Background: Pancreatic cancer is one of the most aggressive human tumors and is virtually incurable. Its incidence in the United States has tripled in the past 50 years. The tumor is a frequent cause of cancer death in both men and women. The current treatment options are inadequate and probably reflect the fact that the etiologic factors and the pathogenesis of pancreatic cancer are unknown.
Methods: The author reviewed recent studies describing some of the molecular alterations that may play a role in pancreatic carcinogenesis.
Results: Most pancreatic tumors arise in the ductal epithelium. Cytogenetic abnormalities and alterations in proliferation, oncogenes and tumor suppressor genes, cell receptors, and growth factors are described.
Conclusions: Preliminary studies have implicated, among others, the insulin-like growth factor-1 receptor, Src, and Stat3 proteins in human pancreatic carcinogenesis. These molecules may represent important predictors of tumor behavior and targets of novel therapeutic modalities in human pancreatic cancer.