li
  • , Xiaobo Li
  • , Xiaotong Li
  • , Xinyue Li
  • , Yilong Li
  • , Han Liang
  • , Sheng-Ben Liang
  • , Peter Lichter
  • , W. M. Linehan
  • , Ole Christian Lingjærde
  • , Dongbing Liu
  • , Eric Minwei Liu
  • , Fei-Fei Fei Liu
  • , Fenglin Liu
  • , Xingmin Liu
  • , Julie Livingstone
  • , Dimitri Livitz
  • , Naomi Livni
  • , Lucas Lochovsky
  • , Markus Loeffler
  • , Georgina V. Long
  • , Armando Lopez-Guillermo
  • , Shaoke Lou
  • , David N. Louis
  • , Laurence B. Lovat
  • , Yiling Lu
  • , Yong-Jie Lu
  • , Youyong Lu
  • , Claudio Luchini
  • , Ilinca Lungu
  • , Xuemei Luo
  • , Hayley J. Luxton
  • , Andy G. Lynch
  • , Lisa Lype
  • , Cristina López
  • , Carlos López-Otín
  • , Eric Z. Ma
  • , Yussanne Ma
  • , Gaetan MacGrogan
  • , Shona MacRae
  • , Tobias Madsen
  • , Kazuhiro Maejima
  • , Andrea Mafficini
  • , Dennis T. Maglinte
  • , Arindam Maitra
  • , Partha P. Majumder
  • , Luca Malcovati
  • , Giuseppe Malleo
  • , Graham J. Mann
  • , Luisa Mantovani-Löffler
  • , Kathleen Marchal
  • , Giovanni Marchegiani
  • , Elaine R. Mardis
  • , Adam A. Margolin
  • , Maximillian G. Marin
  • , Julia Markowski
  • , Jeffrey Marks
  • , Tomas Marques-Bonet
  • , Marco A. Marra
  • , Luke Marsden
  • , John W. M. Martens
  • , Sancha Martin
  • , Jose I. Martin-Subero
  • , Iñigo Martincorena
  • , Alexander Martinez-Fundichely
  • , Yosef E. Maruvka
  • , R. Jay Mashl
  • , Charlie E. Massie
  • , Thomas J. Matthew
  • , Lucy Matthews
  • , Erik Mayer
  • , Simon Mayes
  • , Michael Mayo
  • , Faridah Mbabaali
  • , Karen McCune
  • , Ultan McDermott
  • , Patrick D. McGillivray
  • , Michael D. McLellan
  • , John D. McPherson
  • , John R. McPherson
  • , Treasa A. McPherson
  • , Samuel R. Meier
  • , Alice Meng
  • , Shaowu Meng
  • , Andrew Menzies
  • , Neil D. Merrett
  • , Sue Merson
  • , Matthew Meyerson
  • , William Meyerson
  • , Piotr A. Mieczkowski
  • , George L. Mihaiescu
  • , Sanja Mijalkovic
  • , Tom Mikkelsen
  • , Michele Milella
  • , Linda Mileshkin
  • , Christopher A. Miller
  • , David K. Miller
  • , Jessica K. Miller
  • , Gordon B. Mills
  • , Ana Milovanovic
  • , Sarah Minner
  • , Marco Miotto
  • , Gisela Mir Arnau
  • , Lisa Mirabello
  • , Chris Mitchell
  • , Satoru Miyano
  • , Naoki Miyoshi
  • , Shinichi Mizuno
  • , Fruzsina Molnár-Gábor
  • , Malcolm J. Moore
  • , Richard A. Moore
  • , Sandro Morganella
  • , Carl Morrison
  • , Lisle E. Mose
  • , Catherine D. Moser
  • , Ferran Muiños
  • , Loris Mularoni
  • , Andrew J. Mungall
  • , Karen Mungall
  • , Elizabeth A. Musgrove
  • , David Mutch
  • , Francesc Muyas
  • , Donna M. Muzny
  • , Alfonso Muñoz
  • , Jerome Myers
  • , Ola Myklebost
  • , Peter Möller
  • , Genta Nagae
  • , Adnan M. Nagrial
  • , Hardeep K. Nahal-Bose
  • , Hitoshi Nakagama
  • , Hidewaki Nakagawa
  • , Hiromi Nakamura
  • , Toru Nakamura
  • , Kaoru Nakano
  • , Tannistha Nandi
  • , Jyoti Nangalia
  • , Mia Nastic
  • , Arcadi Navarro
  • , Fabio C. P. Navarro
  • , David E. Neal
  • , Gerd Nettekoven
  • , Felicity Newell
  • , Steven J. Newhouse
  • , Yulia Newton
  • , Alvin Wei Tian Ng
  • , Anthony Ng
  • , Jonathan Nicholson
  • , David Nicol
  • , Yongzhan Nie
  • , G. Petur Nielsen
  • , Morten Muhlig Nielsen
  • , Serena Nik-Zainal
  • , Michael S. Noble
  • , Katia Nones
  • , Paul A. Northcott
  • , Faiyaz Notta
  • , Brian D. O’Connor
  • , Peter O’Donnell
  • , Maria O’Donovan
  • , Sarah O’Meara
  • , Brian Patrick O’Neill
  • , J. Robert O’Neill
  • , David Ocana
  • , Angelica Ochoa
  • , Christopher Ogden
  • , Hideki Ohdan
  • , Kazuhiro Ohi
  • , Lucila Ohno-Machado
  • , Karin A. Oien
  • , Akinyemi I. Ojesina
  • , Hidenori Ojima
  • , Takuji Okusaka
  • , Larsson Omberg
  • , Choon Kiat Ong
  • , Stephan Ossowski
  • , German Ott
  • , B. F. Francis Ouellette
  • , Christine P’ng
  • , Marta Paczkowska
  • , Salvatore Paiella
  • , Chawalit Pairojkul
  • , Marina Pajic
  • , Qiang Pan-Hammarström
  • , Elli Papaemmanuil
  • , Irene Papatheodorou
  • , Nagarajan Paramasivam
  • , Ji Wan Park
  • , Joong-Won Park
  • , Keunchil Park
  • , Kiejung Park
  • , Peter J. Park
  • , Joel S. Parker
  • , Simon L. Parsons
  • , Harvey Pass
  • , Danielle Pasternack
  • , Alessandro Pastore
  • , Ann-Marie Patch
  • , Iris Pauporté
  • , Antonio Pea
  • , John V. Pearson
  • , Chandra Sekhar Pedamallu
  • , Jakob Skou Pedersen
  • , Paolo Pederzoli
  • , Nathan A. Pennell
  • , Charles M. Perou
  • , Marc D. Perry
  • , Gloria M. Petersen
  • , Nicholas Petrelli
  • , Robert Petryszak
  • , Stefan M. Pfister
  • , Mark Phillips
  • , Oriol Pich
  • , Hilda A. Pickett
  • , Todd D. Pihl
  • , Nischalan Pillay
  • , Sarah Pinder
  • , Mark Pinese
  • , Andreia V. Pinho
  • , Esa Pitkänen
  • , Xavier Pivot
  • , Elena Piñeiro-Yáñez
  • , Laura Planko
  • , Christoph Plass
  • , Paz Polak
  • , Tirso Pons
  • , Irinel Popescu
  • , Olga Potapova
  • , Aparna Prasad
  • , Shaun R. Preston
  • , Manuel Prinz
  • , Antonia L. Pritchard
  • , Stephenie D. Prokopec
  • , Elena Provenzano
  • , Xose S. Puente
  • , Sonia Puig
  • , Montserrat Puiggròs
  • , Sergio Pulido-Tamayo
  • , Gulietta M. Pupo
  • , Colin A. Purdie
  • , Michael C. Quinn
  • , Raquel Rabionet
  • , Janet S. Rader
  • , Bernhard Radlwimmer
  • , Petar Radovic
  • , Benjamin Raeder
  • , Keiran M. Raine
  • , Manasa Ramakrishna
  • , Kamna Ramakrishnan
  • , Suresh Ramalingam
  • , W. Kimryn Rathmell
  • , Tobias Rausch
  • , Guido Reifenberger
  • , Jüri Reimand
  • , Jorge Reis-Filho
  • , Victor Reuter
  • , Iker Reyes-Salazar
  • , Matthew A. Reyna
  • , Sheila M. Reynolds
  • , Esther Rheinbay
  • , Yasser Riazalhosseini
  • , Andrea L. Richardson
  • , Julia Richter
  • , Matthew Ringel
  • , Markus Ringnér
  • , Yasushi Rino
  • , Karsten Rippe
  • , Jeffrey Roach
  • , Lewis R. Roberts
  • , Nicola D. Roberts
  • , Steven A. Roberts
  • , A. Gordon Robertson
  • , Alan J. Robertson
  • , Javier Bartolomé Rodriguez
  • , Bernardo Rodriguez-Martin
  • , F. Germán Rodríguez-González
  • , Michael H. A. Roehrl
  • , Marius Rohde
  • , Hirofumi Rokutan
  • , Gilles Romieu
  • , Ilse Rooman
  • , Tom Roques
  • , Mara Rosenberg
  • , Philip C. Rosenstiel
  • , Andreas Rosenwald
  • , Edward W. Rowe
  • , Romina Royo
  • , Steven G. Rozen
  • , Mark A. Rubin
  • , Carlota Rubio-Perez
  • , Vasilisa A. Rudneva
  • , Borislav C. Rusev
  • , Andrea Ruzzenente
  • , Gunnar Rätsch
  • , Radhakrishnan Sabarinathan
  • , Veronica Y. Sabelnykova
  • , Sara Sadeghi
  • , Natalie Saini
  • , Mihoko Saito-Adachi
  • , Gordon Saksena
  • , Roberto Salgado
  • , Leonidas Salichos
  • , Richard Sallari
  • , Charles Saller
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  • , L. van’t Veer
  •  & Christian von Mering

Contributions

M.G., C.J., I.L., S.G., P.A., D.R., D.G.L., P.T.S. and P.V.L. performed timing of point mutations and copy number gains. S.G. and M.G. performed qualitative timing of driver point mutations and analyses of synchronous gains, L.J. timed secondary copy number gains. I.L., T.J.M., D.R., D.G.L., D.C.W. and G.G. performed relative timing of somatic driver events and implemented integrative models. C.J., Y.R., M.G., Q.D.M. and P.V.L. performed timing of mutational signatures. M.G. performed real-time estimation of whole-genome duplication and subclonal diversification. S.G. assessed mutation rates in relapsed samples. C.J., M.G., I.L., Y.R., D.R. and P.V.L. constructed cancer timelines. M.G., C.J., I.L., S.C.D., S.G., T.J.M., Y.R., P.A., J.D., P.C.B., D.D.B., V.M., Q.D.M., P.T.S., D.C.W. and P.V.L. interpreted the results. S.C.D., I.L., J.W., A.D., I.V.-G., K. Yuan, G.M., M.P., S.M., N.D., K. Yu, S. Sengupta, K.H., M.T., J.D., D.G.L., D.R., J.L., M.C., S.C.S., Y.J., F.M., V.M., H.Z., W.W., Q.D.M., D.C.W. and P.V.L. performed subclonal architecture analysis. S.C.D., I.L., K.K., V.M., M.P., X.Y., D.G.L., S. Schumacher, R.B., M.I., M.S., D.C.W. and P.V.L. performed copy number analysis. J.W., S.C.D., I.L., K.H., D.G.L., K.K., D.R., D.C.W., Q.D.M. and P.V.L. derived a consensus of copy number analysis results. K. Yu, M.T., A.D., S.C.D., I.L., D.C.W., M.G., P.V.L., Q.D.M. and W.W. derived a consensus of subclonal architecture results. Y.F. and W.W. contributed to subclonal mutation calls. P.T.S., D.C.W. and P.V.L. coordinated the study. M.G., C.J., P.T.S., Y.R., I.L., Q.D.M., D.C.W. and P.V.L. wrote the manuscript, which all authors approved. S.C.D., I.L., M.G., C.J., K.H., M.T., J.W., A.G.D., K. Yu, S.G., Y.R. and G.M. in the PCAWG Evolution & Heterogeneity Working Group contributed equally. W.W., Q.D.M., P.T.S., D.C.W. and P.V.L. in the PCAWG Evolution & Heterogeneity Working Group jointly supervised the work.

Corresponding authors

Correspondence to Moritz Gerstung or Peter Van Loo .

Ethics declarations

Competing interests.

R.B. owns equity in Ampressa Therapeutics. G.G. receives research funds from IBM and Pharmacyclics and is an inventor on patent applications related to MuTect, ABSOLUTE, MutSig, MSMuTect and POLYSOLVER. I.L. is a consultant for PACT Pharma. B.J.R. is a consultant at and has ownership interest (including stock and patents) in Medley Genomics. All other authors declare no competing interests.

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Extended data figures and tables

Extended data fig. 1 summary of all results obtained for colorectal adenocarcinoma ( n  = 60) as an example..

a , Clustered heat maps of mutational timing estimates for gained segments, per patient. Colours as indicated in main text: green represents early clonal events, purple represents late clonal. b , Relative ordering of copy number events and driver mutations across all samples. c , Distribution of mutations across early clonal, late clonal and subclonal stages, for the most common driver genes. A maximum of 10 driver genes are shown. d , Clustered mutational signature fold changes between early clonal and late clonal stages, per patient. Green and purple indicate, respectively, a signature decrease and increase in late clonal from early clonal mutations. Inactive signatures are coloured white. e , As in d but for clonal versus subclonal stages. Blue indicates a signature decrease and red an increase in subclonal from clonal mutations. f , Typical timeline of tumour development. Similar result summaries for all other cancer types can be found in the  Supplementary Information (pages 46–77).

Extended Data Fig. 2 Comparison of methods used for timing of individual copy number gains.

a , b , Pairwise comparison of the three approaches for timing individual copy number gains. c , Comparison using simulated data, showing high concordance.

Extended Data Fig. 3 Early copy number gains in brain cancers.

a , Three illustrative examples of glioblastoma with trisomy 7. The red arrow depicts the expected VAF cluster of point mutations preceding trisomy 7, which usually contains less than three SNVs. b , Distributions of the number of SNVs preceding trisomy 7 and total number of mutations on chromosome (chr) 7 in n  = 34 GBM samples with trisomy 7. c , Medulloblastoma example with isochromosome 17q. d , Distributions of SNVs on 17q in n  = 95 samples with isochromosome 17q; 74 out of 95 samples have less than 1 SNV preceding the isochromosome.

Extended Data Fig. 4 Validation of relative ordering model reconstruction based on simulated cohorts of whole-genome samples.

a , Relative ordering model (PhylogicNDT LeagueModel) results for a simulated cohort of samples ( n  = 100) from a single generalized relative order of events (with varied prevalence) showing high concordance with the true trajectory. Probability distributions show the uncertainty of timing for specific events in the cohort. b , Relative ordering model results on a simulated cohort of samples ( n  = 95) from a complex mixture of trajectories with different order of events showing high concordance with the expected average trajectory. c , Estimation of accuracy of the relative ordering model reconstruction by simulation of a set of 100 cohorts ( n (samples) = 100) with random trajectory mixtures and quantifying the distance in log odds early/late from perfect ordering. For the vast majority of events (even with low number of occurrences in the cohort), the log odds error does not exceed 1, confirming that very few events would switch between timing categories. The inset box corresponds to the first and third quartiles of the distribution, the horizontal line indicates the median and whiskers include data within 1.5× the IQR from the box. d , Simulated data show concordant timing in cohorts with WGD ( n  = 245). Exclusion of samples with WGD (right, n  = 242) introduces only a mild drop in accuracy, indicating that WGD is beneficial but not necessary for the reconstruction. Red dot = true rank. e , Estimated log odds in observed data including WGD (left, n  = 245) and without (right, n  = 242), across different mutation types. The inset box corresponds to the first and third quartiles of the distribution, the horizontal line indicates the median and whiskers include data within 1.5× the IQR from the box.

Extended Data Fig. 5 Correlation between the league model and Bradley–Terry model ordering.

Direct comparison for each tumour type of the league and Bradley–Terry models for determining the order of recurrent somatic mutations and copy number events. Axes indicate the ordered events observed in the respective tumour types. Correlation is quantified by Spearman’s rank correlation coefficient. A total of n  = 756 ordered events are shown.

Extended Data Fig. 6 Examples of mutation spectrum changes across tumour evolution.

a , Three examples of tumours with substantial changes between mutation spectra of early (top) and late (bottom) clonal time points. b , Three examples of tumours with substantial changes between mutation spectra of clonal (top) and subclonal (bottom) time points.

Extended Data Fig. 7 Overview of early-to-late clonal and clonal-to-subclonal signature changes across tumour types.

a , b , Pie charts representing signature changes per cancer type for early-to-late clonal signature changes ( a ) and clonal-to-subclonal signature changes ( b ). Signatures that decrease between early and late are coloured green; signatures that increase are purple. The size of each pie chart represents the frequency of each signature. Signatures are split into three categories: (1) clock-like, comprising the putative clock signatures 1 and 5; (2) frequent, which are signatures present in ten or more cancer types; and (3) cancer-type specific, which are in fewer than ten cancer types and are often limited to specific cohorts.

