
Nobel Prize in Physiology or Medicine · 1989
Harold E. Varmus
He showed that cancer genes are corrupted copies of our own growth genes, a key step toward drugs that target cancer.
The Nobel citation: “for their discovery of the cellular origin of retroviral oncogenes”
- Born
- December 18, 1939, Oceanside, NY, USA
- Shared with
- J. Michael Bishop
- Affiliation at the time
- University of California School of Medicine, USA
Medicine prize
1989
Shared with 1 other laureate.
Age that year
50years
Born in 1939.
Headline credited impact
1,050–3,900lives saved
Chronic myeloid leukemia deaths averted by imatinib and later BCR-ABL kinase inhibitors, 2001-2025. How it was built
Sources cited
28
Fact-checked September 24, 2026.
- Before medicine he studied English literature, earning a Harvard master's degree focused on Anglo-Saxon and metaphysical poetry.
- He began lab research only as he neared 30, unusually late for a biomedical scientist, and shared a Nobel Prize about two decades later.
- In 1985-86 he chaired an international virus-naming committee that proposed the name the AIDS virus still carries: HIV.
- At the 1989 Nobel banquet he likened the cancer cell to Grendel, the monster in the Old English epic Beowulf.
- He was the first Nobel laureate to run the US National Institutes of Health, whose budget grew from under $11 billion to almost $16 billion on his watch.
The breakthrough
Cancer genes come from our own cells
In the early 1970s many scientists thought viruses might cause cancer by slipping foreign "cancer genes" into cells. Rous sarcoma virus, which gives chickens tumors, carries one such gene, called src. Varmus and Michael Bishop's team at UC San Francisco, with Dominique Stehelin doing the key lab work, built a radioactive probe that stuck only to src. They used it to search the DNA of healthy birds. In 1976 they reported that normal chickens, and other birds as distant as the emu, carry a close relative of src in their own chromosomes. Later work found it in mammals, including humans. In normal cells the gene was split into pieces, as ordinary cellular genes are, and it had been kept through a long stretch of evolution. So the virus had not invented it. Long ago a virus had picked up a normal gene that helps control cell growth, altered it, and turned it into a trigger for cancer. Think of a car's accelerator: every car needs one, but if it sticks, the car races out of control. These "proto-oncogenes" are the cell's accelerators, and mutations, chemicals, radiation or viruses can make them stick. The finding moved the hunt for cancer's causes inside our own genes. Using viruses as guides, researchers had found more than 40 such genes by 1989.[1],[3],[4],[8],[12]
“ways that reveal a cancer cell to be, like Grendel, a distorted version of our normal selves”
What it meant for humanity
Before 1976, much cancer research looked for causes in viruses and outside chemicals. Varmus and Bishop moved the search inside the cell. Once scientists knew that cancer genes are damaged versions of normal growth genes, they could look for the specific broken part in each cancer and try to block it. Many of these genes turned out to make kinases, enzymes that switch other proteins on. The first big payoff came in chronic myeloid leukemia (CML). Its key gene, ABL, was first found as the cancer gene of a mouse leukemia virus and later in a chromosome swap in human leukemia. In 1986 the drug company Ciba-Geigy began searching for chemicals that could block overactive kinases. The result, the pill imatinib (Gleevec), was approved in the United States in 2001. Five years after diagnosis, about 89 percent of patients on it were alive, compared with about 60 percent on the older treatment. The US death rate from CML has fallen by about two thirds since the late 1990s. Imatinib helped establish targeted cancer drugs, a family of treatments aimed at specific genetic faults. Varmus kept working along this path: at Memorial Sloan Kettering his lab helped show which lung cancers respond to EGFR-blocking pills and why they later stop working. His public work mattered too. As head of the National Institutes of Health he helped grow its budget from under $11 billion to almost $16 billion, and he pushed for free online access to research through PubMed Central and the Public Library of Science.
