This review describes the recent advances in the molecular events involved in pancreatic cancer initiation, progression, and metastasis. Additionally, the importance of deregulated cellular signaling elements as potential targets for developing novel therapeutic strategies against incurable forms of pancreatic cancer is reported. The emphasis is on the critical functions gained by numerous growth factors and their receptors, such as epidermal growth factor receptor, hedgehog signaling, and proangiogenic agents such as vascular endothelial factor and interleukin-8 for the sustained growth, survival, and metastasis of pancreatic cancer cells. The molecular mechanisms associated with antitumoral properties and the clinical benefits of gemcitabine alone or in combination with other cytotoxic agents for the treatment of pancreatic cancer are discussed.

This preoperative nomogram has been shown to accurately predict the risk of perioperative mortality following pancreatectomy for malignancy.

The results of the present study demonstrate that after hepatic resection, a significant proportion of patients will need assistance upon discharge. This information needs to be included in patient counselling during pre-operative risk and benefit assessment.

These observations support the potential implication of IFNgamma and TGFbetas in MUC4 regulation in vivo and suggest a complex interaction of TH1 and TH2 signaling in the pancreatic tumor microenvironment. These findings may provide useful insights into the pathobiology of pancreatic cancer.

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