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David Tuveson

Professor
M.D., Ph.D., Johns Hopkins University,1994


Contact
dtuveson@cshl.edu
(516) 367-5246 (p)
  Tuveson Lab Website
Pancreatic cancer is an extremely lethal cancer.  On average, patients who are diagnosed with pancreatic cancer succumb to the disease within 6 months.  Research is the only way to defeat pancreatic cancer.  My lab is making progress toward finding a cure by detecting the disease earlier and designing novel therapeutic approaches.
David Tuveson’s lab uses mouse and human tissue models of neoplasia to explore the fundamental biology of these diseases and thereby identify new diagnostic and treatment strategies. His team’s main focus is pancreatic cancer, a lethal malignancy that has eluded clinical solutions despite intensive study. The lab’s approaches at CSHL run the gamut from designing new model systems of disease to inventing new therapeutic and diagnostic platforms for rapid evaluation in preclinical and clinical settings. For example, they have adopted a new method of culturing tissue fragments indefinitely in cell culture, enabling deep analysis with genetic and pharmacological probes. In addition, therapeutic experiments in mouse models have revealed an important role of redox metabolism and stromal interactions on influencing therapeutic response. This year, they used the mouse model system to identify the mechanism of a promising drug treatment for pancreatic cancer. The lab found that using the drug in combination with more standard chemotherapeutic drugs stopped the tumor growth and lengthened life span for the mice, suggesting that the combination therapy may help overcome the drug resistance that is so commonly found in cancers. Tuveson’s lab also has a strong link to clinical trials locally and internationally, with confirmation in early-phase trials the ultimate goal. Collectively, their strategy in the preclinical and clinical arena is codified as the “Cancer Therapeutics Initiative,” and this initiative will provide these same approaches to the entire CSHL cancer community.

Dr. Tuveson serves as Director of the Lustgarten Foundation Pancreatic Research Laboratory at CSHL and as Director of Research for the Lustgarten Foundation.

Palm, W. and Park, Y. and Wright, K. and Pavlova, N. N. and Tuveson, D. A. and Thompson, C. B. (2015) The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1. Cell

Ponz-Sarvise, Mariano and Tuveson, David A. and Yu, Kenneth H. (2015) Mouse Models of Pancreatic Ductal Adenocarcinoma. Hematology/Oncology Clinics of North America

Espana-Agusti, J. and Tuveson, D. A. and Adams, D. J. and Matakidou, A. (2015) A minimally invasive, lentiviral based method for the rapid and sustained genetic manipulation of renal tubules. Sci Rep 5pp. 11061.

Tuveson, D. and Rai, K. R. (2015) Augmenting NF-kappaB in poor-risk CLL: A general paradigm for other cancers?. J Exp Med 212(6) pp. 830-1.

Jenkinson, Claire and Elliott, Victoria and Evans, Anthony and Oldfield, Lucy and O'Brien, Darragh and Apostolidou, Sophia and Gentry-Maharaj, Aleksandra and Fourkala, Evangelia- O. and Jacobs, Ian and Menon, Usha and Cox, Trevor and Campbell, Fiona and Tuveson, David and Greenhalf, William and Sutton, Robert and Pereira, Stephen and Timms, John and Neoptolemos, John and Costello, Eithne (2015) Decreased serum thrombospondin-1 levels in pancreatic ductal adenocarcinoma patients: an early indicator of disease or diabetes mellitus development?. Pancreatology 15(3, Sup) pp. S28.

Additional materials of the author at
CSHL Institutional Repository