- Imatinib blocks ABL, a cancer enzyme first found through a mouse leukemia virus. Five years after diagnosis about 89 percent of CML patients on it were alive, versus about 60 percent on interferon.[19],[20],[21]
- The US death rate from chronic myeloid leukemia fell from about 1 per 100,000 people a year in the 1970s and 1980s to about 0.3 since 2007, while five-year survival roughly doubled to over 70 percent.[15]
- With Memorial Sloan Kettering colleagues, his lab studied lung cancers with EGFR mutations that respond to gefitinib and erlotinib, and in 2005 was one of two teams to report T790M, a mutation that lets tumors escape these drugs.[11],[13],[28]
- As NIH director from 1993 to 1999 he built support in Congress to raise the agency's budget from just under $11 billion to almost $16 billion, with a plan to reach $26 billion by 2002.[10]
- He helped create PubMed Central, a free online archive that held over three million articles by 2014, and co-founded the Public Library of Science, a nonprofit open-access publisher.[10],[11]
Impact in numbers
Varmus's main contribution was a change of view: cancer is not an invader but our own growth genes gone wrong. That idea, shared with Michael Bishop, underlies modern cancer genetics, tumor gene testing and targeted drugs, so its reach is far wider than any single number. The claim below counts only one well-measured benefit, lives saved by BCR-ABL kinase inhibitors in chronic myeloid leukemia, and credits Varmus with a small share because a long chain of other scientists and drug makers was essential. Other targeted drugs for breast, lung and other cancers are not counted. His public service is also left unquantified: he helped grow the NIH budget, guided the naming of HIV, helped launch PubMed Central, which held over three million articles by 2014, and co-founded the Public Library of Science, which showed that free-to-read journals can work.
HealthFundamental science
Each number is the laureate’s credited share of a real-world outcome, cumulative to 2025. The whole outcome, the share of credit, and the reasoning are shown so you can check the arithmetic. Outcomes shared with other laureates are counted once on the impact page.
- Low confidenceRippleModeledHealth
Chronic myeloid leukemia deaths averted by imatinib and later BCR-ABL kinase inhibitors, 2001-2025
1,050–3,900
lives saved, credited share
That is 3% of 35,000–130,000 lives saved since 2001.
How this number was built
CML deaths averted by BCR-ABL inhibitors (imatinib approved 2001) only, a floor. SEER US age-adjusted CML death rate: 0.85-0.88 in 1996-98, 0.65 in 1999-2000, about 0.30 since 2007. The 1999 step down predates imatinib's approval and coincides with the switch to ICD-10 death coding, so 0.65 is the last comparable pre-imatinib level. Averted = sum of (counterfactual - observed) x US population, 2001-25. Low: 0.65 falling 2%/yr as in 1991-98 = 13,300 US; other high-income countries (3.28x US population) at half the US per-capita gain = 35,000. High: 0.65 held flat = 25,000 US; x4.28 with full gain abroad = 107,000; plus 25,000 in poorer countries (Max Foundation: 100,000+ patients; half CML, half of those saved) = 132,000, rounded to 130,000. Share 0.03: src work set the frame in which ABL was found; Bishop, Baltimore, Witte, Nowell, Rowley, Druker, Lydon, Sawyers were essential.[15],[16],[17],[18],[19],[20],[27]
Sources: National Cancer Institute, SEER Program; World Bank, World Development Indicators API; The Max Foundation; Lasker Foundation; Nature Reviews Cancer; Lasker Foundation; Cancer (American Cancer Society)
The double edge
The oncogene discovery itself caused little direct harm, but the story has real costs. The targeted drugs it helped inspire are expensive: in 2012 imatinib cost about $54,000 a year in the US and newer versions $80,000 to $90,000, and researchers warned that lifelong treatment could be unaffordable in most poorer countries, though generic imatinib was expected to cost far less. Most CML patients must take the pills for life, and cancers often become resistant, as Varmus's own lab showed in lung cancer. As NIH director, Varmus was also at the centre of a sharp ethics dispute. NIH and CDC funded trials in poorer countries that tested a cheaper, shorter AZT regimen against a placebo to stop mothers passing HIV to their babies, even though a longer, proven regimen existed. In 1997 Varmus co-wrote a defense of the design in the New England Journal of Medicine; critics said families in the placebo groups were denied a treatment known to work. The dispute fed into later changes to international research-ethics rules.
