Browse our latest Cancer Biology articles

Testicular microcalcifications arise secondary to local alterations in mineral homeostasis, which in combination with impaired Sertoli cell function and reduced levels of mineralization inhibitors facilitate deposition of hydroxyapatite.

TAK1 plays a negative role in esophageal squamous cancer cell metastasis, which depends on the TAK1-induced phosphorylation of PLCE1 at S1060 and subsequent inhibition of PIP2 hydrolysis.

Cell crowding drives a pro-invasive mechanotransduction pathway in high-grade DCIS, inducing TRPV4 inhibition, calcium and cell volume reduction, and increased invasion, with compensatory plasma-membrane TRPV4 relocation indicating pathway activation.

Cell crowding causes high-grade breast cancer cells to become more invasive by activating a molecular switch that causes the cells to shrink and spread.

Pairwise CRISPR screen identified FYN and KDM4 as key regulator of tyrosine kinase inhibitor resistance in triple negative breast cancer (TNBC).

High-throughput characterization of all possible CDKN2A missense variants identifies functionally deleterious variants and establishes accuracy of variant effect predictors.

In a mouse model of the hotspot mutant TP53^Y220C, the mutant p53 exhibited oncogenic gain of function in males and teratogenic gain of function in females, both correlated with inflammation.