Deletion of the ATM cofactor ATMIN reduces PDGFRA expression and strongly suppresses tumorigenesis in a TP53-deficient mouse model of glioblastoma.

Retention of Caspase-8 confers a selective advantage to glioblastoma and represents a novel therapeutic target.

Hypersensitivity of cohesin-deficient cells to Wnt signaling is concomitant with beta catenin stabilization and offers promise that Wnt agonists could be therapeutically effective in cohesin mutant cancers.

The glial developmental factor, Daam2, promotes glioma tumorigenesis by degrading the VHL tumor suppressor, illustrating how dysregulation of gliogenic factors can impact tumor suppressor activity and promote glioma tumorigenesis.

Cannabidiol binds to TRPV2 via a previously unidentified, but highly conserved, pocket.

The genetic background of a cancer cell and the chromatin organization of the tissue-of-origin impact the amount, length and position of somatic copy number alterations in cancer.

A new paradigm of DNA methylation mediated gene activation and chromatin remodeling provides a general framework to dissect the biological functions of DNA methylation readers and effectors.

Loss of membrane-bound ICAM-1, overexpression of soluble ICAM-1 or ILKAP activity in tumor cells induce resistance to antigen-specific cytotoxic T-cell-mediated killing independently from regulating antigen presentation, PD-L1 expression, IFN-γ, or TNF-α responsiveness.

Correlated magnetic resonance imaging and ultramicroscopy resolves macro- and microvasculature in glioma models and allows treatment monitoring of antiangiogenic therapy.