Benjamin G. Neel
New York University
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Primary Section: 41, Medical Genetics, Hematology, and Oncology Secondary Section: 22, Cellular and Developmental Biology Membership Type:
Member
(elected 2022)
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Biosketch
Benjamin (Ben) Neel is a cancer biologist recognized for his work on signal transduction and mouse models of disease. He is known particularly for his work on oncogene activation by slowly transforming retroviruses and on the role of protein tyrosine phosphatases, particularly PTP1B, SHP1, and SHP2, in normal and cancer cell signaling. Neel was born in Wynnewood, PA and grew up in Philadelphia and Cherry Hill, NJ. He graduated from Cornell University with a degree in biology in 1977, from Rockefeller University with a degree in viral oncology in 1982, and from Cornell Medical College with an MD in 1983, followed by a residency in internal medicine at Beth Israel Hospital (Boston. He completed a postdoctoral fellowship at Harvard University from 1985-88 and served on the faculty of Harvard Medical School from 1988-2006. He was director of research for Princess Margaret Cancer Center and a Canada Research Chair, Tier 1, at University of Toronto from 2007-2015, before assuming his current position as Director of the Perlmutter Cancer Center/Professor of Medicine at NYU Langone. He is a member of both the National Academy of Sciences and the American Association of Physicians.
Research Interests
Ben Neel's laboratory is interested in signal transduction in health and disease and in mouse models of cancer and developmental syndromes. His group focuses on the biology and biochemistry of protein-tyrosine phosphatases (PTPs), particularly PTP1B, SHP1, and SHP2, which they cloned at the onset of the PTP field, on regulation of the RAS/ERK pathway, and on the biology of ovarian cancer. They generated novel mouse models of deficiency and gain-of-function for these and other key disease genes and used them to suggest novel therapies for various malignancies and for RASopathies, a set of genetic syndromes caused by mutations in RAS/ERK pathway genes. They identified roles for PTP1B in glucose homeostasis, body mass regulation, and hypoxia regulation, for SHP1 in inflammation and auto-immunity, and for SHP2 in cancer and development. More recently, they have concentrated on detailed dissections of how signal transduction inhibitors differentially affect cancer cells and cells in the tumor microenvironment, on the molecular and cellular biology of drug resistance and persistence, and on generating novel genetically defined models of high grade serous ovarian cancer.
