Stuart Orkin
| Stuart H. Orkin | |
|---|---|
| Nationality | American |
| Education | Massachusetts Institute of Technology, Harvard Medical School |
| Scientific career | |
| Fields | Pediatric oncology |
| Institutions | Dana–Farber/Harvard Cancer Center |
Stuart H. Orkin is an American physician, stem cell biologist and researcher in pediatric hematology-oncology. He is the David G. Nathan Professor of Pediatrics at Harvard Medical School and is the chairman of pediatric oncology at the Dana–Farber/Harvard Cancer Center. Orkin's research has focused on the genetic basis of blood disorders. He is a member of the National Academy of Sciences and the Institute of Medicine.
Orkin grew up in Manhattan, where his father was a urologist. He studied biology as an undergraduate at the Massachusetts Institute of Technology and earned a medical degree from Harvard Medical School. He did postdoctoral research in molecular biology at the National Institutes of Health under geneticist Philip Leder. While Orkin was completing his training in hematology-oncology, his department chair, David G. Nathan, allowed him to establish his own research laboratory.
Orkin is the David G. Nathan Professor of Pediatrics at Harvard Medical School and chairs the Department of Pediatric Oncology at the Dana–Farber/Harvard Cancer Center. He has been on the Harvard Medical School faculty since the late 1970s and has been a Howard Hughes Medical Institute investigator since 1986.
In the 1970s and 1980s, Orkin conducted research that identified genetic mutations associated with a group of blood disorders known as the thalassemias. Later, he and his team cloned a gene causing chronic granulomatous disease, marking the first time that a disease-causing gene was cloned without the researchers already knowing the protein coded by the gene. Today, his research lab examines transcriptional regulators of cell specification and differentiation. In September 2015, Orkin published a study in the journal Nature showing a small section of DNA which could be responsive to gene therapy for sickle-cell disease.
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