Glycogen synthase kinase-3 beta (GSK-3β) genomic alterations and increased programmed death-ligand 1 (PD-L1) expression in advanced malignancies


Brittany A. Borden, Joanne Xiu, Yasmine Baca, Pilar Ramos, Francis J. Giles, Andrew Mazar, Fabio Tavora, Howard P. Safran, Wafik S. El-Deiry, Benedito A. Carneiro

Glycogen Synthase Kinase-3 beta (GSK-3b) is a serine/threonine kinase with regulatory activity in numerous diseases and implicated in both innate and adaptive immune responses 1,2 • GSK-3b is involved in the pathogenesis of several malignancies 3,4,5 • GSK-3b phosphorylates target pro-oncogenes (C-Jun and C-myc), as well as non-glycosylated forms of PD-L1 leading to its proteasome degradation 6 • GSK-3b inhibitors have advanced to clinical trials in refractory malignancies 7 • Genomic alterations in GSK-3b have been described, yet a comprehensive analysis of these alterations is lacking.

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