Extended Data Fig. 8 Age-dependent mutation burden and relapse samples indicate near-normal CpG>TpG mutation rate in cancer, with moderate acceleration during carcinogenesis.

a , Across all cancer samples, a predominantly linear accumulation of CpG>TpG mutations (scaled to copy number) is observed over time, as measured by the age at diagnosis. b , Cancer-specific analysis of the CpG>TpG mutation burden as a function of age at diagnosis for n  = 1,978 samples of 34 informative cancer types. The dotted line denotes the median mutations per year (that is, not offset), and shading denotes the 95% credible interval of a hierarchical Bayesian linear regression model across all data points. Slope and intercepts are drawn for each cancer type from a gamma distribution, respectively; inference was done by Hamiltonian Monte Carlo sampling. c , Maximum a posteriori estimates of rate and offset for 34 cancer types with 95% credible intervals as defined in b . d , Mutation rate inferred from cancer as in b and from selected normal tissue sequencing studies of n  = 140 normal haematopoietic stem cells, n  = 1 normal skin sample, n  = 182 samples from normal endometrium, and n  = 445 normal colonic crypts; error bars denote the 95% confidence interval. e , Median fraction of mutations attributed to linear age-dependent accumulation, based on estimates from b and the age at diagnosis for each sample. Error bars denote the 95% credible interval. f , g , CpG>TpG mutations per gigabase for ovarian cancer ( f ) and breast cancer ( g ) samples with matched primary and relapse samples. h , Increase in CpG>TpG mutation rate inferred from paired primary and relapse samples for six cancer types. Bars denote the range of the rate increase for different scenarios of copy number evolution, assuming ploidy changes have occurred prior (upper value) or posterior (lower value) to the branching between primary and relapse sample.

Extended Data Fig. 9 Real-time estimates indicate long latencies for some samples caused by the absence of early mutations.

a , Time of WGD for n  = 571 individual patients, split by tumour type with an estimated mutation rate increase of 5×, except for ovary–adenocarcinoma (7.5×) and CNS (2.5×). Error bars represent 80% confidence intervals, reflecting uncertainty stemming from the number of mutations per segment and onset of the rate increase. Box plots demarcate the quartiles and median of the distribution with whiskers indicating 5% and 95% quantiles. b , Scatter plots showing the time of diagnosis ( x axis) and inferred time of WGD ( y axis) with error bars as in a . c , Scatter plot of early (co-amplified) CpG>TpG mutations ( y axis) as a function of the mutational time estimate of WGD ( x axis). The black line denotes a nonlinear loess fit with 95% confidence interval. Colours define the cancer type as in a . d , Total CpG>TpG mutations ( y axis) as a function of the mutation time estimate of WGD ( x axis). Colours and fit as in c . Early molecular timing is thus caused by a depletion of early CpG>TpG mutations, rather than an inflation of late CpG>TpG mutations. e , Estimated median WGD latency of n  = 571 patients as in a for fixed ( x axis) versus patient specific rate increases, depending on the observed CpG>TpG mutation burden, allowing for a higher (up to 10×) mutation rate increase in samples with more mutations ( y axis). Error bars denote the IQR. f , Timing of subclonal diversification using CpG>TpG mutations in n  = 1,953 individual patients. Box plots and error bars for data points as in a . g , Comparison of the median duration of subclonal diversification per cancer type assuming branching and linear phylogenies.

Supplementary information

Supplementary information.

This file contains a more detailed description of all methods, three supplementary notes, and summary pages for each PCAWG cohort, with sample-level figures representing the results of each of the life history analyses: timing of gains, ordering of events, timing of drivers, signature changes and evolutionary timelines.

Reporting Summary

PCAWG Consortium author list: This file contains a full list of consortium members.

Source Data Fig. 1

Source data fig. 2, source data fig. 3, source data fig. 4, source data fig. 5, source data fig. 6, source data extended data fig. 3, source data extended data fig. 5, source data extended data fig. 6, source data extended data fig. 8, source data extended data fig. 9, rights and permissions.

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Gerstung, M., Jolly, C., Leshchiner, I. et al. The evolutionary history of 2,658 cancers. Nature 578 , 122–128 (2020). https://doi.org/10.1038/s41586-019-1907-7

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Comprehensive cancer centers panel 2021

The three comprehensive cancer centers that set the model for a nation

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Directors of the first three NCI -designated Comprehensive Cancer Centers are learning from the past, starting with the National Cancer Act , and mapping an equitable future for oncology.

On July 29, 2021, the Cancer History Project convened panelists Candace S. Johnson, president and CEO of Roswell Park Comprehensive Cancer Center, Craig B. Thompson, president and CEO of Memorial Sloan Kettering Cancer Center, and Peter WT Pisters, president of MD Anderson Cancer Center, for a two hour Zoom session moderated by co-editor Otis W. Brawley. 

A summary of the event is published in The Cancer Letter , and a full transcript and video are available below.

Otis Brawley: Hello. I’m Otis Brawley of Johns Hopkins University and I’m one of the co-editors of The Cancer History Project along with Paul Goldberg, and we’re staffed by Katie Goldberg.  

I want to welcome you to this evening’s discussion, where we’re going to talk about cancer centers and the history of cancer in the United States, especially since the National Cancer Act.  

It was in December of 1971 that Richard Nixon signed the National Cancer Act. There was a lot of buildup politically throughout the 1950s and 60s in order to sign the National Cancer Act. And now 50 years later after we look at what many refer to as Nixon’s War on Cancer, it’s time for an after action report, where we sit back and assess where we’ve come from, what we’ve done, and that’s how we figure out where we’re going in the future. I want to welcome all the viewers.

We’re an international audience. There are people from the United States, people from Canada, people from as far away as Australia who are viewing us this evening.  

We have some wonderful guests. These are three of the leaders in oncology today, three amazing physicians, and—I know them all personally—amazing human beings who lead three of the great cancer centers of our time. They’re going to talk to us today a little bit about cancer centers, the National Cancer Act, and tell us a little about, maybe give us a glimpse as to where cancer research and cancer care is going into our future.  

And so you’ve seen the introductions of Dr. Candace Johnson of Roswell Park, Dr. Craig Thompson of Memorial Sloan Kettering, and Dr. Peter Pisters of the MD Anderson Cancer Center. Thank you for joining us today.

I must say, being with the three of you, I do feel like Forrest Gump. You are all incredibly distinguished in your own right, and you run amazing organizations that have contributed so much and are, and will contribute so much in the fight against cancer.

Let’s start out a little bit talking about the history of cancer centers. What is a cancer center and how did they get founded is where I think we should start it out. And let me start with you, ladies first.

Dr. Johnson, Roswell Park. I know Roswell Park himself was a surgeon, but I don’t even know if he founded the institution. I’ve heard it referred to as New York State Institute for the Study of Malignant Disease—catchy name, by the way—but tell us a little about Roswell Park and where it came from.

Candace Johnson: Roswell Park, you’ve got to remember, this was in the late 1800s. So this was 1898, somewhere around in there. And Buffalo, New York was the second largest city in the country. So, that’s obviously not true now, but we were the Erie Canal. I mean, this was a really booming place. If you look at our downtown, lots of incredible architects built wonderful buildings here and, with the Renaissance, we’re trying to bring that back. So this was a site of much commerce and activity.  

And so Roswell Park was a surgeon. He did found the New York State Institute for the Study of Malignant Disease. He was really a Renaissance man and, actually, Roswell Park IV just passed away during COVID. Not of COVID, he was a longtime multiple myeloma survivor and succumbed to the disease during COVID. But he was Roswell Park IV, he was a professor at Buff State. So we have a long history of Roswell Park, the family.  

And he thought out of the box. He really thought the way we’re going to understand this disease was to study it, sort of the beginnings of translational research, if you were. And in 1898, you were more likely to die of an infectious disease than cancer, perhaps, but he really saw a real need for this.  

And he also thought, and this was very revolutionary for the time, that the government should support this research. And it really goes to the tenet of how prominent a role Roswell Park played in that because he was very well connected to the president, to President Taft at the time, and really advocated for government support for, in cancer.

Brawley: Now over the years, you’ve had some amazing people there. I remember from a… You’re a basic scientist, so I’m going to dabble just a little bit. I remember a little about basic science about glucose being converted to glycogen. As I recall the Coris, a married couple at Roswell Park, won the Nobel Prize for that, right?

Johnson: Yeah, they did. And Roswell was supported by New York State, hence, significantly so during those early years. And really, there were a lot of very famous people that did their training here.  

We still have a summer program and little Roswell Park in Buffalo, New York has trained—people have spent summers at Roswell Park in this training program—and then went on to be leaders in the field. And so it’s really, we’ve played a big part in that.  

PSA was discovered here. Ming Chu and Dr. [Ming C.] Wang developed it. The same sort of test, if you will, that Hybritech uses today. In fact, the tech transfer people will say it was one that got away because we didn’t need anything else. I mean, can you imagine, we wouldn’t have to worry about the NCI because of the times.  

It was an invention that perhaps got away, but we have played a very prominent role in smoking cessation.

I don’t think people realize there was a gentleman in 1938, Dr. Levin— Morton Levin —who really made it his life’s work to [study] the evils of cancer and tobacco and their correlation with cancer. And we were very prominent in getting tobacco out of bars and restaurants in New York state.  

And then the Human Genome Project, where the back arrays that were sort of the foundation for the Human Genome Project were from a Buffalonian. And so a strong history in genetics.  

So, we’ve been a player. Two of the founding members that started AACR came from Roswell Park. They were Roswell Park physicians and scientists. And the first meeting of AACR was held here in Buffalo, New York.  

And so, we have our connection to the history of cancer and cancer research is strong.

Brawley: Now this idea of research and clinical care coming together, that too was done at Roswell Park, right? The hospital and the clinics.

Johnson: Most definitely. And I think we were probably one of the first centers to really not just treat cancer, but to really try to understand it and do research around it so that we could figure it out and treat it better.

Brawley: Dr. Craig Thompson, you’re at Memorial Sloan Kettering, the oldest private cancer center in the world, I am told. Tell us a little about the start of Memorial Sloan Kettering, because it started too at about the same time as Roswell Park, as I believe.

Craig Thompson: Oh, that’s right, Otis.  

So Memorial Sloan Kettering was formed actually in a slightly different way than Candace talked about. It was a group of physicians in 1880 that came together with some of the philanthropists in New York with the understanding that, even though this was, as Candace just said, the dawn of the microbial revolution, where we understood viruses and bacteria caused disease, that cancer seemed to them, as a group of seven physicians, to be somewhat different and that it needed its own research.  

And they got the philanthropic community because a number of well off families had been touched by cancer themselves. And it had this scare to it that it could occur, it seemed, in any organ. And there was dysfunction in that organ and it wasn’t attached to the microbial revolution.  

So we were able to raise, I think at the time, $3 million and proposed to build a hospital dedicated to cancer.

Now, I should say that because there’s international visitors, we weren’t the first private hospital in the world. We modeled ourselves off of The Royal Marsden, which was the very first, it was started in 1865, if I remember the year correctly. And they came together as a cancer research hospital over exactly the same reason, and New Yorkers believed we should have exactly the same thing in New York.  

So our mission was to understand this disease, to put it on the map. And we would do that through what is our tripartite mission, which is research, clinical care, and education—and then we met education in the broadest sense, trained those people that would do the research and the clinical care as Candace just said. And prove that by understanding the disease, we could provide better clinical care that led to our clinical trial efforts.  

And then the education, we are proud every year of the 3000 trainees that come through Memorial Sloan Kettering, and are exposed to the best of cancer research care and go out into the community and practice it throughout the world. We’re very proud of our alumni.  

The hospital was originally on Central Park West. The original hospital still exists on 104th, 105th street. It was actually built with round rotundas because they weren’t really sure that it wasn’t a virus or a bacteria, so they built a hospital with round rooms so there were no corners for microbes to lurk in. That was our proud first hospital.  

Our original hospital was led by surgeons and pathologists, just as Candace said. The leader of that group was William Coley . He was a sarcoma surgeon. He actually was the founder of Coley’s toxins and the idea that immunotherapy would make a difference. And in 1890, he launched our first dedicated research program into immunotherapy, starting with Coley’s toxins.  

We continued that continuously through its work on Lloyd Old and BCG, to our most recent work where Jim Allison realized checkpoint blockade, brought it into the clinic with other physicians here. And to its most recent iteration CAR T-cells led by Michel Sadelain and Isabelle Rivière.

So he was visionary at the very start, but he was at heart a surgeon. It was his care of a young woman who was 19 years old, who had osteosarcoma we believe, that led the Rockefeller family to be devoted to the institution. She was the closest friend of John Rockefeller Jr. and they were devastated with the loss of this close friend of their son. And they became the base of our philanthropy ever since, and brought people to the community. Ultimately Laurance Rockefeller became our chairman for many, many decades.  

Over the years, we started with surgery and pathology. Our first three chairmen are well known to everybody. I talked about Coley. The second was James Ewing, Ewing sarcoma. He was a pathologist. He put the pathology of cancer on the map. He wrote the first definitive pathology texts of the diversity of cancer.

And then the third was actually a practicing surgeon Peter [Pisters] will know well, and that was Allen Whipple, who’s best known for the Whipple procedure and pancreatic cancer as we went forward.  

We weren’t only surgery, though. In 1911, Madame Curie won her second Nobel Prize, which was really for the application of the understanding of radiation and its use in various modalities of therapy—and one that she championed was its use in medicine. And we hired one of her first trainees in the translation of radiation science to start a unit here at Memorial Sloan Kettering.  

I’m not sure where that would have gone, except that we were benefited by someone who took the opportunity to bring his daughter. He was a mining engineer from Denver. His name was James Wallace or James Douglas, excuse me. And his daughter had breast cancer. She had surgery out in the west. Didn’t go well. He brought her here to the surgeons at Memorial Sloan Kettering. Unfortunately, also didn’t go well. And then he took her to Madame Curie in Europe to see if radiation would help.  

Unfortunately for that young woman, it also didn’t go well and she died of breast cancer, but he became devoted because his mining included radium mining in the Denver area. And he committed to Memorial that all the radium he mined would come to Memorial. And between 1917 and 1926 Memorial had more radium than all the rest of the world combined sent to us.  

It was ultimately Madame Curie’s visit, first to Candace’s center to our center to Fox Chase , where she brought the one remaining ounce. We had nine ounces, but she brought one more ounce that was bought by the US government who also wanted to play in this.  

At that point, we became known as a radium hospital and we dedicated a quarter of the institution to exploring whether radiation could improve cancer therapy.

First, it was whole body radiation. Patients were put in the room with radium, but fortunately one of our first faculty that was recruited in 1917, Edith Quimby , who is a legend in the early stages of radiation therapy, brought out the first radiation dosing tables and standardized what the doses were that each tissue could take. And from that, she also, because she understood you could encapsulate radiation, made the first brachytherapy program.  

So we’re very proud of that and what Edith did. It’s had a long tradition in radiation therapy since then.  

We were the first center to use computers to plan the ability to deliver radiation. And from that came IMRT in the later years and, more recently, proton therapy. And we’ve had a great tradition ever since Edith put it on the roll to the rational and scientific use of radiation.  

Medical oncology, like for many of us, came to us after World War II, with people that actually came back to New York having been in—unfortunately—in the chemical warfare research department and came back and said, “We want to do this research for something good.”

Using the example of nitrogen mustard gas, started experimental chemotherapeutic program as a result. And that has continued on to this day.  

And as the formation of our medical oncology, we are able at that time to recruit [M.] Lois Murphy to start our pediatric program.

And so we had all of those programs in full place when the National Cancer Act came and it allowed us to have all three of the major modalities to do our clinical research and to inform our basic science research at the time.  

We’ve been incredibly proud of also our ability, our scope, to be able to bring additional therapies to bear on cancer from Jimmie Holland ’s pioneering work to start psycho-oncology and to build the understanding of the psychologic support that cancer patients need, the end of life work that Kathy Foley and others did around the use of opioids to deal with cancer pain, and the end products of that, and then more recently the basic research that got us to underpinning.  

I’ll just speak to one because it’s what everybody knows: One of our first chairmen of the department was in fact Charlotte Friend , of Friend leukemia virus, and she is actually the first person to ever show that differentiation therapy could actually reduce cancer.  

I think I’m really nervous about saying what’s currently going on. We’ve been proud to be with my two compatriots here, part of precision medicine, part of the immuno-oncology revolution, part of robotic surgery, part of proton therapy, and if I mention one faculty I’ll get in trouble because I won’t mention them all.

We’re very proud though, that they’ve received recognition as was just said by Candace. Seventeen of our faculty are members of the National Academy of Science, 25 of them are members of the National Academy of Medicine. Because in the end we balance the hospital, which is the here and now, to help and give hope to patients that actually face the disease, and our research is the future.  

It gives us the knowledge to engage in something you care about Otis, which is prevention. And to improve diagnosis and treatment, which is why freestanding cancer centers have existed since we started in 1884.

Brawley: As I hear about the early radiation therapy studies, you’re starting to rattle my definition of translational research because it really was translational.

Thompson: Exactly.

Brawley: We didn’t call it that in the 1920s. Of course, you and I didn’t call it anything in the 1920s.  

But anyway, Dr. Pisters, your institution was founded by a cotton man I understand. Tell us a little about MD Anderson, and the early history of MD Anderson.

Peter Pisters: Well, our history goes back to World War II when, presumably, the Texas legislature had been watching, potentially for decades, the innovation going on in New York State—in Buffalo and in New York. And the legislature at that time voted to create a state cancer hospital that would be devoted to research to cancer treatment, and positioned that cancer hospital under the jurisdiction of the University of Texas and its board of regents.  

And the hospital, as you alluded to Otis, received tremendous support from Monroe Dunaway [Anderson] , who was a cotton merchant. And he dedicated his business fortune for a series of charitable causes, including cancer. And so following his death, the hospital was named after him in recognition of the foundation support and the wisdom of the legislature.  

MD Anderson himself is clearly recognized as one of the fathers of the Texas Medical Center—a center that is now viewed as the largest medical center in the world and includes institutions such as MD Anderson, Texas Children’s Hospital, and Methodist.

And the initial MD Anderson facility was housed at the Baker Estate, as in James Baker. This was James Baker’s grandfather, who was a lawyer in Houston, and he donated his estate to create the first location for MD Anderson, which was in downtown Houston.  

And then MD Anderson moved to its present location where all of you probably know, in the Texas Medical Center, in 1954 during R. Lee Clark ’s tenure as president. My predecessors; Clark, LeMaistre , Mendelsohn , and DePinho have really transformed MD Anderson in ways that I think hopefully all of our viewers know and understand.  

We’re known for world-class cancer treatment, for research, for education, and also for the wisdom of Dr. LeMaistre, who inserted prevention into our mission statement. That was a quarter of a century ago, and we’ve made great strides in the science of prevention, in implementation science, and so many other aspects of how prevention could transform society.

All of us know that if we could succeed in prevention, we could put ourselves out of business. And so as we look at so many of the innovations that came out of MD Anderson, there are probably too many to summarize today, but I think one of the most important was the creation of multidisciplinary care centers that were organized around diseases. This was innovative. It aggregated groups of specialists around unique patients with specialized diseases, and that became a prototype for comprehensive cancer care delivery around the world.  

We’re also known for deep fusion, deep integration of clinical care and research. And that, I think, creates the opportunities for discovery. It supercharges physician-scientists who have opportunities to learn at the bedside and take questions back to the lab. And I think that is part of our secret sauce, and one of the reasons that we’ve been consistently identified as a top cancer center.  

When we look at the impact on society, there’s so many ways that that could be measured.

One measurement might be FDA oncology drug approvals. And if we look back over the last 15 years, MD Anderson has participated in one way, shape or form in the approval of 116 out of 251 oncology drug approvals. So it is literally the case that today, on Thursday, patients are receiving treatment at MD Anderson that will be approved by the FDA six months from now or a year from now.  

We’re proud of what we’ve accomplished, and look forward to taking a lot of the advances that Craig and Candace have talked about in driving an exciting future for cancer patients going forward.

Brawley: I just get a little bit emotional when you talk about your predecessors. Ron DePinho is a personal friend and John Mendelsohn and Mickey LeMaistre were also very good friends and mentors of mine. You come from a long lineage of just amazing leaders.  

Now, the three of you are at the top of your game, running leading cancer centers. I want to ask you, and you sort of delved into it a little bit Peter: Some cancer centers are matrix and very heavily integrated in university hospitals; some cancer centers are freestanding institutes as yours are.  

I’m about to ask something, this is sort of devilish of me, what’s the advantage of a matrix center versus a center that’s freestanding? Anybody want to jump in on that?

Johnson: Well, I’ll jump in because I came from University of Pittsburgh—very much a matrix cancer center. I think all of us on this panel would say the advantage of a freestanding center is you have more control.  

You’re not competing with all the other disciplines that are in a medical school for resources and you’re sort of… And the hospital, and matrix centers are many times owned by a different corporation, and so you’re fighting with that as well.  

But I think the advantage of a matrix center as you have all of us and especially for me, we’re in a small market. We don’t have perhaps as many deep pockets and endowments as my other two gentlemen here on this panel. And so for us, we’re sort of out there. So we have to survive and not only survive, we have to succeed and do really well on what we can bring to the table because we don’t have the luxury of being a matrix center and having the safety of the medical school or the university.

And so I think matrix centers are different. They have advantages too, because we’re all cancer here. Every person in this institution thinks, breathes, lives, cancer, regardless of where they come at it.  

The advantage of a matrix center is you have those engineering folks or those structural biologists where you can really, I mean, I always thought it was really fun to get into some of that stuff, because I was a pharmacologist in my research life and looking at how those structure function analysis happens. We don’t have that here at Roswell Park. So I think an advantage of a matrix center is you have more depth and breadth across all different disciplines.  

I’d still rather be a free standing center. And I bet you, you guys would agree with that.

Thompson: So I’ll chime in after Candace, because in fact, I started in the cancer center business as a director of a cancer center that was a matrix center at the University of Pennsylvania.  

There are a couple of huge advantages that speak to what Peter talked about at the end of his presentation. Particularly, academic medical centers that are with a matrix cancer center have one tremendous advantage that we don’t have, and that is a primary care network. And they have a public health mandate and usually a public health service such as the department that you work in at Johns Hopkins, Otis. And that gives you the ability to reach out with the knowledge, the understanding we have to get at all of our goal—the goal of all three of our freestanding institutions is to put ourselves out of business.  

And if we can do that through understanding and better therapies so that we don’t need to exist, our faculty and staff will be thrilled that they accomplished a mission that we’ve been at for 134 years.  

But that being said, there is a huge advantage to focus and that focus has allowed us, particularly in the field that you’re in Otis, to actually become the authority for our region. So when the city wants to have new laws on tobacco restriction, I can go to city council with the authority of our 137-year history to say we have got all the documented evidence that preventing tobacco addiction is absolutely an essential thing that the government needs to do, and be that authority.  

We can be the group that has the resources, as Candace said, to focus on, does it make a difference, now that we know that polyps are pre-malignant, to actually have a colonoscopy program, as Sid Winawer and Ann Zauber did?  

And so we can be the authority, and convene others to do that, to do a clinical trial that has gone on for 25 years, and we’re very proud. Just change the guidelines to 45 years, as the screening time is, sadly, we’ve seen colorectal cancer move earlier and earlier. We can pick our moments to do that.

And then, one of the most exciting projects that’s come out of that authority during my time as the president, was to realize that the largest health care workforce that is not coalesced around a major cancer that is increasing incidence, are dentists. Dentists see everybody in the city and everyone in our catchment area’s mouth. There are 40,000 dentists in New York City that actually are seeing people’s mouths.  

Coalescing them through our CME programs, through our research program that Jamie Ostroff runs, to train them in the standard of practice and do a trial, to do early detection and early prevention of oral lesions, has been tremendous, because it was an untapped resource. And as the convening authority, we could involve clinical trials like that, get the support of the NCI and make it a model for how to do it—and that’s an advantage of a freestanding institution.

Pisters: I think Craig and Candace have made great points. I can double-click on a couple of them just for emphasis. And my experience, obviously, comes back to being a CEO in a matrix environment with Princess Margaret, Toronto General, Toronto Western, a rehab institute, and an affiliation with the University of Toronto. And the clear benefit of the matrix environment, as Candace was alluding to, is that you’ve got a rich ecosystem, and you can be a beneficiary of the talent and the resources, the infrastructure, at the university, and that can foster tremendous collaboration and lots of opportunities.

On the other side of the ledger and the matrix environment, is the dynamic tension and funds flow, oftentimes between the health system CEO, the medical school dean, and the cancer center director, who have somewhat aligned agendas, but not always. And that can create tensions in an environment where the cancer center director has to compete with the organ transplant program, the cardiovascular program, the neuroscience program. And where, institutionally, at an enterprise level, there isn’t the fidelity and clarity on mission that you see in a cancer center. It is separated from the university environment.

When you look at the current situation I’m in, one of the benefits that we talk about internally is that we’re not a university and we’re not a medical school. And so, we can shed ourselves of many of the funds flow issues, the internal politics associated with that, and we can focus on making cancer history.  

And I think as we look closely, internally, we have the benefit of not having those politics, and we have the fidelity and clarity around what is it that we’re actually here to do. And as we think about that internally, and we talk about it, it’s symbolized by the cancer strike-through, it’s put into words by making cancer history.

Everyone in our institution, all 22,000 of our employees, understand why we’re here. It doesn’t matter if you’re a valet parker, a top-shelf neurosurgeon, a researcher, a laboratory technician, or a CEO, everyone knows this is why we’re here. And when you have that fidelity and clarity, you can drive deep engagement around purpose and meaning and work.  

And that, really, is a lot of the special sauce that exists in independent cancer center environments, where you’re freed from a lot of the politics, funds flow, and you can focus on what’s important.

Brawley: Great, great, great. Now I want to note to the audience, the Q&A function is open. And if you have any questions for any of our guests here, please go ahead and add, just write in the Q&A. I will read the questions as they come in, or we might bunch some of them together toward the end of our two-hour session here.  

I want to point out, we now know who MD Anderson is, we now know who Roswell Park. Since I’m from Detroit, I’m going to let folks know, this is a Jeopardy question, I’m sure. Sloan and Kettering were General Motors money. Kettering, actually, is the guy who created the modern-day automobile starter, so you didn’t have to get out in front of the car and crank the car up, as you might see in some old, old movies, the old silent movies.

Now, let’s get back to our point: cancer centers, at the time of the National Cancer Act, your three centers were consensus, comprehensive cancer centers, you need not apply. Everybody just accepted that you guys were the crème de la crème .  

How have cancer centers evolved over time? And I would actually, I’m going to say this—you guys don’t have to—many other institutions have tried to become like you. Just talk a little bit about the evolution of cancer centers and how they have changed over time.

Johnson: So, I think that one of the tenets of the cancer center program and the National Cancer Act was, cancer, it’s a complex disease. I think it was even acknowledged back in the ‘70s that this was not going to be an easy disease to treat. It was very multifactorial and different in every organ, and so forth.  

And so, you needed to have centers of excellence for innovative treatment, research, therapies. And so, it was thought that these centers should be within a day’s drive of every American. And so, if you look at a map, now in the early days, in the ‘70s, they were focused predominantly on the east because of the centers of activity. But if you look at a map today, there is, even in the west, even if you live in Montana, you’re within a day’s drive of an NCI-designated center.

And what it says to an American is that those centers, they’re going to know what to do with your cancer. So you may be treated in your community, but maybe you should go to one of those NCI-designated centers and make sure that there’s not something that you’re missing or there’s not some treatment that you could avail yourselves of.  

The other thing that I think is important is that, of those NCI-designated centers, we work very well together. I know, because Craig and I are not too far away, we’re at both ends of the state. And there will be people that we have sent to Memorial, because they have things that we don’t have.

But we have also gotten patients sent from Memorial to Roswell, because they live closer to us and we have things that Memorial doesn’t have, or they know that they could be treated here just as effectively.  

And so we do share. I mean, I get asked that from so many people. We do share, we do work together, and I think we do this for the betterment of all patients with cancer around this country. And so, I think that’s, to me, one of the real significance of the National Cancer Act is establishing these centers of excellence in cancer, because look at other diseases, you don’t have this

Thompson: Right. So our research mission, as Candace said, and you just alluded to Otis, was put on its legs, really, between 1935 and ‘45, when GM was the largest corporation in the world. Their headquarters were 10 blocks from us, and Alfred Sloan, their CEO, and Charles Kettering, who’s their chief engineer, turned their attention to an unsolved problem. And as Candace just alluded to, we knew it was too complex.  

Surgery wasn’t going to be the end-all and be-all cure. We needed additional things. And Charles Kettering was the proud man, okay, who not only had the starter, he invented the Slant-6, which was the successful car block engine for everybody.

They believed that if they funded our research institute, and we’d left the researchers alone, on their own, just like they invented a car, they would invent a therapy for cancer within five years. That’s actually what was in the document.  

Unfortunately—although we need, as both Candace and Peter have said, those colleagues who are engineers, and cellular engineering is the thing of today—we didn’t achieve that. Because, in fact, they both believed the research institute, a hospital, had to be separated. And it took us until 1960, 15 years of separate governance, but overlapping governance, to realize they were best together.

And so, in fact, in 1960, we formed the Memorial Sloan-Kettering Cancer Center to combine the Sloan-Kettering Institute and the hospital, Memorial Hospital for Cancer and Allied Disease, into one corporate entity, where we drew on each other. And that was timely, because in those next 10 years, we’re going to be part of the backbone, as my two colleagues are, of the reason we needed a National Cancer Act.  

And so what we really learned from that research is why all the other diseases had national institutes that were succeeding and were getting more funding, because they worked on an organ that had a physiology. So you could work on the heart and ask, what did it do and what goes wrong when you have a heart attack? When you have arrhythmia, what goes wrong with the conduction system?

But cancer is just too sporadic. It occurs in every organ. At the time, in 1960, it wasn’t amenable in most cases as patients presented, to surgical care. We didn’t have the diagnostic capability to do it early enough, and we were able to document that by having scientists who take the latest physiologic techniques come together. And so, the Cancer Act—we came together in 1960, the frustrations of coming…  

And I’ll give you our history. Our center grant, our cancer center support grant, started in 1964, four years after we came together. Because we just, simply, no investigator—this is Peter’s point of team-based science. So for us, team-based science started in 1960 when we realized we had to have the researchers and the clinicians working on the same platform, in the same… and bumping into each other in the lunchroom and having those conversations.

Our center grant came because we had 54 funded NCI grants. And the NCI said, “You’re driving us crazy, because you all want the same resources,” and made us bundle them all. We complained it was so much paperwork. We think about the paperwork today—they were complaining in 1964 there was too much paperwork. And the NCI, at least according to our records, threw up their hands and said, “Fine, put them all in one center grant.” And that gave us the resources to have cores that could support all of our clinicians, all of our researchers, to investigate human tissue, human biopsies, human cell line—our cell line program started then—and be able to focus on what now is the paradigm, the human as the subject, what the human natural disease is.

I embarrassed myself when I came 10 years ago to Memorial, when they told me, “We think cancer is 150 different diseases, because we’ve been part of the cancer sequencing projects.”  

And I said, “No, no, that’s way too complicated. We can’t have 100.”  

We unequivocally know there are over 400 entirely separable, need-to-be-treated diseases that are called cancer today. So there isn’t one organ. There isn’t one physiology. And the timing of the Cancer Center Act, the three of us came together and said, “We have to do this on a national level,” for the reason Candace said, so everybody has that hope that a freestanding cancer center is within a short distance of their own home. A network allowed us to take advantage of the revolution that started, also, in 1971, which was molecular biology.

We are the poster child of how much molecular biology can deliver to human health, with the TCGA, with the sequencing projects, the somatic mutations, the predisposition syndromes that have been figured out at a molecular level. That was all because of DNA sequencing, the understanding of molecular biology, and now the therapies that molecular biology provides us to treat this disease.  

It was just very timely for us to come together to understand that the research and the clinical care had to be hand in hand. We had to handle the tissues carefully to understand this disease, because it looked so diverse. And it allowed us to realize advantages that happened in our basic research. Rous sarcoma virus—I’m looking at the building that Rous sarcoma virus was discovered in at our sister institution, Rockefeller University.

My predecessor, Harold Varmus , with his colleague, Mike Bishop , cloned the gene, which was a homologue of a gene to launch the molecular era in the 1970s. The benefit of funding, that doubling of funding, because the National Cancer Act doubled the NCI’s budget—for our junior colleagues, they’ll be horrified, it went from $100 million, to $200 million.

That was a revolution that allowed the molecular era of cancer research to start. We, all three of us, and our colleagues, and all of our patients have benefited from that revolution over the last 50 years. Why do we see cancers’ mortality going down 1% a year, every year since 1990? And now it has accelerated in the last decade to 2% a year.

Brawley: You brought up a very important point. The NCI budget in 1971 was $200 million. Today, it’s about $6 billion.

Thompson: That’s right.  

Brawley: Did I step on you, Dr. Pisters?

Pisters: I’m going to say, Otis, taking into account that we have an international audience, and looking at the benefit of history, I really believe one thing that should be emphasized today is that, by starting out with three exemplars, and then by putting into place a set of criteria, this then became an aspirational goal through university presidents, medical school deans and health system CEOs.  

