FAK and paxillin, two potential targets in pancreatic cancer
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Rajani Kanteti1, Surinder K. Batra2, Frances E. Lennon1 and Ravi Salgia3
1 Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL, USA
2 Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA
3 Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, CA, USA
Ravi Salgia, email:
Keywords: FAK, paxillin, pancreatic cancer, integrins, P53
Received: October 22, 2015 Accepted: February 11, 2016 Published: March 13, 2016
Pancreatic ductal adenocarcinoma (PDAC) is a devastating cancer in large part due to late diagnosis and a lack of effective screening tests. In spite of recent progress in imaging, surgery and new therapeutic options for pancreatic cancer, the overall five-year survival still remains unacceptably low. Numerous studies have shown that focal adhesion kinase (FAK) is activated in many cancers including PDAC and promotes cancer progression and metastasis. Paxillin, an intracellular adaptor protein that plays a key role in cytoskeletal organization, connects integrins to FAK and plays a key role in assembly and disassembly of focal adhesions. Here, we have reviewed evidence in support of FAK as a potential therapeutic target and summarized related combinatorial therapies.
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