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David M. Livingston, MD


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David M. Livingston, MD


  • Charles A. Dana Chair in Human Cancer Genetics
  • Emil Frei III Distinguished Professor of Medicine, Harvard Medical School

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Deceased (1941-2021)

David Livingston was the Deputy Director of the Dana-Farber/Harvard Cancer Center; Chief of the Charles A. Dana Division of Human Cancer Genetics, and the Emil Frei Professor of Genetics and Medicine at Harvard Medical School. From 1996 to 2000, he served as Chairman of the Executive Committee for Research at the Dana-Farber Cancer Institute, leading the senior faculty group that oversees all aspects of the Institute's research program. He reassumed that post in 2005. Dr. Livingston was a Harvard faculty member continuously since 1973.

Dr. Livingston received an A.B. cum laude from Harvard College in 1961, an M.D., magna cum laude, from Tufts University School of Medicine in 1965, and served his internship and residency in internal medicine at the Peter Bent Brigham Hospital in Boston (now Brigham and Women's Hospital). In 1967, he became a Research Associate at the National Cancer Institute (NCI) in molecular biology and biochemistry; he continued his work as a Research Fellow in Biological Chemistry at Harvard Medical School in 1969. Dr. Livingston returned to NCI in 1971 as a Senior Staff Fellow where he began his career in cancer research. He was recruited to Dana-Farber (then the Children's Cancer Research Foundation) in 1973.

Dr. Livingston was an internationally recognized expert on genes that regulate cell growth in the body - genes that, when they go awry, can lead to cancer. These genes are called oncogenes and tumor suppressor genes. Through his research, Dr. Livingston uncovered detailed biochemical steps required to initiate and maintain the transformation of these cells into tumor cells. His focus was on the regulatory controls of signal transduction - the smooth and coordinated flow of special chemical signals from the surrounding environment to the cell, where it is transduced into specific commands that tell cells whether or not to grow - and their role in cancer development. In recent years, his work centered on those key molecular steps that trigger the development of breast and ovarian cancer.

Dr. Livingston was the recipient of numerous awards and honors. He was been elected to the Institute of Medicine of the National Academy of Sciences, the National Academy of Sciences, itself, and the American Academy of Arts and Sciences. He sat on multiple editorial boards, the science advisory boards of other research institutions, and was a member of the Association of American Physicians, the American Society for Clinical Investigation, the American Society for Microbiology, and the American Academy of Microbiology. He was also a Foreign Associate of the European Molecular Biology Organization and served as Vice Chair of the Board of the Damon Runyan Cancer Research Foundation. Dr. Livingston authored more than195 scientific publications.

Recent Awards:

  • Baxter Award for Distinguished Research in the Biomedical Sciences, AAMC 1997
  • Lila Gruber Honor Award for Cancer Research, American Academy of Dermatology 2001
  • Member, American Academy of Arts and Sciences 2001
  • AACR-G.H.A. Clowes Award 2005
  • Boveri Award for Molecular Cancer Genetics, German Cancer Society 2005


Molecular Pathogenesis of Breast and Ovarian Cancer

The Livingston laboratory is dedicated to the study of processes that, when defective, allow human cells to develop malignant characteristics. These processes are, in part, controlled by tumor suppressor loci. We continue to concentrate our efforts on a subset of these loci, all of which exert their functions in the nucleus. Some participate in the control of cell proliferation, others in the control of genome integrity, and still others in mechanisms that underlie the ability of cells to thrive in low-oxygen environments and under other stresses. Based on some unexpected results, we have extended our work over the past two years to explore the events that give stem cells of certain tissues the ability to self-renew.A fraction of our effort is dedicated to understanding the genetics of breast and ovarian cancer development. In particular, we are studying the in vivo biochemical and biological functions of four genes - BRCA1, BRCA2, BACH1, and BARD1 - which encode large nuclear proteins that interact specifically with one another. At least three and likely all four of these proteins are products of tumor suppressing loci. Together, they function as parts of large nuclear complexes that participate in the response of cells to DNA damage, and perhaps in other basic functions as well. When BRCA1, BARD1, or BRCA2 is rendered defective by germline mutation in females, tumor development develops at higher than normal frequencies in the breast and the ovary. A major segment of our ongoing work is aimed at trying to understand how, in biochemical terms, BRCA1 and BRCA2 perform their tumor suppressing effects and why, in the case of BRCA1, these effects are detected in the cells of women but not men.

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