The heterogeneity of immune cell types in glioblastoma tumors depends on the tumor's genetic make-up and treatment status and is an incompletely mined source of novel therapeutic targets.
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.
A novel phenotypic screening platform based on immunofluorescent imaging of histone modifications enables accurate identification of cell fates and environmental perturbations.
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.
Correlated magnetic resonance imaging and ultramicroscopy resolves macro- and microvasculature in glioma models and allows treatment monitoring of antiangiogenic therapy.
DNA lesions formed by alkylating agents trigger double-strand breaks, in the absence of replication, by the action of MMR and BER at nearby O-alkyl and N-alkyl adducts, respectively.
The microenvironment of brain tumors can be modulated by in vivo conditions that change the brain levels of BDNF and IL-15, with effects on innate immune cell activation.
Genetic and molecular analysis of TP53 exon-6 truncating mutations reveal that these mutations, contrary to current belief, promote tumorigenesis and point towards strategies for treating cancers driven by these prevalent mutations.
