INHIBITING FOCAL ADHESION KINASE (FAK) REDUCES THE GROWTH OF UVEAL MELANOMA GNAQ/GNA11-MUTATED CELLS BY TARGETINGTHE PI3K/AKT/MTOR PATHWAY

D.C. RIGIRACCIOLO, X. FENG, R. LAPPANO, M. MAGGIOLINI, J.S. GUTKIND

Article ID: 6471
Vol 32, Issue 4S1, 2018
DOI: https://doi.org/10.54517/jbrha6471
Received: 8 September 2018; Accepted: 8 September 2018; Available online: 8 September 2018; Issue release: 8 September 2018

Abstract

Uveal melanoma (UM) represents the most common intraocular malignancy in adults andapproximately 50% of patients develops metastatic disease. The new genomic sequencing technologies onUM tumors allowed to identify mutations in the Gq alpha subunits GNAQ and GNA11. These mutationsappear in a mutually exclusive manner and are consequently of prognostic importance (Van Raamsdonket al., Nature 2009). FAK (focal adhesion kinase) is a cytoplasmatic tyrosine kinase localized at thesites of cell adhesion to the extracellular matrix. FAK is overexpressed in several tumors and mediatesdiverse signaling promoting cancer growth and metastasis. To date, it has been considered as a potentialtarget for cancer therapeutics (Sulzmaier et al., Nat Rev Canc 2014).



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