Evolution of tumor suppressor genes can involve a trade-off because the acquisition of certain anti-cancer characteristics diminishes the ability to regenerate damaged tissue.

Tissue microarrays, a high-throughout approach to quantifying biomarkers used in hundreds of cancer studies every year, are susceptible to batch effects that can alter results but that are readily addressable.

Infrared high-pulse-energy low-pulse-repetition-rate excitation advances deep intravital microscopy in strongly scattering tissues such as skin tumors and thick bone, thereby bringing previously inaccessible tumor areas in reach with subcellular resolution.

Nutrient limitation elicits differential responses in cells lacking the tumor suppressor PTEN and in normal cells, resulting in hyperplastic overgrowth of PTEN mutant tissue independent of additional mutations.

Bariatric surgery reversed obesity-exacerbated tumor burden and increased efficacy of anti-PD-L1 immunotherapy.

RNA-level regulation of gene expression is negatively associated with protein-level regulation across cellular pathways in normal tissues and cancer.

AIDPS derived by 76 machine-learning algorithm combinations in 13 independent multicenter cohorts exhibited superior capability than clinical traits and 86 published prognostic signatures and could serve as an ideal biomarker for stratified management and individualized treatment of pancreatic cancer.

Mouse genetic studies reveal that let-7 performs potent tumor suppressive roles, but at the expense of regeneration and tissue homeostasis in the liver, findings with unanticipated therapeutic implications.

Weakly migratory cancer cells facilitate their own escape from the primary tumor by releasing microvesicles that activate fibroblasts to remodel matrix and facilitate cancer cell metastasis.

Loss of polarity in epithelial cells leads to mitogenic cytokine upregulation, via coincident activation by JNK and atypical protein kinase C (aPKC), and Polycomb derepression.