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

NMNAT is genetically required for glioma development and promotes glioma growth by allowing a higher tolerance to DNA damage and inhibiting DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD⁺-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53.

A geneome-scale shRNA screen identifies five genes whose suppression promotes cell death upon PI3K inhibition both in vitro and in vivo, thus suggesting potential combination therapies involving PI3K inhibition.

Interactions between Neuropilin-1 and VEGFR2, rather than VEGF-Neuropilin-1 binding, underlie Neuropilin-1's critical function in VEGF-mediated vascular development.

Analyses of discovered cancer-driving nucleotides (CDNs) reveal their evolutionary, biochemical, and therapeutic characteristics that are often shared among multiple cancer types.

A common genomic deletion in various human cancers disrupts mitochondrial protein homeostasis in a way that might be targeted by existing drugs.

Co-mutation of two powerful oncogenes in certain cell types may have a lethal effect that explains the mutual exclusivity of the mutations.

The development of an integrative computational-experimental approach for identifying small molecules that can disrupt RNA:protein interactions in vitro and in cells led to the identification of several inhibitors of YBX1 in the micromolar range, including a previously approved drug.