And oftentimes, that is really what led them on a pathway to create an NCI-designated Comprehensive Cancer Center. It infused the understanding of many of the complexities of cancer care delivery that Candace has really talked about, and that Craig has really elaborated on.

And it helped, really, to create geographic distribution that has been so beneficial to cancer patients. And I think that in the modern area, this has led to a degree of consumerism where the term cancer center is understood by lay people in fairly detailed terms, as a result of the fact that so many universities and medical schools really chartered a pathway and put into strategic goals, spoke to philanthropists, talked to their community, and now, we have an unbelievable network of 51 NCI-designated Comprehensive Cancer Centers that benefit society in ways that don’t exist, frankly, in other countries.

Brawley: Is the expectation of the American people that a cancer center is both a place that treats and a place that does basic and translational research? Am I right that people have come to expect that?

Pisters: I believe so. It’d be interesting to hear what my colleagues think. I really believe that increasingly, particularly as we move past the AIDS epidemic and into, now, a pandemic, people are understanding the value of medical research.  

Now, we’re in an era where we can get a COVID vaccine generated and into people’s arms in six months. These are unbelievable triumphs of science that the general public is becoming much more aware of, and therefore, hopefully, continuing the long-standing, bi-partisan support for NIH funding.

Johnson: I agree with that. I think, actually though, I’m not sure we’re always as effective lobbyists for getting more money from the federal government for the NCI.  

I mean, if you look over time at the NCI budget, and the paylines and so forth, it’s gone up, it’s gone down in my career. I’ve seen lots of that, sometimes it was stable. And if you look at who was president, who was in charge of the Congress at the time, you can’t really correlate excess research dollars with any political affiliation.

Because you could see on both sides of the spectrum, you can find where we had prosperous times. And I think that when you talk to people in the federal government, they all support us, they all think what we do is wonderful, they all want more money. It’s prioritizing—and it’s too easy to cut our budget.  

And I think we need to be more bold, and maybe the general public, especially coming out of COVID, where research is so important, can help us with that. Because I think we’re not as good an advocate as we could be to advocate for more dollars.

Thompson: So, I agree with that, Otis. And just to add a little bit of color to what both—and I completely agree with what Candace and Peter said—I think the public does understand what comprehensive cancer centers [are].  

My chief operating officer, when I first came here, John Gunn , used to say the biggest value of our cancer care is actually people seeing how many people are committed to the team that will make them better and find a new therapy.  

You come on our main campus, and you see the number of people involved in research, you see the number of people involved in clinical care, and it gives patients and their caregivers hope. And that is a message that gets out into the community, and it matters.

Because we still don’t—and it’s to Candace’s point—we haven’t done a good enough job of explaining, yes, we have all these new tools, but we only have half the tools we really need to make cancer history, as Peter just said, in his dialogue.  

We still need funding, we’ll still need research, because of the complexity of the diseases that come under the rubric of cancer. We have to exist for rare cancers that no single community hospital or regional hospital even sees one of in a year. We have at each of the three centers, a clinic every afternoon of the week, seeing people from around the country to come for that combined expertise.

At the same time, we have to see the common cancers for our training missions. And that often confuses people, “Well, if I have a common cancer, why can’t I go to my local cancer center?” I can come to a comprehensive cancer center, because you’re participating in improving our knowledge about that.  

And we do need to be better at getting that communication. As Peter said, sometimes people think of cancer treatment just as a commodity. It’s odd it happens in these conversations that Candace is talking about, rather than when you actually talk to patients and their families. They really do understand the importance of this.

The public’s ability for philanthropy—we have averaged over my presidency, a million donations a year. But the average donation is a couple hundred bucks, and that’s the [public]. We don’t touch that many people—people believe in the mission.  

George Gallup told me in 2008, that the leading thing Americans now fear in health for their family, is actually getting cancer. The World Health Organization doubled down [on] that in 2012, it’s the leading fear around the world in developing and developed nations.  

And so, our opportunities to give hope through combining that expertise, the team-based research, is a tremendous benefit, and we don’t do enough to shine a light on it. I hope the Cancer History Project actually shines the light on that as we go forward.

Johnson: Yep.

Brawley: Thank you. I’ll take that as an opportunity to do the one commercial of the two-hour interview. The Cancer History Project, at CancerHistoryProject.com is a website free to anyone who wants it, that allows people to go look at some of the sentinel events that have happened in cancer medicine, not just in the 50 years since the National Cancer Act, but in the history of cancer. You get to see things donated from various cancer centers and universities, various distinguished scientists, archives of records. So you can actually see the first protocol that looked at lumpectomy and radiation versus mastectomy, for example. You can read the actual protocol. Now that’s for the commercial, CancerHistoryProject.com .

Craig, you really want me to go in two directions, or you’re encouraging me to go at two directions. What I want to talk about, how, over the last 50 years, we, and we as the cancer centers at the lead, have really changed the definition of what cancer is. People didn’t realize it was a genetic disease in the 1950s and ‘60s. Many people thought it was metabolic. Talk a little bit about that. You’re a true basic scientist. Talk about how the definition of what cancer is has evolved. You mentioned the 400 different diseases, explain that to the lay person a little bit.

Thompson: So, I think a couple of major insights have come in the last 50 years. First of all, the discovery, as I’ve mentioned, by Harold Varmus and Mike Bishop, of oncogenes, genes that drive proliferation and survival of cells, that are recurrently mutated to define certain classes of genes. And so they come as a large group, the kinases, but each individual cell and each individual cell type relies on a different member of that family. And so, you have to treat relative to what’s driving this accumulation of cells.

When I started in medical oncology, I was taught that every cell had a risk of becoming cancerous. That’s not true. We now know that every tissue in our body, as a long-lived animal, a mammal, we have regeneration. When you cut yourself—I cut myself this morning on my hand—I know it will heal over time. But that regeneration activates lineage-specific cells of my skin to repopulate the tissue. And that duplication, because it is a genetic disease, inherited in the DNA that you’ve talked about, it’s those mutations, that accumulate over lifetime, that make cancer a disease of aging. And because we are constantly damaging ourselves and regenerating, we understand why things, like tobacco smoke, like UV light or radiation, increase our risk, because they damage DNA during that repair process.

We understand why Hepatitis B and Hepatitis C cause liver cancer. We understand why HPV over a long time causes cervical cancer and head and neck cancer, and we can build preventative strategies, HPV being one of the biggest opportunities going forward.  

We had to have a molecular understanding, because it wasn’t one organ. Every organ can get cancer, but it’s the regenerative cells of that tissue that make a difference.  

That leads us to our last frontier of why all three of us continue to believe in freestanding cancer centers. We’re terrific now at treating anybody whose cancer is caught early enough, that it’s only in the local organ that it starts in.

Peter’s surgeons, Candace’s surgeons, my surgeons, radiation oncology surgeons, any major cancer center—all of them that participate in the comprehensive [designation] can cure that person with the modalities they have.  

The problem is cancer metastasizes, and that’s the last frontier. If we can understand why it is that cancers acquire the ability to metastasize, because it’s not a simple mutation. We’ve now sequenced thousands of metastases. Yes, they have a little more diversity than the cancer, but there aren’t oncogenes of metastasis. There aren’t tumor suppressors of metastasis. And so we’ve got a whole new frontier, because that’s, unfortunately, why there’s still residual cancer that we can’t handle. And, ultimately, when we understand the biology of that, we’ll get to the future.

And so, we had this tremendous advance that gave us precision medicine. Charles Sawyers who leads the program here, and his work on Gleevec with others at Peter’s institution, as well as at the University of Oregon, really proved to us that understanding mutations, and treating for those mutations, would give us better outcomes. And so, the use of Gleevec and CML revolutionized the disease that I used to take care of and had fatality within 36 months.  

Now, the cohort that they studied in a phase I study that was never closed, those patients are living longer than their age-matched controls, as Brian Druker continues to follow them at Oregon. And that’s amazing that precision therapy delivered that.

And then, we understood that to be able to be successfully metastasized, they had to fool the police of our body, the immune cells, and that led to Jim Allison ’s insight about checkpoint blockade. Those are two revolutions that given us tools for the metastatic disease, so we can see melanoma be cured, lung cancer, which I never thought in my lifetime we’d see cured, but it doesn’t work for everybody. So there’s lots more we need to know. And that both demonstrates the promise of things we didn’t expect, from the discovery of oncogenes and tumor suppressors in molecular detail, with the sequencing of the human genome, and then the sequencing of cancer genomes compared to the germline.

And then, this discovery that the rest of the body is co-opted by the cancer cell of the metastasis problem, and if we can reactivate the cops, we’ll do well, but there’s other cells involved in helping a tumor be successful, that we’ve got to learn how to get them to stand down or fight back against the cancer, which has fooled them.  

And so there’s a tremendous need for this network of comprehensive cancer centers to solve that problem, and then deliver that answer in a way it can be practiced everywhere in the country, for every oncologist, every patient that has the disease.

Brawley: Dr. Johnson, you are a world-renowned pharmacologist, a drug developer, what’s the future of the cancer center and drug development?

Johnson: So, I think drugs have taken a different turn than from, well, when I started in this business, because they were all poisons, [with] their side effects. They still have a place today. But I’d like to think that pharmacology, we’ve gotten a little more sophisticated. And some of our drugs, pharmacologists would even say that a checkpoint inhibitor is a drug, and there are pharmacologists that work on those sorts of areas.  

But I think the future for us is more targeted therapy. As Craig said, the genomic era has really offered us such an opportunity to identify genomic signatures. And there are, really, only about a handful of drugs that recognize certain genomic signatures, where you can actually see a response in a patient.

Now, if you have that, if you find that gene where there is a companion drug for it, you have a good chance to see a response, and it’s a wonderful thing—but it’s limited. And so I think there’s lots of room for new drug development, and for drugs that are attacking and looking only at that specific target. So I think, there’s still a place.  

Pharmacologists, in the old days, when you’d go to an ASCO or an AACR meeting, there’d be lots of pharmacologists, lots of drug-discovery efforts, and so forth. And now, it’s all immunology, and the pharmacologists are sort of sitting in the corner.

But I think that immunopharmacology is a really important area. And I think that what all of us are doing in the immune space, in the immunotherapy space, is really exciting. I mean, we’re seeing the “C-word”—cure—in patients that you just wouldn’t have seen this before.  

As we’ve all said, this is a very complex disease. We’re not going to solve it with just drugs alone, and we’re not going to solve it just with immunotherapy alone, where it’s going to take all of this. It’s a complex process.

Brawley: Yeah. Dr. Pisters, you’re a surgeon—you already knew that, I guess. The minimally invasive surgery, when I first started in medicine in the 1980s, surgery caused a lot of morbidity and there were efforts, tremendous efforts to decrease morbidity from surgery. Limb sparing sarcomas surgeries, and that sort of stuff. It seems like surgery has progression and minimally invasive surgery with robotics, with scoping, and that sort of stuff, has become more and more on the forefront.  

Can you tell me just a little bit about cancer centers and developing those sorts of things, and convincing the FDA and the American public that you really don’t have to be totally unzipped in order to have a good colon cancer operation?

Pisters: Well Otis, your question really makes the point that minimally invasive surgery has transformed many aspects of surgical care, not just cancer surgery. It was brought to cancer patients and done so in the ways that your question really illustrates, that it really reduces morbidity. It has comparable mortality rates, where mortality is often driven by the other comorbidities rather than the surgery itself.  

And over time, we’ve been able to demonstrate that on oncologic outcomes, in some but not all cancers, are comparable, and this has really created advantages. Unfortunately, those advantages don’t extend to cost, where increasingly the costs of the reusables associated with this drives up the cost of a given operation, and as we all become more cost-focused, this will become an issue over time.  

We also have seen that in many cases across the nation, a lot of aspects of minimally invasive surgery had been driven by the industry, and this has created a situation where there’s been really a dearth of randomized data, particularly in cancer.

When you look closely at subsets of cancers and you look at the randomized data, or the trial that we led in gynecologic cancer, we found contrary to the hypothesis, that patients who had open surgery had superior oncologic outcomes. This was practice changing. It prompted lots of questions over time, and really demonstrates the point that when new technology is introduced, particularly expensive technology, it has to be subject to randomized controlled trials that look at all aspects of the short-term morbidity, look at cost data and look at oncology outcomes.

Brawley: Thank you. The cancer centers as a group, the NCI-designated Cancer Centers, have gotten a mandate to do community outreach and engagement recently. Now, the original National Cancer Act in 1971 told the NCI that it needed to do public education regarding cancer, and this COE, or community outreach and engagement mandate, is really a follow through of that. And it’s actually manifested itself in a number of different ways.  

The three of you were co-signatories of a very powerful, incredibly powerful letter—I wish we had some similar thing for coronavirus vaccine. A letter encouraging every parent in the United States to get their children, boys and girls, vaccinated against HPV.  

Just tell me a little bit about what your cancer centers are doing for other aspects of education beyond that—diet, exercise, smoking cessation, so forth. Just give us some examples of what your cancer centers are doing and what other cancer centers ought to be doing. I’ll start with you Candace.

Johnson: Our catchment area is characterized by poverty, obesity, smoking. We’re the second poorest city in the country, and so it’s a real issue for us. We have a large number of African-Americans, Hispanics in our community, and also we have the indigenous population. There are many Seneca reservations that are around our catchment area as well.  

And so it’s something that we really pay attention to. And I think that even before the community outreach and engagement component of centers’ grants, this was something that we put center stage, is reaching out to our community. I applaud the NCI for focusing on this because it, and quite honestly, many of our efforts that we’ve done in cancer, really helped us to reach folks for COVID vaccines because they trusted us, because we’ve spent a lot of time in trying to develop trust in many of these groups that don’t trust us. It’s helped us in so many ways, education, screening, and so forth.

We have, Christine Ambrosone leads a very distinguished group and is interested in molecular risk factors in breast cancer, and has really reached out in the African-American community and collaborated with many centers around the country to look at a number of factors, including breastfeeding to decrease mortality in breast cancer. And in prostate cancer, we have outreach in many of our African-American communities here as well.  

One of our faculty members is a member of the Seneca tribe, so we have a big study and looking at obesity and trying to make connections in the indigenous population, and I want to tell you, it’s a whole other level of mistrust, if you will. And so we’ve made great strides in helping to, in our screening programs, to get these folks in.

I think that it’s one of the most positive things that we can do, as a cancer center, is to be that nexus, not only for screening, but for education, as it relates to a whole variety of diet.  

I’ve already mentioned our footprint in smoking cessation, but now that’s also expanded into, I mean, vaping, which is a huge problem and looking at the effects, and it’s not without its issues.  

And so I think that the community outreach and engagement has really made our centers. We talk about, those of you that know about the CCSG, excuse me, the depth to be a comprehensive center. You have to have depth and breadth across all of the basic science, clinical and population science, and education. And I think the community outreach and engagement really has given all of our centers depth and breadth, because it shines a light on these so important things that we do for our communities. So I could go on and on, but I’ll turn it over to Craig or Peter.

Thompson: So I’ll just pick up where Candace said. I think each of us serve major cities, as Candace said. When their center started, Roswell Park started, it was the third largest city in America and had a booming economy. As small industry has moved away, she’s faced the economic challenges.  

For us, we are still the largest city. We have 34 million people within 100 miles of me right now, so that’s one in 10 Americans, and we have to serve, to get through that whole diversity. So for rare cancers, things like that.  

But in terms of the outreach to the community, Otis, the critical things that we’ve seen, that we uniquely can do, are some of our aspects of immigrant health and cancer disparities that Fran Gany leads. We have a very active program that reaches out into the Hispanic community that’s moving up from the Caribbean, from Central and Latin America, and reaching out because they don’t have that kind of cancer information that they need.

So we have a big program in getting HPV vaccine into that community. Signing that letter didn’t impact that community as much as I would like to have. So we have a terrific program around that.  

We have a huge obesity problem that Candace mentioned and it is socioeconomic—it goes across America, America is the fattest nation. And today, at least in our city, tobacco is not the number one preventable cause of cancer, it’s actually obesity, type 2 diabetes, and poor diet and lack of exercise-related cancers as seen by the statistics published by the National Cancer Institute . So I was really proud among… We could all talk about ratings, but I was really proud of our, the recent ratings come out, the US News and World Report, because we’re 18th in the country in our diabetes program. Because we need to understand why is this cancer incidence going up in the obese population to serve our community.  

But at the other end of the spectrum, because of the socioeconomic challenges that Candace said, we have a huge number of patients we deliver care that are food insecure. So we have a hospital-based food security program to make sure our patients have the nutrition to successfully get through their therapies. We reach out and make sure that all of our patient population is doing that.  

For prevention strategies, we’ve learned, as I said earlier, to partner. So right now in northern New Jersey, we’ve got to get people back to their cancer screening. We have a public service message announcement going out with our partner there, Hackensack Medical Center. They have 20 hospitals that serve all of northern Jersey. They have the screening facilities, we have that imprimatur to say, “You have to go and do that.” Those partnerships with all the community-based organizations really work to get the word out on our community.  