- Moderate
Defending placebo-controlled HIV prevention trials
In the 1990s, placebo-controlled trials of cheaper ways to stop mothers passing HIV to their babies enrolled more than 12,000 HIV-positive women in 16 countries, with NIH and CDC among the principal funders. Varmus and his co-author argued in 1997 that the trials sought affordable options for the poorest countries. Critics writing in the same journal called withholding a proven regimen unethical.[22],[23]
- Moderate
Targeted drugs priced beyond reach
In 2012 imatinib cost about $54,000 a year and second-generation CML drugs $80,000 to $90,000. Because most patients need the drugs for life, researchers warned that the cost could be prohibitive in most emerging countries and heavy even in rich ones. Generic imatinib, expected after 2014, was forecast to cost far less.[16]
- Minor
Resistance and lifelong treatment
Targeted drugs rarely cure in the strict sense. Fewer than 5 percent of CML patients could safely stop imatinib as of 2012, and tumors evolve resistance mutations, such as T790M in lung cancer, which Varmus's lab helped identify.[13],[16],[19]
Against the odds
Varmus describes his Long Island childhood as easy and fortunate. His grandparents were part of the great Jewish migration from Eastern Europe around 1900: his father's father came from a village near Warsaw, and his mother's parents from villages near Linz. The family knew hardship: his father's mother died in the 1918 flu epidemic, and his father had to leave Harvard College after two years for lack of money. Varmus was born in December 1939, as World War II was beginning, and spent the war years in Florida, far from the fighting, where his father was posted to a military hospital. The wider climate for American Jews was harsher than his own story. After World War I, nativism and antisemitism rose, and from the 1920s most American medical schools capped Jewish admissions. Columbia University adopted an explicit quota in 1918, and a New York State investigation after World War II found that Jewish, Black and Italian Catholic applicants were being selectively turned away from Columbia's and Cornell's medical schools. The quotas faded after the war and were gone by 1970. Varmus entered Columbia's medical school in 1962, after Harvard Medical School turned him down; no source links that rejection to his background. Compared with Jewish laureates who fled Europe, he faced little personal discrimination.
Jewish background
Varmus was born to Frank Varmus, a family doctor, and Beatrice Barasch Varmus, a social worker, both children of Jewish immigrants. His father's father came from a village near Warsaw; his mother's parents came from farming villages near Linz, Austria, and opened a children's clothing store in Freeport, New York. He opens his Nobel autobiography by placing himself in the early-1900s migration of Eastern European Jews to New York. The sources we found do not describe religious practice; his public life has centred on science, literature and public service.[2],[6],[26]
Key dates
December 18, 1939
Born in Oceanside, New York, to a family doctor and a social worker, both children of Jewish immigrants.[1],[2]
1962
Earns an MA in English at Harvard, then enters Columbia's medical school after a rejection from Harvard Medical School.[6],[7]
1966
Receives his MD from Columbia's College of Physicians and Surgeons.[7]
1968
Joins Ira Pastan's NIH lab through the Public Health Service, his first real research and an alternative to the Vietnam draft.[7],[14]
1970
Moves to UC San Francisco as a postdoctoral fellow with Michael Bishop, beginning a long partnership on cancer-causing retroviruses.[2],[7]
1971
His mother dies of breast cancer; her diagnosis had helped draw him toward tumor viruses.[2],[14]
March 11, 1976
With Stehelin, Bishop and Vogt, reports in Nature that normal bird DNA carries a close relative of the src cancer gene.[7],[12]
May 1986
The virus-naming committee he chairs proposes the name human immunodeficiency virus (HIV) for the AIDS virus.[7],[9]
October 9, 1989
Nobel Prize in Physiology or Medicine announced, shared with J. Michael Bishop, for the cellular origin of retroviral oncogenes.[1],[3]
November 1993
Becomes director of the National Institutes of Health, the first Nobel laureate in the post.[6],[10]
January 2000
Becomes president of Memorial Sloan Kettering Cancer Center; the same year he co-founds the Public Library of Science.[10],[11]
2005
