Abstract
Objective: The aim of this study was to determine potential proteomic mechanisms by which activating CTNNB1 exon 3 mutations may drive angiogenesis in endometrial cancer (EC). CN-low and MSI endometrioid EC patients with these mutations tend to have poorer outcomes than wildtype (WT) patients. β-catenin is thought to increase VEGFA expression and tumor vascularity. Results from clinical trial GOG-86P suggested an improved outcome for patients with CTNNB1 mutations treated with bevacizumab (Bev), an antiangiogenic drug that targets VEGFA.
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