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FAK and paxillin, two potential targets in pancreatic cancer.
Kanteti, Rajani; Batra, Surinder K; Lennon, Frances E; Salgia, Ravi.
Afiliación
  • Kanteti R; Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL, USA.
  • Batra SK; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA.
  • Lennon FE; Department of Medicine, Section of Hematology/Oncology, University of Chicago, Chicago, IL, USA.
  • Salgia R; Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, CA, USA.
Oncotarget ; 7(21): 31586-601, 2016 May 24.
Article en En | MEDLINE | ID: mdl-26980710
ABSTRACT
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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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Carcinoma Ductal Pancreático / Quinasa 1 de Adhesión Focal / Paxillin Límite: Humans Idioma: En Revista: Oncotarget Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Carcinoma Ductal Pancreático / Quinasa 1 de Adhesión Focal / Paxillin Límite: Humans Idioma: En Revista: Oncotarget Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos