Recent genomic analyses of pediatric glioblastoma, a poorly understood tumor with dismal outcome, have identified mutations in histone H3 variants that affect critical amino acids in the tail. The findings extend discoveries of chromatin regulator inactivation and gain-of-function mutations by documenting alteration of a modifiable histone residue in human cancer.
A tell-tail sign of chromatin: histone mutations drive pediatric glioblastoma.
Cancer cell