His lab and colleagues report the T790M mutation that lets lung cancers resist gefitinib and erlotinib, days apart from another team's report.[13],[28]
July 12, 2010
Becomes director of the National Cancer Institute, appointed by President Obama.[7],[26]
March 31, 2015
Leaves the NCI and returns to New York as Lewis Thomas University Professor of Medicine at Weill Cornell.[6],[7]
Sources
- 1.Harold E. Varmus - Facts · NobelPrize.org (Nobel Prize Outreach)
- 2.Harold E. Varmus - Biographical · NobelPrize.org (Nobel Foundation, from Les Prix Nobel 1989), 1989
- 3.The Nobel Prize in Physiology or Medicine 1989 - Press release · The Nobel Assembly at the Karolinska Institute, 1989
- 4.Retroviruses and Oncogenes I (Nobel Lecture, 8 December 1989) · NobelPrize.org (Nobel Foundation), 1989
- 5.Harold E. Varmus - Banquet speech · NobelPrize.org (Nobel Foundation), 1989
- 6.Biographical Overview (The Harold Varmus Papers, Profiles in Science) · US National Library of Medicine
- 7.Brief Chronology (The Harold Varmus Papers, Profiles in Science) · US National Library of Medicine
- 8.Retroviruses and the Genetic Origins of Cancer, 1970-1993 (The Harold Varmus Papers, Profiles in Science) · US National Library of Medicine
- 9.AIDS and HIV: Science, Politics, and Controversy, 1981-1993 (The Harold Varmus Papers, Profiles in Science) · US National Library of Medicine
- 10.Basic Science and Congressional Politics: NIH Director, 1993-1999 (The Harold Varmus Papers, Profiles in Science) · US National Library of Medicine
- 11.Memorial Sloan Kettering Cancer Center, 2000-2010, and National Cancer Institute, 2010-2015 (The Harold Varmus Papers, Profiles in Science) · US National Library of Medicine
- 12.DNA related to the transforming gene(s) of avian sarcoma viruses is present in normal avian DNA (Stehelin D, Varmus HE, Bishop JM, Vogt PK), Nature 260:170-173 · Nature, 1976
- 13.Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain (Pao W, ... Varmus H), PLoS Medicine 2:e73 · PLoS Medicine, 2005
- 14.Free Radical (Jamie Shreeve) · Wired, 2006
- 15.Cancer Stat Facts: Leukemia - Chronic Myeloid Leukemia (CML) · National Cancer Institute, SEER Program, 2026
- 16.Estimations of the increasing prevalence and plateau prevalence of chronic myeloid leukemia in the era of tyrosine kinase inhibitor therapy (Huang X, Cortes J, Kantarjian H), Cancer 118:3123-3127 · Cancer (American Cancer Society), 2012
- 17.Population, total (SP.POP.TOTL): high-income countries and United States, 2001-2024 · World Bank, World Development Indicators API, 2025
- 18.The Max Foundation (home page: people served and countries reached) · The Max Foundation, 2026
- 19.Molecularly targeted treatments for chronic myeloid leukemia (2009 Lasker~DeBakey Clinical Medical Research Award: Druker, Lydon, Sawyers) · Lasker Foundation, 2009
- 20.Role of ABL family kinases in cancer: from leukaemia to solid tumours (Greuber EK, Smith-Pearson P, Wang J, Pendergast AM), Nature Reviews Cancer 13:559-571 · Nature Reviews Cancer, 2013
- 21.How Imatinib Transformed Leukemia Treatment and Cancer Research · National Cancer Institute, 2018
- 22.Can context justify an ethical double standard for clinical research in developing countries? (Landes M), Globalization and Health 1:11 · Globalization and Health (BioMed Central), 2005
- 23.Ethical complexities of conducting research in developing countries (Varmus H, Satcher D), New England Journal of Medicine 337:1003-1005 · New England Journal of Medicine (PubMed record), 1997
- 24.Why Did the United States Medical School Admissions Quota for Jews End? (Halperin EC), American Journal of the Medical Sciences 358:317-325 · American Journal of the Medical Sciences (PubMed record), 2019
- 25.Jewish American Heritage Month: The Forgotten History of Quotas in American Medical School Admissions · Himmelfarb Health Sciences Library, George Washington University, 2023
- 26.Harold E. Varmus · Wikipedia
- 27.Fundamental discoveries, academic leadership, public advocacy (2021 Lasker~Koshland Special Achievement Award: David Baltimore) · Lasker Foundation, 2021
- 28.EGFR mutation and resistance of non-small-cell lung cancer to gefitinib (Kobayashi S, ... Halmos B), New England Journal of Medicine 352:786-792 · New England Journal of Medicine (PubMed record), 2005
Fact-checked on September 24, 2026 by a separate AI fact-checking pass that re-opened the sources, with 12 corrections made. How we check
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