Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [p16]

The goal of this study is to identify the senescent cells expressing high level of p16Ink4a (p16Ink4a Hi) in GBMs and characterize their action on the tumor microenvironment at an early timepoint. We introduced the p16-3MR transgene in the GBM mouse model to selectively delete p16Ink4a Hi senescent cells upon ganciclovir (GCV) injection. We compared p16-3MR+GCV to WT+GCV control GBMs that were harvested 7 days after the last GCV injection. Bulk RNAseq of five p16-3MR + GCV vs four WT + GCV mouse GBMs at early timepoint (7 days after the last treatment shot)