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| Name |
Andrews, Nancy C. |
| Location
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Boston Children's Hospital |
| Primary Field
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Medical Physiology and Metabolism |
| Secondary Field
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Medical Genetics, Hematology and Oncology |
 Election Citation
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Andrews has been a leader in the renaissance of iron biology. She pioneered using mouse models to discover genes important in iron transport, understand iron homeostasis in vivo and elucidate the pathogenesis of hemochromatosis, the anemia of chronic disease, and (first described by Andrews) iron-refractory iron deficiency anemia. |
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Research Interests
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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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