Nancy C. Andrews

Harvard University


Primary Section: 42, Medical Physiology and Metabolism
Secondary Section: 41, Medical Genetics, Hematology, and Oncology
Membership Type:
Member (elected 2015)

Biosketch

Nancy Andrews is Executive Vice President and Chief Scientific Officer at Boston Children’s Hospital. She assumed that position after more than a decade at Duke University, where she served as Dean of the School of Medicine. Earlier in her career, she was the George Richards Minot Professor of Pediatrics at Harvard Medical School and Boston Children’s Hospital and an investigator of the Howard Hughes Medical Institute. Her laboratory discovered molecules important in mammalian iron homeostasis and worked out the molecular causes of several diseases characterized by abnormal iron handling. In addition to the NAS, Andrews is an elected member of the NAM and the American Academy of Arts and Sciences. She is a past president of the American Society of Clinical Investigation and a past Chair of the Board of the American Academy of Arts and Sciences. She currently serves on the Boards of Directors of Novartis, Charles River Laboratories and Maze Therapeutics. Andrews earned her B.S. and M.S. from Yale, her Ph.D. from M.I.T., and her M.D. from Harvard Medical School. She did her clinical training in pediatric hematology and oncology at Boston Children’s Hospital and Dana-Farber Cancer Institute.

Research Interests

Nancy Andrews’ primary research contributions have been in mammalian iron homeostasis and its disruption in human diseases. Through positional cloning of the affected genes in classical rodent mutants with anemia, her group identified key molecules involved in iron handling, including the first mammalian transmembrane iron transporter and demonstrated its importance in intestinal iron absorption and red blood cell differentiation. They characterized a second transmembrane iron transporter that releases iron from cells and showed that insufficiency of a peptide that regulates that transporter is fundamentally important in the pathogenesis of hemochromatosis, an iron overload disorder. They proposed that diminished cellular iron export plays a major role in the anemia of inflammation and, with others, confirmed that hypothesis. Starting with a patient that Andrews treated, her group identified the gene responsible for a disorder that they named iron-refractory iron deficiency (IRIDA). In addition, the Andrews lab identified new roles for the classical transferrin receptor, suggesting that iron and the transferrin receptor may have relevance to a variety of diseases that have not generally been considered iron disorders.

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