Associate Professor, Department of Obstetrics & Gynecology and Women's Health
Phosphatidylinositol-3-kinase (PI3K) is a crucial mediator of receptor-initiated signaling cascades, through the production of phosphatidylinositol (3,4,5)-triphosphate (PIP-3). Among the major effectors of PI3K is the AKT kinase, which is activated upon PIP-3-mediated membrane recruitment and, in turn, phosphorylates an ever-growing list of target proteins, regulating key processes such as proliferation, survival, cell size, genome stability, metabolism, and mRNA translation. This cascade is counteracted by the PTEN tumor suppressor, which opposes PI3K activity by dephosphorylating PIP-3 to PIP-2. Somatic deletions, mutations and epigenetic inactivation of PTEN have been identified in a large fraction of tumors (endometrial, glioblastoma, prostate, thyroid, melanoma), placing PTEN among the most commonly mutated genes in human cancer.
The central focus of my laboratory is the identification and characterization of the specific biological processes and signaling pathways that are controlled by the PI3K/PTEN/AKT cascade. Our research is centered on tumors originating in the thyroid gland: we utilize genetically engineered mouse models to identify and deconstruct the signaling cascades altered during early neoplastic transformation, to understand through which signaling nodes the PI3K cascade intersects with other growth-promoting pathways, and to design and test in vivo innovative, rationally designed therapeutic approaches.
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Albert Einstein College of Medicine
Michael F. Price Center
1301 Morris Park Avenue , Room 302
Bronx, NY 10461