Focal adhesion kinase signaling and function in pancreatic cancer

Front Biosci (Elite Ed). 2011 Jan 1;3:750-6. doi: 10.2741/e283.


In the United States and the European Union, pancreatic cancer is the fourth leading cause of cancer death in both men and women. Chemotherapy and radiation therapy have had little impact on survival, prompting the National Cancer Institute to declare that survival for pancreatic cancer has remained unchanged for three decades and its treatment has consistently been identified as an area of unmet medical need. Clearly, additional agents are needed to improve outcomes in this aggressive disease. Clinicians must translate the available knowledge of the molecular basis of this disease into rationale and effective therapeutic strategies for treatment. Pancreatic cancer has been found to have several genetic alterations and is, in fact, one of the tumors with the highest number of genetic mutations of any solid malignancy. These mutations include activation of K-ras and inactivation of p53, p16, and DPC4. Other alterations include upregulation of angiogenic factors and matrix metalloproteinases, dysregulation of growth factor receptors, and cytoplasmic kinases including focal adhesion kinase (FAK) and Src. The role of FAK in the pathogenesis of pancreatic cancer is discussed below and efforts aimed at the development of inhibitors of FAK for this disease are reviewed.

Publication types

  • Review

MeSH terms

  • Female
  • Focal Adhesion Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Focal Adhesion Protein-Tyrosine Kinases / genetics
  • Focal Adhesion Protein-Tyrosine Kinases / metabolism*
  • Humans
  • Male
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / physiopathology*
  • Signal Transduction / physiology*


  • Focal Adhesion Protein-Tyrosine Kinases