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Sci. Signal., 26 March 2013
Vol. 6, Issue 268, p. pe10
[DOI: 10.1126/scisignal.2004021]

PERSPECTIVES

Disrupting the Scaffold to Improve Focal Adhesion Kinase–Targeted Cancer Therapeutics

William G. Cance1,2,3*, Elena Kurenova1,3, Timothy Marlowe1, and Vita Golubovskaya1,3

1 Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA.
2 Department of Surgery, University at Buffalo, State University of New York, Elm and Carlton Streets, Buffalo, NY 14263, USA.
3 CureFAKtor Pharmaceuticals, LLC, 14 Rockdove Lane, Orchard Park, NY 14127, USA.

Abstract: Focal adhesion kinase (FAK) is emerging as a promising cancer target because it is highly expressed at both the transcriptional and translational level in cancer and is involved in many aspects of tumor growth, invasion, and metastasis. Existing FAK-based therapeutics focus on inhibiting the kinase’s catalytic function and not the large scaffold it creates that includes many oncogenic receptor tyrosine kinases and tumor suppressor proteins. Targeting the FAK scaffold is a feasible and promising approach for developing highly specific therapeutics that disrupt FAK signaling pathways in cancer.

* Corresponding author. E-mail: william.cance{at}roswellpark.org

Citation: W. G. Cance, E. Kurenova, T. Marlowe, V. Golubovskaya, Disrupting the Scaffold to Improve Focal Adhesion Kinase–Targeted Cancer Therapeutics. Sci. Signal. 6, pe10 (2013).

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