MTAP loss promotes stemness and epigenetic reprogramming in Glioblastoma

Methylthioadenosine Phosphorylase (MTAP) loss is one of the most frequent genetic alterations in Glioblastoma and has been associated with poor clinical outcomes in several cancer types. Here we used patient derived glioblastoma cell lines and manipulated MTAP status to create isogenic pairs with which to study the effects of this alteration on epigenetics, gene expression, and cell identity Comparison of GBM cells with or without functional MTAP protein