Browse our latest Cancer Biology articles

Coregulators mediate selective interactions between DNA-bound androgen receptor and other transcription factors, which control distinct prostate cancer biology, suggesting disruption of critical interactions in these complexes as a novel therapeutic strategy.

The inhibitory or deletion effect of MELK does not impair the proliferation of basal-like breast cancer cell lines.

Lin37 is essential for cell-cycle gene repression by the DREAM complex in cellular quiescence and a combined loss of Lin37 and Rb prevents cell-cycle exit in response to growth-limiting signals.

Functional and mechanistic analyses of cancer cells containing homozygous deletion of TP53 and FXR2 reveal that inhibition of FXR1 blocks cell proliferation in a collateral lethality manner, opening an avenue to develop therapies targeting such cancers.

Epigenetic regulation of the glucocorticoid receptor in castration-resistant prostate cancer can be targeted via the use of BET bromodomain inhibitors.

Radiomics allows automated quantification of the radiographic phenotype of a tumor across diverse patient cohorts and is connected to the underlying molecular pathway activities, which together determine the clinical outcome.

Cell culture models widely used in cancer research do not reflect metabolism in tumors; by altering culture systems to better model tumor metabolism we find that environmental cystine promotes tumor glutamine metabolism.

Radiomics has the potential to improve the management of cancer patients, but further research is required before it can be adopted into routine clinical practice.

PTEN organizes multicellular architecture by non-catalytic scaffolding of spatially localized β-Arrestin1/ARHGAP21/Cdc42 protein complexes to control mitotic spindle orientation, multicellular configuration and lumen formation.

GDE3 is a transmembrane GPI-specific phospholipase C that sheds the urokinase receptor (uPAR) from the cell surface resulting in loss of uPAR function in breast cancer cells and reduced tumor growth.