Molecular targeted therapies for pancreatic cancer

Am J Surg. 2008 Sep;196(3):430-41. doi: 10.1016/j.amjsurg.2008.04.009.

Abstract

Background: Pancreatic cancer cells express different mutations that increase the aggressiveness and confer resistance to conventional chemotherapy and radiotherapy. Molecules that selectively bind and inhibit these mutations are effective in other solid tumors and are now emerging as a complementary therapy in pancreatic cancer. The objective of this review is to describe the effect of drugs that inhibit specific mutations present in pancreatic cancer with special emphasis on clinical trials.

Data sources: We reviewed the English-language literature (MedLine) addressing the role of drugs that target mutations present in pancreatic cancer. Both preclinical and clinical studies were included.

Conclusions: Preclinical evidence supports the combination of conventional approved therapies plus drugs that block epidermal growth factor receptor and vascular growth endothelial factor or induce apoptosis. However, most of the current clinical evidence is limited to small phase I trials evaluating the toxicity and safety of these regimens. The results of additional randomized trials that are still undergoing will clarify the role of these drugs in pancreatic cancer.

Publication types

  • Review

MeSH terms

  • Antibodies, Monoclonal / therapeutic use
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • Apoptosis / drug effects
  • ErbB Receptors / antagonists & inhibitors*
  • Humans
  • Mutation
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / therapy*
  • Protein Kinase Inhibitors / therapeutic use
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors*

Substances

  • Antibodies, Monoclonal
  • Antineoplastic Agents
  • Protein Kinase Inhibitors
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • Receptors, Vascular Endothelial Growth Factor