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Review
.2010 Dec;10(10):722-34.
doi: 10.2174/187152010794728657.

Evolving therapies and FAK inhibitors for the treatment of cancer

Affiliations
Review

Evolving therapies and FAK inhibitors for the treatment of cancer

Kelli Bullard Dunn et al. Anticancer Agents Med Chem.2010 Dec.

Abstract

Despite advances in medical and surgical therapy, cancer kills more than half a million people in the United States annually, and the majority of these patients succumb to metastatic disease. The traditional approach to treating systemic disease has been the use of cytotoxic chemotherapy. However, chemotherapy is rarely curative and toxicity is often dose limiting. In addition, the effects of chemotherapy are nonspecific, targeting both malignant and normal tissues. As a result, recent efforts increasingly have focused on developing agents that target specific molecules in tumor cells in order to both improve efficacy and limit toxicity. This review summarizes the history and current use of targeted molecular therapy for cancer, with a special emphasis on recently developed inhibitors of Focal Adhesion Kinase (FAK).

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Conflict of interest statement

CONFLICT OF INTEREST

Dr. Vita Golubovskaya discloses potential conflict of interest with CureFAKtor Pharmaceuticals.

Figures

Fig. 1
Fig. 1
Activation of an RTK induces dimerization and downstream phosphorylation of non-receptor tyrosine kinases. Major signaling cascades include the RAS/RAF/MAPK pathway, MEK pathway, and the PI3kinase/AKT pathway. (Adapted by permission from Macmillan Publishers Ltd:Nature Reviews Cancer, Zhu & Parada,Nature Reviews Cancer, 2002, 2: 616–626, copyright 2002.)
Fig. 2
Fig. 2
Progression through each phase of the cell cycle is regulated by cyclin/CDK interactions. (Copyright of Renaic, with kind permission of Renaic Corporation and Sysmex Corporation.)www.sysmex-lifescience.com
Fig. 3
Fig. 3
FAK plays a key role in a signaling cascade that can lead to some of the tumorigenic properties of cancer cells. FAK activation induces cell proliferation, motility, survival, invasion and metastasis. SABiosciences.www.sabiosciences.com
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References

    1. American Cancer Society. Cancer Facts & Figures 2010. American Cancer Society; Atlanta: 2010.
    1. Heffler M, Golubovskaya V, Bullard Dunn KM. Evolving molecular therapies and their applications to surgical oncology. ACS Surg Principles Pract. 2010 (in press)
    1. Arora A, Scholar EM. Role of tyrosine kinase inhibitors in cancer therapy. J Pharmacol Exp Ther. 2005;315(3):971–9. - PubMed
    1. Robinson DR, Yi-Mi Q, Su-Fang L. The protein tyrosine kinase family of the human genome. Oncogene. 2000;19:5548–5557. - PubMed
    1. Arnold D, Seufferlein T. Targeted treatments in colorectal cancer: state of the art and future perspectives. Gut. 2010;59:838–858. - PubMed

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