Andre Nussenzweig
National Institutes of Health
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Primary Section: 41, Medical Genetics, Hematology, and Oncology Secondary Section: 26, Genetics Membership Type:
Member
(elected 2023)
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Biosketch
Andre Nussenzweig, PhD is a Distinguished NIH investigator and Branch Chief of the Laboratory of Genome Integrity within the Center for Cancer Research at the National Cancer Institute. He earned his BA in physics at New York University, and subsequently obtained a Ph.D. in physics at Yale University. After doing a postdoctoral fellowship in physics with Serge Haroche at the Ecole Normale Superieure in Paris, France, he became interested in a career in biological science, and began researching DNA repair mechanisms at Memorial Sloan-Kettering. In 1998, he established his independent research group at the National Cancer Institute in Bethesda Maryland. Awards include the Arthur S. Flemming Award, the National Cancer Institute and NIH Director’s Awards, and the Basser Global Prize for BRCA Research. He is an elected a member of EMBO, the National Academy of Medicine, the American Academy of Arts and Science, and the National Academy of Sciences.
Research Interests
Andre Nussenzweig has contributed to our understanding of genomic instability, a precursor and hallmark of all cancers. His work demonstrated that the eukaryotic non-homologous end joining repair pathway is a major genome caretaker and a powerful barrier against cancer, that a core histone protein functions as a tumor suppressor, and that BRCA1-deficient cancers can become rewired in ways that restore their capacity for homologous recombination. He has also been at the leading-edge of developing pioneering genomic technologies that have helped identify new classes of fragile sites which reside at conserved topological domain borders which are commonly translocated in cancer. He further utilized these technologies to uncover a novel biomarker within microsatellite unstable tumors that is being used to develop new drug targets for multiple cancer types, and discovered that human neurons harbor high levels of endogenous ‘programmed’ DNA damage at regulatory genomic elements, a finding with implications for mutagenesis associated with aging and neurological diseases.
