Histone H3.3K27M Represses p16 to Accelerate Gliomagenesis in a Murine Model of DIPG

This study shows that H3.3K27M mutation and PDGF signaling act in concert to accelerate gliomagenesis in a genetic mouse model and identifies repression of p16 tumor suppressor as a target of H3.3K27M, highlighting the G1–S cell-cycle transition as a promising therapeutic avenue. Mol Cancer Res; 15(9); 1243–54. ©2017 AACR.

Source: Molecular Cancer Research - August 31, 2017 Category: Cancer & Oncology Authors: Cordero, F. J., Huang, Z., Grenier, C., He, X., Hu, G., McLendon, R. E., Murphy, S. K., Hashizume, R., Becher, O. J. Tags: Oncogenes and Tumor Suppressors Source Type: research