And then finally, COVID has allowed us to reconnect because, in fact, cancer exposed you at greater risk to COVID.

We reached out to the communities, at the request of New York City, to stand up vaccine centers with our colleagues in Harlem. We partnered with the Abyssinian Baptist Church. Tremendously successful program that’s vaccinated over 10,000 people that were otherwise vaccine-hesitant. Reverend Butts has been amazing in leading that program, and we were proud to be a nation center where the First Lady, Dr. Biden came to visit with Tony Fauci to actually talk about why we had to be engaged in the communities.  

We’re really proud of those efforts, we’ll never be able to… I mean, we’ll keep doing as many as we can, but connecting with the community, becoming that trusted authority, which COVID has allowed us to reinvigorate, because of our response, is something that all the cancer centers really do embrace.  

But each of our areas and the service we can provide is unique, and it’s different as we’ve talked about for a matrix center, which has a public health score in primary care network, versus a Comprehensive Cancer Center, that needs partnership to get to those primary care givers or the dentist that I talked about earlier.

Pisters: Otis, just to add a little bit to what Candace and Craig have said, and for our international audience, I think COE is a uniquely American adaptation to changes and interventions that have occurred in the jurisdictional level in other developed countries that have single payer systems.  

Other developed countries that have better health outcomes than the United States use a jurisdictional approach to cancer prevention and screening. That’s what we had in Ontario with Cancer Care Ontario: an entire provincial agency that sent letters to everyone in the province at a moment in time when you needed to have colorectal cancer screening or a mammogram.  

And what we’ve done instead, for a variety of reasons related to structural issues in the American healthcare system, we’ve created this construct of COE as a best practice, or as an adaptation, to try to extend prevention and screening benefits, as well as anti-cancer living benefits, to larger populations, not just those who enter our organizations.  

So it would be important for us at a policy level to learn lessons from other countries that are, frankly, better at this than we are. Yeah.

Thompson: I want to double down on what Peter said, because that international program… For us in New York, if we look at the patients that come to our hospital, to be able to adequately inform them of their healthcare, we need to engage with them in their primary language.  

In many parts of America, that will be English, and increasingly Spanish. For us, we have five languages where more than 5% of our patients, it’s their primary language at home. And so learning to get that content and how to communicate it, we can do through our international collaborators, to learn how to interact in different dialects of Spanish. We’ve used the UN, a unique resource we have, to do reverse translation, because just translating in one direction, you often don’t… When it’s [not] reverse translated, you didn’t say what you meant to say.

And language, because America is this great melting pot of diversity, language is something we have not embraced enough in explaining the complexities of cancer to patients, so they feel comfortable with the authority that we’re providing. So language is a huge barrier in the metropolitan areas in the United States, but I think it’s everywhere. Every community has a language of the immigrant population that came there, right?

Johnson: Do you know Craig, even in Buffalo and we’re a very small market, we have over 70… We translate over 70 different languages and have capabilities for that. So it’s difficult, but you have to be able to do it. It’s so, so important.

Thompson: And increasingly we could draw on an international community where they have that language content, and we could adopt it because many times that reverse… We were shocked when we started this reverse translation system, that our translation into these guys… We have 80, like Candace, 85 languages we provide interpreters versions, but when you translated it back, it didn’t come back exactly in what the first English version was.  

So we have lots to learn in the community delivery of that care, in our messaging, in our prevention strategies, and that’s why we need to engage the community and provide research into what makes a difference. Because for us, the biggest thing that drives disparity is not understanding, and it’s that language barrier.

Brawley: Now the NCI doesn’t call this community outreach and engagement, but I think it’s one thing that cancer centers might be able to do. Can you speak to what you’re doing to influence how people are treated in your catchment area who don’t come to the cancer center? Whether they get… How doctors are recommending mammography screening, or how doctors dose chemotherapy, or how doctors might even perform operations, or when. Are the Cancer Centers really involved in trying to drive quality of care? And here, I’m thinking about your involvement with NCCN as well, and so one of you may want to explain to the population here, what NCCN is.

Pisters: I can just start this one just with our example. Houston is situated in Harris County, and Harris County, Texas has the largest number of uninsured citizens in the country—1 million. And what we’ve done is to look at the county hospitals, and to partner. We have two county hospitals, Ben Taub and LBJ. Baylor College of Medicine provides oncology care at Ben Taub, and MD Anderson provides oncology care at LBJ Hospital.  

And the way we’ve done that, is to really bring the doctors to the patients, and so our faculty have a clinic at LBJ. We provide the services there, at our standards, with our doctors, and we bring, increasingly, our clinical trials to that environment so we can enroll a larger population, a much more diverse population of individuals, into our clinical trials.  

We’re working now with the UT System to increase our investment and build an MD Anderson facility at LBJ Hospital with donor support and with support from the University of Texas Board of Regents. So I’m really excited about these changes. It’s an excellent example of what other cancer centers can do to really make a material difference in their own regions.

Johnson: I mean, NCCN has really played a huge role in standardizing things across this country, and all of us are members of NCCN and on this panel, to improve quality across the board. We also try, with pathway-driven care, to try to standardize the way some of our physicians in the community—and sometimes that’s embraced and sometimes it’s not. But I think we owe it to our community to be the leaders and be the gatekeeper if you will, of this high quality care at every turn. So I think it is a really important thing that we do.

Thompson: Right, so I’ll just double down on NCCN, which is where the comprehensive centers came together to set common standards, so that everywhere… 85% of oncology care is still given in community hospitals throughout the nation, and to have a standard reference to go back, to have a compendium of recommended therapy that is kept constantly updated, is what NCCN has started, and that’s been a great offshoot of the Comprehensive Cancer Center network.  

I do want to say that the biggest hit that we’ve seen in COVID, and in our mission, has actually been our ability to serve as the CME center for cancer in our catchment area. We never had a week go by without at least two groups of three or 400 physicians coming to be re-educated on their part of cancer to this institution. I’m sure Peter and Candace would say the same thing. And we haven’t been able to convene them, and it’s not the same thing as them coming and talking to our experts, finding out that insight, understanding why that new treatment makes a difference, that communication.

When immunotherapy came, the average person didn’t know how to deal with the side effects. That was a way we communicated it, and that ability to come together with CME, we’ve all got to reinvent.  

And then I just want to speak to something Candace mentioned and Peter reminded me of, which is that we have a huge and wonderful—you heard a lot about from them—of safety net hospitals in this city, that in COVID were amazing in how they stood up here. We partnered with them to take their cancer patients who shouldn’t be exposed to COVID. It was a great partnership. But the real important, long-lasting thing is that those safety net hospitals don’t have the molecular testing that allows them to decide whether they could achieve NCCN guidelines because they don’t have the molecular testing.

And so Dr. Carol Brown , who is our chief health equity officer, has been standing up programs in partnership with health and hospitals to get those people tested through our impact testing. Those people that get a cancer diagnosis, now the hospitals can find out if they’re eligible for a clinical trial, if they can get that molecular testing. And we have that at a number of pilot programs in Queens, in Brooklyn, throughout the city, to be able to do that.  

That’s where we become that authority, that Candace is talking about. We have to make those trials available to everybody, the latest recommendations. You have to have the diagnostics right to do that, and that’s where we are falling down, and why we’ve got to convince the Federal Government that molecular testing is the right way forward with cancer. That’s not yet fully approved in terms of reimbursement.

Brawley: Cancer centers have always had a lot of political support. One of my old bosses while I was at the NCI, an NCI Director, used to always say, “The thing about cancer centers is every one of them has two senators and at least one congressman.” I don’t think that the cancer centers are going to be removed from the NCI budget in the near future, but we still have a payline that’s hovering between 9 and 10%. I worry about the investigators who work in the cancer centers. How are we going to fund the future? How are we going to keep young people in research?  

And I ask this question, knowing that the three of you do an amazing job of finding alternative streams of money to support young investigators. But how long can we keep doing this? And what are some of the ways—you might want to mention some of the ways that you’ve been working to support young investigators, because I don’t think many people outside of the community of cancer center executives know the work that you do, the hard work that you do to support, especially young investigators. I’m talking about the people who are in their 30s, who are just building their career.

Johnson: I mean, I can start. I’m the small fry here, but I actually think Buffalo, Roswell Park, we’re sometimes the last bastion of the clinician-scientist, because the young clinician-scientist, we really try to incentivize them and support them early on in their career, especially to push that translational envelope, as well as our basic scientists, the young folks who get very discouraged at a 9% pay line, that’s for sure.  

Our philanthropy is a lot smaller, I’m sure, than my colleagues on the panel, but we do a really incredible job at raising money in Buffalo. And we use that philanthropy very judiciously to help support some of these programs, and to help give some of these young individuals a chance for pilot studies to be able to garner bigger and more comprehensive grants from the NIH or NCI or DOD or other mechanisms, but it is a challenge.

We also utilize our clinical revenues to help support our research mission. Hence why it’s so important for us to drive that, because it helps to fund these young investigators. But you have to be committed to it. And I think cancer centers are the place to do this, and I know my colleagues agree with me. It’s what distinguishes us. Our innovation and our ability to generate these incredible discoveries is what distinguishes us from a non-NCI-designated Cancer Center, a cancer center who is more of a community center. That’s what designates us and distinguishes us, and so I think it’s really important that we don’t lose that.  

And it will become more and more of a challenge Otis, you’re exactly right as we go forward, because those dollars are going to be harder and harder to come by.

Pisters: I think that, just to add briefly to what Candace said, as we think about it and our diverse faculty, it’s very important that we value all contributions to the mission.  

Research is very important, it’s a very important component of our societal contributions, and we want to create dedicated protected time for a subset of our faculty who engage in research. We want to give them all the resources, all the time, access to the platforms.  

And then, as we talk about it internally, we make investments in three specific areas to fuel the kind of production that we need and to enhance the ability to come above the payline.  

One of them is investment in talent, where we’re recruiting the right kind of collaborators.  

Second area is investment in partnerships, very important, academic partnerships illustrated recently by Breakthrough Cancer, and industry partnerships that are very, very important to our research community.

And the last area of investment, very important, is the facilities and infrastructure. Not just cores. I’m talking about ideation space, new research buildings, different way of allocating space over time so that highly productive researchers get rewarded for that and they get more space over time. And that we help researchers who, for whatever set of reasons and circumstances, can’t achieve reasonable research productivity to find other ways to contribute to our mission.  

So it’s really understanding that not everyone needs to be engaged in wet lab-based research, those who are engaged need to be supported in [every] possible way, so that they can be successful with the investments in the talent, the partnerships, and the infrastructure.

Thompson: Yeah, so I’ll just re-echo what both Peter and Candace said. We have a big program to fund at the junior investigator level, new pilot ideas, new grant ideas, that will give them the opportunity and the resources to be able to develop a portfolio of results at every level, whether it’s basic, translational, or clinical science, to move forward to getting funding from a federal agency or a patient interest group. And those funds are absolutely essential for success at the junior level. To have that chance, that satisfaction, that you can investigate your own new idea.  

The new thing is, what Peter said, translational research is the mantra of today. Demonstrating it can happen, that’s much more team-based. You need to bring together the expertise. That means we have to have promotion systems that recognize people are going to share the credit. It’s not what the movies show us, as one doctor sitting in a laboratory coming up with something. And so we have to change the standards of team-based research, of embedded investigators junior in their career, so that they can explore their ideas in the framework of a larger group of people working on that.  

So team-based science, collaborative science is really something we’re pushing hard to support our junior investigators, and get them to understand the complexity of modern biomedical research.

Brawley: What about investigator-initiated research versus directed research? There’s increasingly, I’m seeing… For the audience, over the last 50 years, a lot of our learning has come about because people in the laboratory or groups of people in laboratories at cancer centers, universities, have written grants, sent them to the NIH, said, “This is my idea and this is why it should be funded.” That’s an investigator-initiated grant. More and more, there are movements by certain elements to have more directed research, where some smart person somewhere says, “I want to give you money to do this or that.”

Are you seeing… I think this is becoming more and more prevalent. Are you seeing this, and do you think this is a good idea? Because we’ve learned an awful lot through investigator-initiated research in terms of what’s going on in the cancer cell. And I’ve even gone off and said, for example, the mRNA vaccines for coronavirus, they weren’t created in six months. It was huge investments in basic research over several decades that all came together and happened to be applied in a short period of time to develop those vaccines. But it was primarily investigator initiated research that brought us that—and I’m talking too much. Do you see a problem here?

Thompson: So Otis, let me just speak to this because in researching, and this is relevant to the History Project, one of the real debates and what started the National Cancer Act was the commission that took place in the Senate as Nixon came in and Johnson left. Mary Lasker convinced the Senate to have, along with Sidney Farber, to have a commission that looked at what should happen in cancer.  

The biggest debate in Congress, if you read those records, was whether the new money should be a contract or a grant. And thank goodness, the scientific community stood up and said, “It cannot be a contract. This is not just delivering this number of doses. We need to investigate the science of this and to have those investigator-initiated ideas, and a way to do that.”  

It’s a time where that debate’s happening again, Otis, and that’s what you said. And so I think we need to look at what happened for that 50 years, because we stuck to the idea that these are grants, that people get to follow their new hypothesis driven idea with the new tools of science, with the new tools of medicine. And we have to really double down that. And we need to use, collectively, our authority as cancer centers, say this is critical in driving cancer forward and keeping the talent that’s involved in our education, our training missions as we go forward.

Johnson: Agreed. Totally.

Brawley: Yeah. Peter?

Pisters: I think that it’s very important for us, in each of our organizations, and I presume colleagues across the country and around the world, are trying to find the sweet spot. In other words, you need to support a curiosity-based discovery research, exemplified as Craig said, by Jim Allison’s work on the fundamental biology of the immune system and how it can be used for cancer. And that’s had massive impact on society.  

You also need to see the opportunities that are created with team-based science. And that when we solve for a problem like a breast cancer, or glioblastoma, by putting research teams together from different institutions, or partnering with industry, team-based science creates tremendous benefit. The poster child for team-based science on a foundation of curiosity based science that you pointed out, Otis, was the development of the COVID vaccine.

And so we need in our institutions to have both. And really the challenge is to define the sweet spot, so that individuals feel like they can pursue their own hypothesis-driven ideas in a rich resource-based environment, and other individuals, or perhaps the same individuals at different points in their careers, can join teams that are doing great things together.

Brawley: Wonderful. I’m going to ask a couple of the questions here and anybody who wants to add into the Q&A session, please go ahead. One person who worked for the NCI said that they’ve witnessed examples of discretionary resources being directed toward achievement of cancer center metrics rather than toward the most exciting science. That’s their opinion. Do you have suggestions for improving the NCI designation process? Anybody?

Johnson: I hope we go back to in-person site visits.  

I’ve done a bunch of those site visits and it’s difficult to sort of get the chemistry of the team. I don’t want to joke around, obviously, the person that asked the question.

I would like to think at our center that we don’t spend—if it’s directed towards the CCSG metric, it’s actually going to help the institution and it’s going to incentivize the best science. So I don’t know the specifics of that question, but I think that, most of us, the metrics actually are positive ones too, that we achieve.

Brawley: Yeah. I will say, having sat near the front office at the NCI, there is a concern about unfunded mandates on the part of the NCI. There’s a desire not to do unfunded mandates, near oftentimes pressures for certain mandates that are from places you would never, never dream of.

From one of our Canadian friends, please comment on the cancer centers’ global mandate. Should the US model be replicated in every country around the world? And what’s the nature of cancer centers, US cancer centers global mandate?

Johnson: I can start out. We are probably not as global outreach as my panelists, but I think it is important for us to be in the global scene. They have a lot to offer to us.  

We have a longstanding collaboration with Cuba. And the Cubans are really an incredible group of scientists and have achieved much with very little. And so I think we at Roswell Park have been enriched through our collaborations, and I think we are bringing things to Cuba, and they are bringing things to us.

We have some outreach in Africa, where there is much needed attention to quality and care for those individuals, and in the Caribbean, and so forth. So I think a global presence is really important for every NCI-designated center, because I think it enriches. It’s just like diversity. It enriches us, and it enriches them because you’re bringing a different culture and you’re learning more things about them.  

Thompson: I just want to echo what Candace said, and not talk about specific programs. All of us, and everyone at our centers, wants to reduce to practice advances in cancer prevention, diagnosis, and treatment, that won’t be just practiced in our center, but will be adopted—are capable of being adopted—for every one of the 8 million cancer victims every year throughout the world.

But what we have to appreciate is, which has been a very important part of our international program is, that there are cultural differences in how people approach health. And we need to be sensitive to that and knowledgeable about that. And that means a partner that is involved in the primary delivery of care throughout the world.

So our global missions are almost always in partnership in all the continents where we have major programs, to find a partner hospital similarly dedicated to elevating the quality across their nation or their region’s cancer care, and deliver that in a culturally sensitive way, that actually makes a meaningful difference.

