Focal Adhesion Kinase as a Cancer Therapy Target

ISSN: 1875-5992 (Online)
ISSN: 1871-5206 (Print)


Volume 16, 12 Issues, 2016


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Anti-Cancer Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Cancer Agents

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  • 27th of 59 in Chemistry, Medicinal

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Editor-in-Chief:
Michelle Prudhomme
Universite Blaise Pascal - C.N.R.S
Aubiere Cedex
France


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Focal Adhesion Kinase as a Cancer Therapy Target



Anti-Cancer Agents in Medicinal Chemistry, 10(10): 735-741.

Author(s): Vita M Golubovskaya.

Affiliation: Department of Surgical Oncology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY, 14263, USA.

Abstract

Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that resides at the sites of at focal adhesions. The 125 kDa FAK protein is encoded by the FAK gene located on human chromosome 8q24. Structurally, FAK consists of an amino-terminal regulatory FERM domain, a central catalytic kinase domain, and a carboxy-terminal focal adhesion targeting domain. FAK has been shown to be an important mediator of cell adhesion, growth, proliferation, survival, angiogenesis and migration, all of which are often disrupted in cancer cells. Normal tissues have low expression of FAK, while primary and metastatic tumors significantly overexpress this protein. This review summarizes expression of FAK by immunohistochemical staining in different tumor types and presents several FAK inhibition therapy approaches.

Keywords:

Adhesion, cancer, Focal Adhesion Kinase, inhibitor, metastasis, tumor, Breast Cancer, Hepatocellular Carcinoma, Acute Myeloid Leukemia, HBV, FRNK, Troglitazone, Neuroblastoma, IHC, EGFR.



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Article Details

Volume: 10
Issue Number: 10
First Page: 735
Last Page: 741
Page Count: 7
DOI: 10.2174/187152010794728648
Price: $58
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