Michael M. Gottesman

National Institutes of Health


Election Year: 2018
Primary Section: 26, Genetics
Secondary Section: 41, Medical Genetics, Hematology, and Oncology
Membership Type: Member

Biosketch

Michael M. Gottesman is the Deputy Director for Intramural Research at the National Institutes of Health and Chief of the Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute. He obtained his M.D. from Harvard Medical School, completed his internship and residency in medicine at the Peter Bent Brigham Hospital in Boston, and received his postdoctoral research training in molecular genetics with Martin Gellert at the NIH before returning to Harvard Medical School as an Assistant Professor of Anatomy. Positions at NIH include Chief of the Molecular Cell Genetics Section of the Laboratory of Molecular Biology, NCI NIH, in 1980, and Chief of the Laboratory of Cell Biology in 1990. In 1992 he was Acting Director of the National Center for Human Genome Research. Since 1993 he has been the NIH Deputy Director for Intramural Research. Recognition has included election to the Institute of Medicine (now the National Academy of Medicine) in 2003, to the American Academy of Arts and Sciences in 2010, and to the National Academy of Sciences in 2018.

Research Interests

Dr. Gottesman developed somatic cell genetic systems for the analysis of drug resistance in cancer cells. Those studies led to the cloning of the human MDR1 (ABCB1) gene, an ATP-dependent multidrug efflux pump, and the elucidation of its function in normal tissues and in cancer cells. Structure-function studies on the ABCB1 transporter have led to models accounting for the broad range of substrates recognized by this transporter. These genetic and beiochemical studies have resulted in recognition of ABCB1 and other ABC transporters as essential determinants of drug pharmacokinetics and components of the blood-brain barrier and blood-placental barrier. The Gottesman lab continues to focus on identifying mechanisms of multidrug resistance in cancer and in determining the clinical relevance of these mechanisms with the intent to find ways to circumvent or exploit multidrug resistance and improve the treatment of cancer.

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