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[Cancer Research 61, 4827-4836, June 15, 2001]
© 2001 American Association for Cancer Research

Molecular Biology and Genetics

Fragile Histidine Triad Expression Delays Tumor Development and Induces Apoptosis in Human Pancreatic Cancer1

Kristoffel R. Dumon2, Hideshi Ishii2, Andrea Vecchione, Francesco Trapasso, Gustavo Baldassarre, Fatima Chakrani, Teresa Druck, Ernest F. Rosato, Noel N. Williams, Raffaele Baffa, Matthew J. During, Kay Huebner and Carlo M. Croce3

Kimmel Cancer Center, Thomas Jefferson University [K. R. D., H. I., A. V., F. T., G. B., F. C., T. D., R. B., M. J. D., K. H., C. M. C.], and Department of Surgery, Hospital of the University of Pennsylvania [K. R. D., E. F. R., N. N. W.], CNS Gene Therapy Center, Department of Neurosurgery, Jefferson Medical College, Philadelphia, Pennsylvania 19107

The fragile histidine triad (FHIT) gene is a tumor suppressor gene that is altered by deletion in a large fraction of human tumors, including pancreatic cancer. To evaluate the potential of FHIT gene therapy, we developed recombinant adenoviral and adenoassociated viral (AAV) FHIT vectors and tested these vectors in vitro and in vivo for activity against human pancreatic cancer cells. Our data show that viral FHIT gene delivery results in apoptosis by activation of the caspase pathway. Furthermore, Fhit overexpression enhances the susceptibility of pancreatic cancer cells to exogenous inducers of apoptosis. In vivo results show that FHIT gene transfer delays tumor growth and prolongs survival in a murine model mimicking human disease.




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