Treatment-associated <i>TP53</i> DNA-binding domain missense mutations in the pathogenesis of secondary gliosarcoma

Abstract

TMZ-induced <i>TP53</i> gain-of-function mutations can have a driving role in secondary gliosarcoma pathogenesis. Analysis of variants identified in <i>ex vivo</i> TMZ-treated gliomaspheres may have utility in predicting GBM evolutionary trajectories <i>in vivo</i> during standard chemoradiation.