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In explaining why mutations in the gene TP53 tend to cluster in “hot spots,” a new study lays the groundwork for ability to identify the function of any mutation in any cancer gene.

Risk scores arise, scrutinizing cells' nutrient sensors, learning about lncRNAs, and more.

Researchers predicted these cancer-specific peptides, dubbed "retained intron" neoantigens, by computationally sifting through melanoma patients' tumor RNA.

Long thought to be genetically stable and identical, cancer cell lines harbor significant levels of genetic variation, which may help explain why it can be hard to reproduce findings in cell line-based research.

Mapping mouse airways, brown fat and exercise, and cancerous dependencies.

A common prostate cancer mutation retargets an epigenetic complex to force prostate cells down a malignant path, creating a possible therapeutic opportunity in the process.