Clinical Research Division, Fred Hutch
Public Health Sciences Division, Fred Hutch
Raisbeck Endowed Chair for Pancreatic Research
Dr. Sunil Hingorani studies the cellular and molecular mechanisms involved in the initiation and progression of pancreatic cancer. The goals of his laboratory and clinical research are to develop new strategies for detection and treatment that transform the management of this disease. Dr. Hingorani’s team has designed several mouse models of pancreatic cancer that accurately mimic the human disease. Their research has revealed key secrets of pancreatic cancer’s resistance to treatment and drive to spread, or metastasize. Through their “mouse clinical trials program,” Dr. Hingorani and colleagues rigorously assess new strategies for early detection, diagnosis and treatment to accelerate their translation to the clinic. Dr. Hingorani founded the multidisciplinary Pancreatic Cancer Specialty Clinic at Seattle Cancer Care Alliance and the Center for Accelerated Translation in Pancreas Cancer within the Fred Hutch/University of Washington Cancer Consortium.
University of Washington
Director, Center for Accelerated Translation in Pancreas Cancer (CATPAC)
Fred Hutch/SCCA/University of Washington
B.S.: Yale University, Molecular Biochemistry & Biophysics, 1985
M.D.: Yale University, Medicine, 1994
Ph.D.: Yale University, Cellular & Molecular Physiology, 1994
Residency: Brigham and Women's Hospital
Fellowship: Dana-Farber/Partners Cancer Care Program
The Hingorani laboratory investigates the molecular and cellular mechanisms that drive the pathogenesis of pancreas cancer. The inability to detect the disease early together with multiple mechanisms of chemical and radiotherapeutic resistance contribute to the extreme lethality of PDA. Our goal is to identify the most compelling strategies to translate to the clinic in order to cure this disease.
We have undertaken a systematic effort to deconstruct the cell autonomous and non-cell autonomous factors that cooperate to produce this unusually aggressive and lethal disease. To this end, we have helped to develop a number of genetically engineered, highly faithful animal models of preinvasive, invasive and metastatic PDA through the targeted endogenous expression of mutations in a key oncogene and select tumor suppressor genes. These models faithfully recapitulate the clinical syndrome, pathophysiology and molecular features of the distinct histopathologic routes to human pancreas cancer, including manifesting the unique stromal and immune responses that constitute the characteristic “desmoplastic reaction.” These models also serve as the primary platforms for our Murine Clinical Trials Program (“Mouse Hospital”) designed to accelerate the translation of early detection, diagnostic and treatment strategies to the clinic. As recent examples, our insights into combined stromal and epithelial cell targeting form the basis for international, randomized clinical trials currently underway. We have also characterized unusual physicomechanical properties of this cancer, with respect to an abundant interstitial gel-fluid phase, as well as identified a concerted transcriptional program that drives metastasis.
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