And we can become, as I just said—as we do in the US in our local region—we become the authority that they can exercise to say, here’s the science of it, here’s how we can adopt it within our healthcare system to make a difference. Because ultimately, all three of us and the cancer centers that are in the conference right now, are incredibly proud of the quality we deliver to the individual patients that come to our care.

But that’s only a small fraction of the US cancer patients that we need to help, and the international patients, because cancer is a disease in every country in the world. And so we really want to understand how to best do that.

And this is an unfunded mandate, but one thing we need to do is share best practices and learning how to do that. And we will often learn as much as we give back for the language issues that I talked about before, for understanding what often that partnership says; “you guys are too academic. You have too many visits that have to be done in a clinical trial.” We could do it with four, and we learn to get simpler, and that’s more patient-centric and more focused.

So the partnerships are good when they are a partnership with the primary caregivers of cancer delivery throughout the world, in our global initiatives.

Pisters: Otis, this is a great topic for discussion. And, in fact, the question you pose is one that was part of our strategic planning and conversations in many meetings. And it comes from experience that we have: we operate a cancer center in Madrid, we do work in partnership in Sub-Saharan Africa.  

And the net result of our strategic planning conversations is that we reached the conclusion that single institutional efforts are highly inefficient. And our resources are probably best allocated in partnership with the WHO, with UICC, where we can come together and take full advantage of their talent, their infrastructure, their footprint, in some of these areas of the world where there’s massive unmet need.

So I think as you see us moving forward, you’ll see us working to expand our partnerships with organizations that already have a global health mandate, and helping them with oncology care delivery and new ways of extending prevention and screening into the developed world.

Brawley: Question: does each institution have an institutional historian, number one; if so, do you know what year you became an NCI-designated Comprehensive Cancer Center? Did you have to apply? And was there peer review, and what did peer review look like at that time?  

I should point out to the people who asked those questions that all four of us were not in grade school when this happened.

Johnson: So yeah, I could start. So, we don’t know the exact year. We’ve tried to find it. We were one of the first. We did not have, because we were, as I’ve said before, we were a large city for its size, we had preeminence of this longstanding cancer center.

And so we got designation without even applying, and we were one of the first of just a handful of centers that got designated initially. We were also, when we did have an application, we were one of the first folks to get comprehensive status officially, and so forth.

But we do have an historian on our staff. Roswell Park, as you could well imagine—I mean, this, I don’t know if you guys can see this. This is a tobacco box that was Roswell Park’s. It sits on my desk. And I don’t use it for tobacco anymore.

We have a lot of his: his desk, his file folder, x-ray folder, all wood, very beautiful furniture, still sits at Roswell Park. We have it where people can look at it. We have many. We have his death mask. We have archives of records and documents.

And so we have, yes, we have an historian who pays attention to all these things. So a very rich history here.

Thompson: So I will say I envy Candace. We do not have an historian per se, but we have a tremendous library service with a number of people with PhDs in information science, so they’re good at finding that, and we have tremendous archives that we keep that we can draw from the record.

So I can tell you that our first grant that is a cancer center grant was the one I talked about in 1964, that our team was able to drag out.  

What I understand is that there were three outcomes that were relevant to us for the National Cancer Act:

The first was, the chair of our board became the head of the National Cancer Advisory Board—that was Benno Schmidt because Laurence Rockefeller didn’t want to serve. So that’s the historical record. And he nominated Benno Schmidt , and Mary Lasker and Richard Nixon picked him to be the first head of the National Cancer Advisory Board, which started as part of the Cancer Act to oversee this issue and continues to oversee the NCI.

It allowed three cancer centers—because in the act it was anticipated that there would be comprehensive cancer centers—three cancer centers passed through until 1973 to actually be the founding ones without a further application.

And the current directors were in grade school then—Candace, Peter, and myself—because we represent those three institutions that were already considered without an application to do that. That doesn’t mean every five-year since then we had to do it.

Johnson: No, it doesn’t.

Thompson: Exactly, but we were allowed to do that.  

And the one thing that I just want to say, because it’s a very proud part of our tradition that Benno Schmidt brought as part of the NCAB, because there was great concern.

What you may not know is that the director of HEW, which is where the NCI was under at that time, was against the National Cancer Act. And there was a large number of really high quality scientists, some of whom ultimately were chosen to go into the NCAB, who believed, because cancer didn’t have this physiology history, that the money would be wasted on trying to do things that were too close to the clinic and not fundamentally grounded in science.

And the one thing that happened for every center, and it came because Mary Lasker timed the National Cancer Act ask perfectly—you may not know this, but she started the ask immediately after the landing on the moon. And she said, “This is the next thing we’re going to do.”

It was the way we channeled the excitement of going to the moon that Kennedy launched into the Cancer Act, and every center increased their funding over the next decade.

And so, not only did basic science funding—because there were grants increased for cancer—not only did cancer center grants happen, but it raised the molecular biology revolution, and the US’s ability to lead it in every discipline, because Congress got the message that this was an opportunity.

So it’s a tremendous celebration, this 50 years, of what it’s delivered and that delivery, I’m proud to say, happen at every field because cancer touches every organ.

So the other institutes that are dedicated to organ-specific disease benefited as well. And we’re really proud in our history with our role in that, around Benno Schmidt’s role in the first NCAB and making that message clear to Congress, as he did.

Pisters: We’re very much like Sloan-Kettering in the sense that we don’t have a historian, but we do have archives and excellent librarians. I think the flip side to your question, Otis, is, a lot of old history can really be put together with memos and letters that are in paper files. And now we’ve moved to a digital environment—I’m completely paperless myself.

And every now and then I’m wondering, how is the history of this period ever going to be documented? Because it’s in a bunch of deleted emails, it’s on a bunch of servers. How are we going to take the archivists of the modern era and help them to chronicle today’s history?

Brawley: That’s a really, really good point.

Johnson: We have a book that I have to mention that’s pretty special. So it was a bound book that had blank pages in it. Roswell Park started it, so it starts back in 1898, and every time a visitor came and gave a seminar, you signed—or a dignitary or something.

And so, we still have that book. And we’re not using it for people that are coming now anymore for seminars, because we want to preserve it, but, to page through it, it’s remarkable the people that came through, and it’s a very treasured item. So I think it’s important to—I agree with Peter—we don’t want to lose our past.

Brawley: We have 10 minutes left. There’s a couple of questions here about “what are your cancer centers doing to advance health equity,” or “what are you doing to overcome health disparities?”  

I’m going to take the moderator’s prerogative and say that I believe that that’s not just the cancer centers’ obligation—that’s more of a global obligation for society at large. And I’ll even invoke my own personal belief that the cancer centers have done a lot more than a lot of other people in terms of this.  

But anyway, let me give you the opportunity to address that, and, at the same time, because this is probably the last time we go around, what do you expect for the future of the cancer center? I don’t know who wants to go first.

Johnson: I can go first. I think one of the things—we’ve talked about some of the things that we’re doing in our [centers], for our disparate populations across the board and all, both Peter and Craig, we’ve all done and, Otis is exactly right, it’s sort of the mantra of an NCI-designated center.

But I have to tell you, the recent times, with what’s happened in our country, has made me reflect even more on this. I don’t think it’s enough just to go into our community and do the kinds of community engagement kind of things that we’re doing, as it relates to CCSG.

I think that the way we’re going to really make connections is we have to have more physicians, nurses that are African American, or indigenous population, or LGBT.

We need to be more. You know, all of our centers are very diverse. That’s the thing I love about this field is you meet people from all over the world, diverse backgrounds, religions, gender, everything. And it really adds to the richness of each one of our organizations, but we could do more.

And I think that I’ve been very sensitive to trying to make sure that Roswell Park is a place of inclusion, where people can come here and feel safe and be able not only to work here, but also to be treated here.

And I think it goes to—it’s a little bit bigger than just some of the community engagement things that we have. And I think it’s important. I feel a responsibility in this area, and in our community.

Thompson: So, I’ll just echo what Candace said. I think the recent events have reminded us of how important, as part of health care delivery, that people come to see commonality with their caregivers, so that they feel that trust. That convenience is that we’re seeing that’s driving vaccine hesitancy and other things about.

We probably already had a chief diversity officer, and across our whole workforce, we do mirror New York. And we’re very proud of that. We needed to reach out to the populations that were underserved in every way, shape and form in New York to even a greater extent than we’ve talked about.  

An example:

I was very pleased that last summer we were able to have Carol Brown take our chief equity officer position, that we started as part of this, to redouble our efforts, as Candace just said. We needed to understand that we don’t have enough diversity in our senior ranks, particularly of our physicians and our senior researchers.  

We are not as diverse as the community we serve and we need to do better. So we have tremendous programs that, quite honestly, The Cancer Letter has profiled in the last bit of time about our educational mission at high school, at college.

They reach out to diverse communities, but we also needed to do that at the top of the organization.  

We’ve done that for women—more than 50% of our leadership is now female. So that’s worked nicely over the last decade, but it doesn’t mirror the rest of the diversity that we need to achieve.

And so we have asked, and had our diversity council that we stood up, that represents all aspects, in order to set real stretch goals about how we as a leadership match the diversity of our community. We are going to do our best to match that.

I think this was, as Candace said, a wake up call for all of us, that we were not doing enough. But, as you’ve said Otis, this is central to our mission. If we’re going to get the trust of the community to drive cancer care forward, to have people take prevention strategies, which we’ll never know whether they worked or not, we’ve got to be able to represent them in every way in which they feel we are their community. And that’s what we’ll do over the next few years.

Brawley: Peter?

Pisters: Yeah. Just to build on what my colleagues have said, I think that, as we formulated our strategic plan, we spent a lot of time looking at these societal issues and things such as our carbon footprint or a commitment to diversity, equity, inclusion received tremendous internal discussion during the process of co-creating our strategic plan.

With respect to DEI, what we didn’t want as a landing spot was an archipelago of tiny initiatives within the organization that could be at the sub-unit level or in an academic department. But we needed an institutional approach.  

By building it into our strategic plan, we know that resources will be allocated, there’ll be an executive committee that reports to me with defined metrics, and we can really drive change that’s meaningful over time.

As we really look at the issues of health disparity, we have an entire academic department that’s focused on the elimination of disparities that is very, very important to us. And we want to really conduct systematic research to better understand the drivers of disparity, and what our role is in addressing those gaps.

So I think that the issues that our country has faced in the aftermath of George Floyd, a lot of the discussions that have taken place, and the COVID pandemic, have highlighted the disparities that are present in our own country. And it really galvanized academic medical centers around the country to really lean in on this topic.

We know how important it is to our workforce. We know how important it is to our community. Houston is the most diverse city in the United States. We need to reflect that diversity, we need to embrace that diversity, and we need to define how we’re going to get all elements of diversity and inclusion.

Diversity and inclusion are not the same. Diversity is a descriptive fact, inclusion requires acts—and deliberate acts, and strategy. And that’s the conversation that we’ve had as we embark on a big institutional effort on DEI.

Brawley: We only have a couple of minutes left and, the issue of disparities—one element is cost. Costs are going crazy. I prescribed a drug yesterday and patient, told me that it was $15,000 a month for his oral medication. How are we going to overcome this—we don’t have time for that.  

Tell me, are you optimistic? And if so, why? Overcoming disparities, overcoming costs, getting increased access? Are you optimistic? Yes or no? And if, if yes, why?

Johnson: Yes, because—I will answer it immediately—I’m a very optimistic person. And I know the challenges are great, and cost is a big one. And that’s a whole—we could spend a whole other two hours just on that. But I’m optimistic that the future is bright for us, and we will find a way.

And I think some exciting things are going to be coming around. I think science, I think there’s so much exciting out there right now, that I think I’m very optimistic about the future for us in cancer, in cancer investigation.

Thompson: So I’m of two minds. I, like Candace, I think that the science and the advances are going to deliver and the healthcare costs of actually being in the hospital or receiving chemotherapy. It shouldn’t be that there’s a higher copay for an oral medication when you don’t need infusion. And you can do that Otis, as you just pointed out. I think that’s going to happen and it’s going to quickly come down. Right now, the costs are too high.  

What I am worried about is the financial toxicity as we recover from COVID, and we go through all this, that are not part of the health care costs.

To get the best out of cancer care right now, you need a caregiver, you need somebody else that can take it. In a family that’s living close to the poverty line, that’s losing two incomes if both members of the household work: the caregiver and the patient with the disease.

We find the financial toxicities of loss of time from work, loss of pay, the cost of transportation, of food security, are really the things we are going to have to struggle with going forward.

We have institutional resources for all of those, but they are just not sufficient to meet the toxicity that people are facing, as they face a cancer diagnosis right now. And, oddly, the government rules don’t allow us to supplement on certain levels, as you may know.

Brawley: Yeah. Dr. Pisters?

Pisters: Otis, let me just say the obvious: I am wildly optimistic. When you look at four of us on this panel discussion today, it’s accurate to say we’ve all been in this business for decades. And the reality is that the last decade has been like no other decade in our professional lives.

When you look at the strength of our institutions, you look at 51 Comprehensive Cancer Centers across the United States, there couldn’t be a better time to be in oncology. The kind of innovations, the discovery, the amazing things that are going to happen in the next 10 years… I can’t wait to see it happen.

Brawley: I’m just going to end by saying, you know, I saw a guy yesterday. He’s had stage four non-small cell lung cancer for 12 years. I don’t think I would have thought that possible 20 years ago.

Johnson: Yeah, I know. Amazing, I know.

Brawley: This has been a great conversation. I want to thank Dr. Candace Johnson of Roswell Park, Dr. Peter Pisters of MD Anderson, and Dr. Craig Thompson of Memorial Sloan Kettering.

I really enjoyed this conversation. I want to thank you, not just for being the leaders of incredible cancer centers, but for being incredible scientists, and for your contributions, and also being incredible personal friends of mine.

I want to thank you and have a good evening. This is a recording for the Cancer History Project, and it’ll be available on CancerHistoryProject.com .  

I want to thank Katie Goldberg, who has orchestrated this whole thing. And I want to acknowledge my partner in the Cancer History Project, the co-editor Paul Goldberg. So, good evening folks.

Thompson: Thank you. It was a privilege for all of us to participate.

Johnson: Thanks, Otis.

Pisters: Thanks a lot.

Johnson: Thanks Craig, Peter. Great to see you.

make cancer history

Table of Contents

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How Fred Hutch, UW and Seattle Children’s helped revive NCI-designated consortium cancer centers

  • July 16, 2021

Edith Mitchell on her path from Tennessee farm to becoming a cancer doctor and brigadier general

  • February 18, 2022

Panel: Knudsen, Hudis, Hughes-Halbert, Leader, Willman propose action plan on health equity

  • May 13, 2022

Anna Gray to the Rescue

  • March 1, 2022

50th Anniversary of the Johns Hopkins Kimmel Cancer Center Podcast Series – Public Health and Cancer Prevention

  • July 26, 2023

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Health United States 2020-2021

History of Cancer

History of cancer represents both newly diagnosed (incident) and pre-existing cases of cancer ( 1–3 ). Cancer history is a key public health indicator because it reflects cancer’s burden on the population and health care system.

Featured Charts

Explore data, definitions, key findings.

Sparkline: This is a line graph showing the percentage of self-reported history of cancer among adults aged 18 and over for 2009 through 2018 (line) and at 2019 (point).

The age-adjusted percentage of adults aged 18 and over who reported a history of cancer remained stable from 5.8% in 2009 to 6.1% in 2018. In 2019, 6.6% (age adjusted) of adults aged 18 and over reported a history of cancer. See Featured Charts for additional analysis and Notes for more information about analyzing trends using NHIS data.

SOURCE: National Center for Health Statistics, National Health Interview Survey. See Sources and Definitions, National Health Interview Survey (NHIS) and Health, United States, 2020–2021 Table CanHst .

  • Estimates are based on the civilian noninstitutionalized population. See Sources and Definitions, Population .
  • For information on the methods used to assess trends, see Sources and Definitions, Statistical testing .
  • Age-adjusted estimates are presented to eliminate differences that result from changes in the distribution of age in the population over time. Some estimates are shown by a specific age group because of the strong effect of age on most health outcomes. See Sources and Definitions, Age adjustment .
  • In 2019, the NHIS questionnaire was redesigned, and other changes were made to weighting and design methodology. Data for 2019 have not been fully evaluated for comparability with earlier years; therefore, trends through 2019 are not shown. For more information on the 2019 NHIS redesign and evaluation of the redesign on selected indicators, see: https://www.cdc.gov/nchs/nhis/2019_quest_redesign.htm .

Reported history of cancer was higher in women than in men in 2019.

Figure 1 is a line graph showing the percentage of respondent-reported history of cancer among adults aged 18 and over, by sex for 2009 through 2018 (line) and at 2019 (point).

