FAK and Interacting Proteins as Therapeutic Targets in Pancreatic Cancer

In this: publication
By this: publisher
In this Subject: Oncology ,&nbsp; Pharmacology
By this author: A. Ucar, Deniz ;&nbsp; N. Hochwald, Steven

Authors: A. Ucar, Deniz; N. Hochwald, Steven

Source: Anti-Cancer Agents in Medicinal Chemistry- Anti-Cancer Agents), Volume 10, Number 10, December 2010 , pp. 742-746(5)

Publisher: Bentham Science Publishers

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Abstract:

Pancreatic cancer is the fourth leading cause of cancer death in the United States. Chemotherapy and radiation therapy have had minimal ability to alter the natural course of the disease. Clearly, additional agents are needed to improve outcomes in this aggressive cancer. Pancreatic cancer has been found to have several genetic alterations including 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. Clinicians must translate the available knowledge of the molecular basis of this disease into rationale and effective therapeutic strategies for treatment. 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.

Keywords: Pancreatic Cancer; Focal Adhesion Kinase; Review; Therapeutic Targets; Pancreatic Cancer; Chemotherapy; K-ras; angiogenic factors; src; siRNA; gemcitabine chemotherapy; Malignant; MMPs; VEGF; FRNK