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T antigen glycosylation, which marks metastatic cancer cells, is modulated on a small set of proteins by a conserved multipass transmembrane protein to allow tissue invasion by Drosophila macrophages.

Targeting Werner syndrome helicase might constitute a novel opportunity for the treatment of a clinically defined subset of patients harboring MSI-H/MMR-deficient tumors.

Genetic variation determines whether or not UV exposure accelerates melanoma development.

Mice get melanoma faster when they have common, inherited variants in a few genes that control cell-wide changes but also respond to the environment.

The pro-apoptotic BH3-protein Bim contains two distinct binding sites for anti-apoptotic proteins that together confer resistance of Bim/Bcl-2 and Bim/Bcl-XL complexes to BH3-mimetic drugs under development for use in humans.

Editors' Summary: This Replication Study did not reproduce those experiments in the original paper that it attempted to reproduce.

Cancer is a consequence of the release of basal cellular functions inherited from our unicellular ancestors from the control of regulatory networks that evolved during the emergence of multicellularity.

Endothelial cells express a soluble isoform of the L1CAM cell adhesion molecule that is generated by the splicing factor NOVA2 and induces angiogenesis, with relevant implications for ovarian cancer vascularization.

Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.

Inhibition of FGF2-FGFR1 signaling in bone marrow stroma attenuates secretion of FGF2-laden exosomes and subsequent protection of leukemia cells.