Open AccessMoving Beyond VEGF for Anti-angiogenesis Strategies in Gynecologic Cancer
Author(s) -
Duangmani Thanapprapasr,
Wei Hu,
Anil K. Sood,
Robert L. Coleman
Publication year - 2012
Publication title -
current pharmaceutical design
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 159
eISSN - 1873-4286
pISSN - 1381-6128
DOI - 10.2174/138161212800626201
Subject(s) - angiogenesis , cancer research , metastasis , cancer , ovarian cancer , focal adhesion , endometrial cancer , medicine , cervical cancer , cancer cell , ezh2 , pathology , oncology , biology , signal transduction , epigenetics , microbiology and biotechnology , biochemistry , gene
Gynecologic cancer is a major burden in both developed and developing countries. Almost a half million deaths from gynecologic cancer are reported each year. Understanding the molecular biology of cancer is a principle resource leading to the identification of new potential therapeutic targets, which may be parlayed into novel therapeutic options in gynecologic cancer. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase, which plays a pivotal role in many aspects of malignant growth including cancer cell survival, migration, invasion, angiogenesis and metastasis. Various human cancer tissues have demonstrated high expression of FAK or activated FAK, which has been correlated with survival of cancer patients. Among gynecologic cancers, reports have emerged demonstrating that FAK is involved in the pathogenesis of ovarian, endometrial, and cervical cancers. In addition, the polycomb group protein enhancer of Zeste homologue 2 (EZH2), Dll4/notch and EphA2 has also emerged as important regulators of endothelial cell biology and angiogenesis. Herein, we review the role of these new targets in tumor angiogenesis and the rationale for further clinical development.