NOTE: “Stable” refers to no statistically significant trend during the period. SOURCE: National Center for Health Statistics, National Health Interview Survey. See Sources and Definitions, National Health Interview Survey (NHIS) and Health, United States, 2020–2021 Table CanHst .

  • From 2009 to 2018, the age-adjusted percentage of adults aged 18 and over who reported a history of cancer remained stable for both men and women.
  • In 2019, reported history of cancer (age adjusted) in adults aged 18 and over was higher in women (7.2%) than in men (5.9%).

Reported history of cancer decreased in adults aged 45–54 from 2009 to 2012 and increased in adults aged 75 and over from 2009 to 2018.

Figure 2 is a line graph showing the percentage of respondent-reported history of cancer among adults, by age group for 2009 through 2018 (line) and at 2019 (point).

NOTES: APC is annual percent change. “Stable” refers to no statistically significant trend during the period. SOURCE: National Center for Health Statistics, National Health Interview Survey. See Sources and Definitions, National Health Interview Survey (NHIS) and Health, United States, 2020–2021 Table CanHst .

  • From 2009 to 2018, reported history of cancer increased for those aged 75 and over. From 2009 to 2012, reported history of cancer decreased for those aged 45–54 and then was stable through 2018. Reported history of cancer for other adult age groups did not change significantly from 2009 to 2018.
  • In 2019, reported history of cancer increased by age group, with the lowest percentage in adults aged 18–44 (1.8%), followed by adults aged 45–54 (5.2%), 55–64 (9.9%), 65–74 (16.9%), and 75 and over (24.7%).
  • Age-adjusted estimates are presented to eliminate differences that result from changes in the distribution of age in the population over time. Some estimates are shown by a specific age group because of the strong effect of age on most health outcomes. See Sources and Definitions, Age adjustment.

Reported history of cancer increased in non-Hispanic White adults from 2009 to 2018.

Figure 3 is a line graph showing the percentage of respondent-reported history of cancer among adults aged 18 and over, by race and Hispanic origin for 2009 through 2018 (line) and at 2019 (point).

NOTES: NH is not Hispanic. APC is annual percent change. “Stable” refers to no statistically significant trend during the period. SOURCE: National Center for Health Statistics, National Health Interview Survey. See Sources and Definitions, National Health Interview Survey (NHIS) and Health, United States, 2020–2021 Table CanHst .

  • From 2009 to 2018, the age-adjusted percentage of adults aged 18 and over who reported a history of cancer increased for non-Hispanic White adults while it did not change significantly over time for non-Hispanic Black, Hispanic, and non-Hispanic Asian adults.
  • In 2019, among adults aged 18 and over, non-Hispanic White adults (7.5%) were more likely than non-Hispanic Black (4.9%), Hispanic (4.6%), or Non-Hispanic Asian (2.4%) adults to report a history of cancer (age adjusted). Non-Hispanic Asian adults were least likely to report a history of cancer.
  • Estimates are presented according to the 1997 Office of Management and Budget’s “Revisions to the Standards for the Classification of Federal Data on Race and Ethnicity” and are for people who reported only one racial group. See Sources and Definitions, Race.
  • Data on Hispanic origin and race are presented in the greatest detail possible considering the quality of the data, the amount of missing data, and the number of observations. This affects the availability of reportable data for populations such as the Native Hawaiian or Other Pacific Islander and the American Indian or Alaska Native populations. Statements about findings refer to the data presented in the figure.

Download the data

Respondent-reported history of cancer in adults aged 18 and over, by selected characteristics: united states, selected years 1997–2019.

SOURCE: National Center for Health Statistics, National Health Interview Survey.

  • Hispanic origin : People of Hispanic origin may be of any race. See Sources and Definitions, Hispanic origin .
  • History of cancer : Based on a question about whether respondents had ever been told by a doctor or other health professional that they had cancer or a malignancy of any kind. Data exclude squamous cell and basal cell carcinomas. See Sources and Definitions, Cancer .
  • Race : Estimates are presented according to the 1997 Office of Management and Budget’s “Revisions to the Standards for the Classification of Federal Data on Race and Ethnicity” and are for people who reported only one racial group. See Sources and Definitions, Race .
  • National Cancer Institute. Available cancer prevalence statistics. Rockville, MD. Available from: https://surveillance.cancer.gov/prevalence/statistics.html .
  • Miller KD, Nogueira L, Mariotto AB, Rowland JH, Yabroff KR, Alfano CM, et al. Cancer treatment and survivorship statistics, 2019. CA Cancer J Clin 69(5):363–85. 2019.
  • National Cancer Institute. Cancer prevalence statistics overview. Rockville, MD. Available from: https://surveillance.cancer.gov/prevalence/ .

Cancer Deaths

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The History of Cancer: Discovery and Treatment

History of cancer.

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Frequently Asked Questions

Cancer may have been “discovered” and written about thousands of years ago. However, the disease itself has actually existed since before the evolution of humans.

It was first documented in Egypt about 5,000 years ago. Since that time, people from cultures all over the world have written about the disease and its potential treatments.

This article will look at what we know about the history of cancer. It will also talk about how our understanding of what causes cancer and how it can be treated has changed over time.

  • 3000 BCE : The world’s earliest known mention of cancer was found in a papyrus document from ancient Egypt. It described tumors found in the breast . The cancer was treated by destroying the tissue with a hot instrument called “the fire drill”—a technique we now call “cauterization.” Some writings have shown that the ancient Egyptians could distinguish between cancerous (malignant) and noncancerous (benign) tumors.
  • 460 BCE : In ancient Greece, Hippocrates thought there were four fluids in the body that influenced health: blood, phlegm , yellow bile , and black bile. He believed that having too much black bile in a part of the body caused cancer. For the next 1,400 years, people believed cancer was caused by too much black bile.
  • 1628 : William Harvey, physician to King James I of England, dissected animals and human cadavers to learn more about how the body worked. When he published a book about the circulatory system, it upended ancient ideas and opened the door for more research on the workings of the human body.
  • 1761 : Giovanni Morgagni of Padua published a book based on hundreds of autopsies he had performed on former patients of his, looking at both their clinical symptoms in life and his postmortem observations of their organs. This laid the groundwork for modern autopsies to determine the cause of someone’s death.
  • 1775: A British surgeon named Percivall Pott discovered that testicular cancer was common in chimney sweeps. This was the first time a cancer was connected to an environmental cause.
  • 17th century : The discovery of the lymphatic system led to new ideas about cancer. The lymphatic system includes the tissues, vessels, and organs that move a substance called lymph around your body. Lymph is an important part of your immune system. When the lymphatic system was discovered, it brought about the possibility that problems in this part of the body could cause cancer. This idea was called the lymph theory. It replaced Hippocrates’ theory about black bile and cancer.
  • 1838 : Johannes Mueller, a German pathologist, showed that cancer is made of cells, not lymph. Mueller’s student, physician Rudolf Virchow, figured out that all our cells—even cancerous ones—come from other cells. However, he thought cancer spread in the body “like a liquid.”
  • 1860 : A German surgeon named Karl Thiersch was the first person to prove that cancer spread through malignant cells.

How Cancer Was Named

Although most people cite Hippocrates as the first person to use the word cancer, he actually used the Greek words karkinos and karkinoma when he wrote about tumors. These words were related to the Greek word for “crab” because Hippocrates thought the insides of the tumors looked like crabs.

The Roman physician Celsus was the first to translate the word into the Latin word “cancer.”

20th Century to Present Day

The 20th century was an exciting time in cancer research. Carcinogens,  chemotherapy , radiation therapy, and better ways to diagnose cancer were all discovered in these years. Some of the most important discoveries of the 20th century include:

  • 1915 : Katsusaburo Yamagiwa and Koichi Ichikawa at Tokyo University applied coal tar to the skin of rabbits, inducing cancer and showing that some substances are carcinogens or cancer-causing.
  • 1962 : James Watson and Frances Crick won a Nobel Prize for discovering the chemical structure of DNA.
  • 1970s : Scientists discover oncogenes and tumor suppressor genes.
  • 1981: Japanese professor Takeshi Hirayama published the first research linking lung cancer to second-hand smoke.  
  • 1982: Baruch S. Blumberg helped develop a vaccine against hepatitis B, a cause of liver cancer.
  • 1989: The first gene therapy cancer treatments began to evolve.
  • 1994: Scientists discovered the BRCA1 gene. This was the first known gene found to predispose a person to developing breast or ovarian cancer.
  • 1999: Jan Walboomers and Michele Manos found evidence implicating human papillomavirus (HPV) to 99.7% percent of cervical cancers.

Today, we are still learning more about cancer. We have found ways to prevent and treat some forms of cancer and even cure others. Clinical trials have allowed scientists to test new ways to find and treat cancer. Some of this century’s notable discoveries so far include:

  • 2006: The first vaccine against the HPV virus was approved in the United States.
  • 2009: Researchers find that immunotherapy improves cure rates for children with neuroblastoma.
  • 2011: Low-dose computed tomography (CT) scans help reduce lung cancer deaths by finding early-stage cancer in high-risk people.
  • 2016: Researchers find evidence that a type of gene therapy called (CAR) T can produce remission in some people with B-cell hematologic cancers.
  • 2021: The OncoKB, a genetic variant database, was recognized by the FDA as a tool for predicting drug responses in people with cancer. This will help oncologists find the best individual treatments for people with specific types of cancer.

Humans have known about cancer for millennia, but our modern understanding of cancer has only developed in the past few centuries. New advancements are being made all the time, and huge leaps have been made in the last few decades alone. This bodes well for the future of cancer treatments and therapies.

A Word From Verywell

How we look at cancer and its treatments has significantly changed in the last few centuries. Even decades ago, we had limited treatment options and less research. Learning about cancer and treatment history can be interesting when seeing how far we’ve come in such a short time. With new research and discoveries occurring all the time, the future of cancer research is an exciting topic.

Cancer has been around since humanity began recording its history and likely existed even before that time. The oldest description of cancer originates from Egypt around 3000 BC in a text called the Edwin Smith Papyrus, which also describes the Egyptian process of tumor removal using a method of cauterization.

Cancer was treated throughout most of the 1800s using surgery to remove cancerous tumors and affected organs. The discovery of X-rays in 1895 by a physicist named Wilhelm Konrad Roentgen helped to diagnose cancer cases and helped pave the way for radiation therapy.

In 1838, a pathologist known as Johannes Müller showed that cancer cells are what make up cancer. Before this, it was believed that cancer was made up of lymph.

It was first treated by surgery, although early physicians realized that cancer often came back after surgery.

The German chemist Paul Ehrlich started working with drugs to treat infectious diseases in the early 1900s. He coined the term “chemotherapy” to describe the use of chemicals to treat disease. He wasn’t very optimistic about medicine to treat cancer, though.

Cancer is more common with age, and more people are living longer, increasing the risk of cancer. A better metric of progress is the cancer death rate, which is decreasing, indicating that we are developing better treatments for cancer.

Di Lonardo A, Nasi S, Pulciani S. Cancer: we should not forget the past . J Cancer . 2015;6(1):29-39. doi:10.7150/jca.10336

American Cancer Society. Understanding cancer causes: ancient times to present .

National Cancer Institute. Cancer: a historic perspective .

Bolli R. William Harvey and the discovery of the circulation of the blood: part II . Circ Res . 2019;124(9):1300-1302. doi:10.1161/CIRCRESAHA.119.314977

Ghosh SK. Giovanni Battista Morgagni (1682-1771): father of pathologic anatomy and pioneer of modern medicine . Anat Sci Int . 2017;92(3):305-312. doi:10.1007/s12565-016-0373-7

Walter E, Scott M. The life and work of Rudolf Virchow 1821-1902: "Cell theory, thrombosis and the sausage duel" .  J Intensive Care Soc . 2017;18(3):234–235. doi:10.1177/1751143716663967

Faguet GB.  A brief history of cancer: age-old milestones underlying our current knowledge database .  Int J Cancer . 2015;136(9):2022-2236. doi:10.1002/ijc.29134

Iida K, Proctor RN. 'The industry must be inconspicuous': Japan Tobacco's corruption of science and health policy via the Smoking Research Foundation . Tob Control . 2018;27(e1):e3-e11. doi:10.1136/tobaccocontrol-2017-053971

Gerlich WH. Medical virology of hepatitis B: how it began and where we are now . Virol J . 2013;10(1):1-25. doi:10.1186/1743-422X-10-239

National Institutes of Health. Gene therapy turns 30 years old .

Takaoka M, Miki Y. BRCA1 gene: function and deficiency . Int J Clin Oncol . 2018;23(1):36-44. doi:10.1007/s10147-017-1182-2

Okunade KS. Human papillomavirus and cervical cancer . J Obstet Gynaecol . 2020;40(5):602-608. doi:10.1080/01443615.2019.1634030

National Cancer Institute. The HPV vaccine .

National Cancer Institute. Harnessing the power of our immune systems to treat neuroblastoma: discovery of Ch14.18 immunotherapy .

National Cancer Institute. Lung cancer screening saves lives: the National Lung Screening Trial .

Park JH, Geyer MB, Brentjens RJ. CD19-targeted CAR T-cell therapeutics for hematologic malignancies: interpreting clinical outcomes to date . Blood J Am Soc Hematol . 2016;127(26):3312-20. doi:10.1182/blood-2016-02-629063

Food and Drug Administration. FDA recognizes Memorial Sloan-Kettering database of molecular tumor marker information .

American Cancer Society. Understanding what cancer is: ancient time to present .

American Cancer Society: The Cancer Atlas. History of cancer .

American Cancer Society. History of cancer treatments: surgery.

Valent P, Groner B, Schumacher U, et al. Paul Ehrlich (1854-1915) and his contributions to the foundation and birth of translational medicine . J Innate Immun . 2016;8(2):111-120. doi:10.1159/000443526

National Cancer Institute. Cancer statistics.

By Jaime R. Herndon, MS, MPH Jaime Herndon is a freelance health/medical writer with over a decade of experience writing for the public.

Roderic Pettigrew on a career as a “physicianeer” and the early days of the MRI: “You don’t make advances without technological innovation.‪”‬ The Cancer History Project

In this conversation, Roderick Pettigrew speaks with Robert Winn, guest editor of The Cancer Letter and the Cancer History Project during Black History Month, about Pettigrew’s contributions to research, how he became an early self-taught expert on Nuclear Magnetic Resonance Imaging, or the MRI, as well as when he became founding director of National Institute of Biomedical Imaging and Bioengineering. Pettigrew is chief executive officer of Engineering Health (EnHealth) and inaugural dean for Engineering Medicine (EnMed) at Texas A&M University in partnership with Houston Methodist Hospital, and the Endowed Robert A. Welch Chair in Medicine and founding director of the National Institute of Biomedical Imaging and Bioengineering. Winn is the director and Lipman Chair in Oncology at VCU Massey Comprehensive Cancer Center, and senior associate dean for cancer innovation and professor of pulmonary disease and critical care medicine at VCU School of Medicine.

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The Unique Hell of Getting Cancer as a Young Adult

Women Dealing With Mental Health

W hen I got diagnosed with Stage 3b Hodgkin Lymphoma at age 32, it was almost impossible to process. Without a family history or lifestyle risk factors that put cancer on my radar, I stared at the emergency room doctor in utter disbelief when he said the CT scan of my swollen lymph node showed what appeared to be cancer—and lots of it. A few days away from a bucket list trip to Japan, I’d only gone to the emergency room because the antibiotics CityMD prescribed to me when I was sick weren’t working.I didn’t want to be sick in a foreign country. So when the doctor told me of my diagnosis, the  only question I could conjure was: “So Tokyo is a no-go?”

Around the world, cancer rates in people under 50 are surging, with a recent study in BMJ Oncology showing that new cases for young adults have risen 79% overall over the past three decades. In the U.S. alone, new cancer diagnoses in people under 50 hit 3.26 million, with the most common types being breast, windpipe, lung, bowel, and stomach. A new feature in the Wall Street Journal highlights the mad dash among doctors and researchers to determine what’s causing this troubling rise. Strangely, overall cancer rates in the U.S. have dropped over the past three decades, while young people—particularly with colorectal cancers—are increasingly diagnosed at late stages. “We need to make it easier for adolescents and young adults to participate in clinical trials to improve outcomes and study the factors contributing to earlier onset cancers so we can develop new cures,” says Julia Glade Bender, MD, co-lead of the Stuart Center for Adolescent and Young Adult (AYA) Cancers at Memorial Sloan Kettering in New York City (where I am currently a patient.)

Doctors suspect that lifestyle factors and environmental elements, from microplastics to ultra-processed foods, could be to blame. But many adults in their 20s and 30s, such as myself, were otherwise healthy before their diagnoses. It felt like all those years of forcing myself to run, eat high-fiber foods, and choke down kombucha were for nothing. 

Cancer is hell at any age, but the challenges facing young adults are especially steep, as the disease disrupts a formative period for building a career, family, and even healthy self-esteem, from body image to gender identity. It’s critical that our approach to treating and supporting these patients reflects the severity of this disruption. In recent years, a growing number of cancer hospitals have developed young adult-specific programming like support groups, information sessions on dating and sexual health, and even mobile apps to help counter social alienation. But there is still a long way to go.

Read more: Why I Stopped Being A “Good” Cancer Patient

Shockingly enough, canceling my trip to Japan was the least of my worries. Beyond the excruciating physical side effects of high-dose chemotherapy and a number of life-threatening complications, cancer pulverized my self-esteem into nothingness, as I watched peers get married and promoted from my bed. Thankfully, after switching to a new hospital, I found support groups that connected me with a community of peers who got it, as well as social workers who work exclusively with young adults and thus recognized many of my biggest challenges, like social isolation, financial strain, the dating nightmare, and hating my bald head.

Perhaps the biggest reason I resented cancer was for disrupting a milestone I’d worked for my whole life: a book launch. (My diagnosis came two months before my first book was published.) Young adulthood is meant to be littered with these kinds of professional and personal benchmarks, many of which are hard enough to accomplish without tumors; dating, for instance, is impossible for me even as a healthy person. Now I have to re-enter the pool older, weaker, and more traumatized? 

“Young adult patients may be trying to assert independence from parents, establish a career or intimate relationship, or even be parents themselves,” says Bender. “Most will be naïve to the medical system or a serious health condition.” And so they require flexible, creative clinicians who can help navigate them “to and through the best available therapy and back to their lives, inevitably ‘changed’ but intact.” Not only do these patients need specialized psychosocial support, but research initiatives should prioritize developing treatments that minimize long-term toxicities.

Given that many young patients haven’t yet built financial stability and are often in some form of debt, organizations like Young Adults Survivors United (YASU) have emerged to support young adult survivors and patients through the financial overwhelm. Stephanie Samolovitch, MSW and founder of YASU, says that there’s still an enormous need for resources supporting young adult cancer patients and survivors.

“Cancer causes a young adult to be dependent again, whether it’s moving back in with parents, getting rides to appointments, or asking for financial help,” says Samolovitch, who was diagnosed with leukemia in 2005, two weeks before her 20th birthday. “Young adults never expect to apply for Medicaid or Social Security Disability during our twenties or thirties, yet cancer doesn't give us a choice sometimes. That causes stress, shame, depression, and anxiety when trying to navigate the healthcare system.”

Read more: How to Create an Action Plan After a Cancer Diagnosis

When Ana Calderone, a 33-year-old magazine editor, was diagnosed with stage 2 breast cancer at 30, the most challenging part of getting diagnosed so young was “everything.”

“I felt like it set my whole life back, which sounds stupid because I was literally fighting for my life,” she says. “Who cares if I had to delay my wedding a year because I was still getting radiation treatment? But it was really hard at the time. Everything was delayed, and still is.”

During chemo, Calderone’s doctors gave her a shot that she still receives to try and preserve her ovaries, and she’s been able to try IVF twice. She says she had to proactively advocate for those things with her care team. While Calderone is currently cancer free, she still must take medication that has further delayed her plans to build a family. “I’m fairly confident I’d have a child by now if I didn’t get cancer. That’s been the most devastating part,” she says. “My oncologist would consider letting me get pregnant in two more years, which would be 4.5 years post-diagnosis, and even that is still a risk.”

For 32-year-old Megan Koehler, whose son was one and a half when she was diagnosed with Hodgkin Lymphoma, the hardest part “was knowing the world continued on while I spent days in bed,” she says. “My coworkers still worked on projects I was supposed to be part of, and the worst was knowing my son was growing up, learning to speak sentences, and just becoming a toddler without me – or so it felt that way.” 

She remembers crying for most of his second birthday because she was in bed post chemo, feeling devastated that she didn’t have the energy to spend the day with him. During a 50-plus day hospital stay caused by an adverse reaction to a chemotherapy drug, she would Facetime him and cry when he spoke in sentences, because he wasn’t doing that before she was admitted. While she’s grateful for the support she had from her husband and mother, she felt alienated. “I spoke to a few people my age via social media, but no one in person. My center mostly catered to the older generations, so it was somewhat isolating. I did have a great relationship with a few of the infusion nurses who were around my age.”

While oncologists may be rightly focused on saving patients’ lives, there must be more consideration for quality of life during and after treatment – both physical and mental. “More questions need to be asked about their relationships, fertility options, and any mental health concerns or symptoms,” says Samolovitch. From a research perspective, initiatives must expand to pinpoint not only the reason for the rise of cancer in young adults, but find ways to screen and diagnose earlier.

Towards the beginning of my treatment, before I switched hospitals, my oncologist seemed to treat my concerns about self-esteem and hair loss as trivial compared to the real work of saving my life. At my weakest, I had to advocate repeatedly to get accurate information on cold capping, a process of scalp cooling that can preserve most of your hair during chemotherapy, and I had to beg again and again for a social worker to reach out to me, which took weeks. 

It’s a beautiful thing that more young adults with cancer are surviving their illnesses. But that means they’ll have decades of life ahead of them. Providers must do a better job supporting young adult patients through all the collateral damage that comes with cancer and its treatment.  

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Home > Cancer Research Catalyst > The More You Know About Cancer Prevention

The More You Know About Cancer Prevention

The World Health Organization estimates that 30% to 50% of all cancer cases are preventable.  

Yes, much of that can be attributed to healthy lifestyle choices, including physical activity , better nutrition , lack of smoking , and light to moderate alcohol consumption , but knowledge can also be a powerful cancer prevention tool. According to the American Association for Cancer Research (AACR) Cancer Progress Report 2023 , the United States experienced a 33% decline in overall cancer mortality between 1991 and 2020 largely thanks to public health campaigns and policy initiatives implemented to reduce smoking and increase early detection of cancers, based on study findings in CA: A Cancer Journal for Clinicians . 

Bar graph of modifiable cancer risks with tobacco smoking having the highest percentage of cancer cases in the U.S. in adults over 30 attributed to that cause followed by excess body weight, alcohol consumption, ultraviolet radiation exposure, poor diet, pathogenic infections, and physical inactivity.

As they say (or at least a series of public service announcements did in the ’90s), “The More You Know.” And in this case, the more you know about your cancer risks can be lifesaving, and what you don’t know can have negative consequences. A series of recent studies have found that some people may lack a certain level of clarity and/or awareness about some cancer prevention techniques such as screening and vaccination. This may cause gaps in ensuring benefit from available methods that can help detect cancer much earlier or outright prevent it. 

Some Stool Samples Aren’t Fit to be Tested  

One of the several initial screening options for colorectal cancer  (CRC) is a self-administered fecal immunochemical test (FIT) in which an individual provides a stool sample to be examined for hidden blood. The FIT is either administered at a health care office (often with verbal instructions) or via a mail-order program (with written and/or info-graphical instructions). But 1 in 10 FITs could not be processed due to unsatisfactory samples, according to results from a study published in  Cancer Epidemiology, Biomarkers & Prevention , a journal of the AACR. 

At least part of the issue is individuals don’t fully comprehend what is required to provide a sample that is deemed satisfactory for testing, according to Rasmi Nair, MBBS, PhD , co-first author of the paper and an assistant professor at the Peter O’Donnell Jr. School of Public Health of UT Southwestern Medical Center. That was especially true for the mail-order program, which was 2.66 times more likely to produce unsatisfactory results. 

Nair and her colleagues examined electronic health record (EHR) data of 56,980 individuals aged 50 to 74 who underwent FIT screening between 2010 and 2019 within the Dallas-based Parkland Health system. Parkland, which is considered a safety-net hospital, provides care to more than one million low-income, uninsured Dallas County residents. Overall, of the 10.2% FITs considered unsatisfactory, 51% were due to an inadequate specimen, 27% were attributed to incomplete labeling, 13% of the stool specimens were too old, and 8% had a broken or leaking container. Additionally, only 40.7% of individuals with unsatisfactory tests received follow-up FIT or colonoscopy screening within 15 months of the failed test. 

Nair suggested that minimizing language and health literacy barriers could help, and the study authors pointed to visual instructions that showed positive results in improving sample collection in other studies. The authors also suggested that testing facilities include previously affixed patient labels or barcodes to minimize labeling errors as well as policy changes to allow using the sample ordering, mailing, or receiving date as the collection date—if the date is missing on the label itself and the sample is sent within the two-week widow. Finally, the authors also want to see a better system put in place to ensure proper follow-up.   

“The fact that, in most instances, unsatisfactory FIT was not followed by a timely subsequent test highlights the need for systems to have a better, more comprehensive approach to tagging and following up unsatisfactory FIT,” said co-first author Po-Hong Liu, MD , a gastroenterology fellow at UT Southwestern Medical Center. 

The Need for More HPV Vaccine Awareness  

The vaccine for human papillomavirus (HPV) has shown tremendous results in preventing cervical cancer . In fact, a recent study examining cervical cancer cases in Scotland found zero cases among women born between 1988-1996 who were fully vaccinated against HPV between the ages of 12 and 13, according to a paper published in the Journal of the National Cancer Institute .  

The HPV vaccine, however, can benefit men and protect against other cancers as well, including anal , oral, and penile cancers. But this fact may not be properly presented to Hispanic and Latino men who identify as sexual minorities, according to results presented at the  16th AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved . 

Between August 2021 and August 2022, Shannon M. Christy, PhD , assistant member in the Department of Health Outcomes and Behavior at Moffitt Cancer Center in Tampa, Florida, and her colleagues surveyed individuals between the ages of 18 and 26 who were born male and were living in Florida and Puerto Rico, identified as Hispanic or Latino, had sex with a man or were attracted to men, and were able to read and understand Spanish. Among the 102 participants who said they had not received the HPV vaccine, 56% responded incorrectly or “do not know” to a question about whether most sexually active individuals are at risk for being infected with HPV; 20% responded incorrectly or “do not know” to a question assessing whether men can be infected with HPV; and more than half responded incorrectly or “do not know” to questions about the link between HPV and anal (54%), oral (61%), or penile (65%) cancers.  

Fifty-six percent did hear about the HPV vaccine, yet only 19% said a provider had recommended it to them. Currently, the Centers for Disease Control and Prevention recommends HPV vaccination for adolescents around ages 11 or 12 and even encourages the vaccination of young adults up to age 26 if they did not receive it when they were younger. The U.S. Food and Drug Administration has approved the HPV vaccine for people ages 9 to 45. 

A breakdown of the current HPV vaccination recommendations including the CDC recommending two doses given six months apart for adolescents younger than 15 and three doses for those between 15 and 26 or with weakened immune systems.

“Sexual minority men are a population group at higher risk for HPV infections and subsequent HPV-related health concerns, including anal cancer,” said Christy. “Prior research has demonstrated suboptimal HPV vaccine uptake among young adults, including sexual minority men. Additional efforts are needed to ensure that all age-eligible community members can benefit from this effective cancer prevention method.” 

One place to start would be more Spanish-language materials about HPV vaccination for young adults, as Christy and her collaborators found a lack of such education and no materials culturally adapted for Hispanic and Latino sexual and gender minority community members. “To reduce HPV-related cancer disparities, it is essential that information be relevant and actionable and available to age-eligible people in their preferred language,” said Christy. 

Your Genetics Know What You May Not about Cancer Prevention 

Whole-exome sequencing can be used as a screening technique to identify if an individual has any genes predisposed for hereditary diseases, including some cancers. The National Comprehensive Cancer Network (NCCN) has established a set of guidelines—including ones for breast, ovarian, and pancreatic cancers and colorectal cancer —to identify individuals who should undergo genetic testing, but guidelines like these might not be catching everyone who should be screened, according to  N. Jewel Samadder, MD , a professor of medicine at the Mayo Clinic College of Medicine and co-leader of the precision oncology program at the Mayo Clinic Comprehensive Cancer Center. 

“These criteria were created at a time when genetic testing was cost-prohibitive and thus aimed to identify those at the greatest chance of being a mutation carrier in the absence of population-wide whole-exome sequencing,” Samadder said. “However, these conditions are poorly identified in current practice, and many patients are not aware of their cancer risk.” 

Samadder presented results from the  Tapestry  clinical trial at the  AACR Annual Meeting 2023 that showed that 39.2% of individuals who consented to whole-exome sequencing and were identified as carriers of predisposition genes for hereditary breast and ovarian cancer (HBOC) or Lynch syndrome would not have qualified under current guidelines. At the time of data cut-off, 44,306 patients from Mayo Clinic sites in Minnesota, Arizona, and Florida had provided a saliva sample. For this part of the trial, researchers used whole-exome sequencing to evaluate samples for BRCA1 and BRCA2, denoting HBOC, and MLH1, MSH2, MSH6, PMS2, and EPCAM, denoting Lynch syndrome. 

A diagram with lines pointing to various body parts and then a list of the genes associated with potential inherited cancer risk for that body part.

Of the 387 individuals with HBOC and 163 with Lynch syndrome identified, 52.1% did not know prior to this study they had a cancer predisposition condition and 39.2% did not satisfy the existing NCCN criteria for genetic testing. Among the patients who were newly diagnosed with HBOC or Lynch syndrome during this study, 60% were ineligible for genetic testing per the current guidelines. Samadder explained that patients with HBOC have up to an 80% lifetime risk of developing  breast cancer  and a markedly increased risk, relative to the general population, of developing  ovarian cancer ,  pancreatic cancer ,  prostate cancer , and  melanoma . Meanwhile, patients with Lynch syndrome have up to an 80% lifetime risk of colorectal cancer and up to 60% lifetime risk of  endometrial cancer , plus increased risks of upper gastrointestinal, urinary tract, skin, and other cancers.  

Knowing about their increased genetic risk can help patients take appropriate next steps, Samadder said. For example, patients with Lynch syndrome can undergo regular colonoscopies, blood and urine screening, and prophylactic hysterectomy, while patients with HBOC can be proactive through advanced breast imaging and prophylactic mastectomy and/or oophorectomy.  

“The knowledge that comes from genetics,” Samadder said, “can empower patients to take control of their disease risk and increase their likelihood of avoiding a deadly cancer diagnosis or catching it at an early stage when it is highly curable.”  

Like they say, the more you know.  

To see how much you know about cancer prevention, take the AACR’s Cancer Prevention Quiz .   

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Make Cancer History

We can – and must – cure cancer now

What is Make Cancer History?

Make Cancer History is a non-profit organisation based in Tokyo. We’re working to cure all cancers, including late stage cancers (metastatic cancer). With your help we can cure cancer and make it a thing of the past.

Is it really possible to cure cancer?

Yes. Currently some cancers can be cured if the disease is found in an early stage. But the percentage of patients cured is extremely low. We will change that.

What kind of organisation is Make Cancer History?

We’re currently an Unincorporated voluntary association (任意団体) In early 2022 we’ll become a Non-profit Incorporated Association (非営利型一般社団法人 ) This is similar to a 501(c)(3) NPO in the US.

How can I help cure cancer?

There are two ways you can help. You can make a donation  and you can volunteer .

Patient makes history by overcoming prostate cancer through clinical trials at UW-Health

MADISON, Wis. (WSAW) - Gary Davey, originally from the UK, was diagnosed with metastatic prostate cancer in 2010. After first consulting doctors, his fate seemed bleak, but he has since defied the odds.

“My doctor said, ‘If you don’t find the best surgeon, you won’t make it to Christmas, Gary,’” Davey said.

According to the American Cancer Society , about 1-in-44 men will die from prostate cancer but as fate would have it Davey is defying the odds.

“Thirteen years later, I’m here,” Davey said.

When Davey found UW-Health., they initially tried surgery and radiation therapy, but his cancer remained resistant. Looking for more options, Dr. Josh Lang , a Medical Oncologist at UW-Health, decided to put him on a clinical trial. According to Dr. Lang, the trial tested a precision therapy that combined niraparib, a cancer drug that inhibits cancer cells from repairing damaged DNA, and abiraterone, a hormone therapy.

“It was combining a drug that targets a specific genetic mutation called niraparib, and another drug that targets hormones in prostate cancer,” Dr. Lang said. “So this trial is actually just asking if it is safe to combine these treatments.”

Dr. Lang had faith the trial would work but was blown away by just how well it did.

“Especially for a disease that’s as common as prostate cancer is, is an incredible advance,” Dr. Lang said. “We need to make sure we’re doing this genetic testing for all men with metastatic prostate cancer.”

He’s hoping to use this case to pave the way for more success.

“(It is) kind of this revolution of precision medicine,” Dr. Lang said. “It’s for the patient who’s sitting in front of us today, but also the patient’s who are gonna come in the future.”

“If you’d have known me beforehand, you probably wouldn’t have thought I would be this optimistic,” Davey said. “Every day since, I don’t know why I’m here, but (I know) there’s a reason why I’m here. That’s for sure.”

Davey continues to receive the combination treatment each month. The drug combination has recently been approved by the U.S. Food and Drug Administration.

Copyright 2024 WSAW. All rights reserved.

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COMMENTS

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