PIK3CA variants selectively initiate brain hyperactivity during gliomagenesis.

ABSTRACT: Glioblastoma is a universally lethal form of brain cancer that exhibits an array of pathophysiological phenotypes, many of which are mediated by interactions with the neuronal microenvironment^1,2. Recent studies have shown that increases in neuronal activity have an important role in the proliferation and progression of glioblastoma^3,4. Whether there is reciprocal crosstalk between glioblastoma and neurons remains poorly defined, as the mechanisms that underlie how these tumours remodel the neuronal milieu towards increased activity are unknown. Here, using a native mouse model of glioblastoma, we develop a high-throughput in vivo screening platform and discover several driver variants of PIK3CA. We show that tumours driven by these variants have divergent molecular p

SUBMITTER: Yu K 

PROVIDER: S-EPMC7577741 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature