Nancy C. Andrews

Duke University


Election Year: 2015
Primary Section: 42, Medical Physiology and Metabolism
Secondary Section: 41, Medical Genetics, Hematology, and Oncology
Membership Type: Member

Biosketch

Nancy Andrews is a hematologist recognized for her work elucidating mammalian iron metabolism. Her laboratory identified and characterized mechanisms for transmembrane iron transport and its regulation, providing insight into the pathogenesis of genetic hemochromatosis, the anemia of inflammation and iron-refractory iron deficiency anemia. Andrews was born in Syracuse, New York in 1958. She graduated from Yale University with BS and MS degrees in molecular biophysics and biochemistry in 1980, from MIT with a PhD in biology in 1985 and from Harvard Medical School with an MD in 1987. She completed residency training in pediatrics at Children's Hospital Boston and fellowship in pediatric hematology/oncology at Children’s and Dana-Farber Cancer Institute. After 14 years on the faculty and several leadership roles at Harvard she moved to Duke University in 2007 to become dean of the school of medicine. She has been president of the American Society for Clinical Investigation, has served on the board of directors of the American Academy of Arts and Sciences and is a member of both the National Academy of Sciences and the National Academy of Medicine.

Research Interests

Nancy Andrews' laboratory is interested 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 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). Recently, the Andrews lab has determined 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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