Gene transfer techniques now allow further opportunity to inhibit function of this oncogene. DPC-4, p16, and Rb A unique genetic alteration in pancreatic cancer has been recently discovered which functions in a tumor suppressor fashion. By providing normal copies of DPC4, gene transfer provides a potential avenue to restore appropriate signal transduction within pancreatic cancer cells. Both p16 and Rb represent additional targets in pancreatic carcinogenesis. The cytotoxicity of chemotherapeutic agents and radiation is often promoted through a process called apoptosis, or programmed cell death.
Apoptosis is regulated by a balance of proapoptotic and antiapoptotic mediators.
Potential gene transfer approaches to augment apoptosis in cancer cells include blocking Bcl-2 function and overexpressing proapoptotic mediators. Recently, another putative tumor suppressor gene has been identified in pancreatic carcinoma cell lines. Presently, the role of FHIT inactivation in pancreatic tumorigenesis is unknown.