Mutated is a marker of increased expression: analysis of 7,525 pan-cancer tissues.

Anti-angiogenic therapies are an important class of anti-cancer treatment drugs. However, their efficacy is limited to certain tumors and would benefit from identifying a biomarker predictive of therapeutic response. (tumor protein p53) is a tumor suppressor gene frequently mutated in cancer and implicated in cell-cycle regulation, apoptosis, and angiogenesis. Data from 7,525 unique tumor samples (representing 30 tumor cohorts) were retrieved from the TCGA database to analyze the relationship between mutation status and expression. Univariate analyses were done using a Mann-Whitney univariate test or Fisher's exact test. Parameters with a p-value (p)≤0.1 in univariate analysis were selected for follow-up multivariate analyses, including mutation status, cancer cohorts, cancer subtypes, and expression. Our analysis demonstrates statistically significant increases in mRNA tissue expression in -mutated adenocarcinomas (but not in squamous cancers) compared to wild-type tumors. This association holds true in multivariate analyses and remains independent of and overexpression. Our findings provide additional evidence that mutations are linked to the VEGF pathway, potentially offering insight into the mechanism behind increased sensitivity to anti-angiogenic therapies observed in some mutant tumors.