Browse our latest Cancer Biology articles

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.

The MondoA transcription factor localizes to the outer mitochondrial membrane where it coordinates an adaptive transcriptional response to elevated cellular energy represented by high cytoplasmic glucose and high mitochondrial ATP.

In addition to increasing glycolysis, some proliferating cells exhibiting the Warburg effect also increase oxidative phosphorylation through mitochondrial fusion.

Prostate cancer cells maintain heterogeneous androgen receptor transcriptional activity through upregulation of AR-regulated coactivator GREB1, and cells with high activity rapidly develop resistance to antiandrogen therapy in a GREB1-dependent manner.

Bazedoxifene's SERD activities enable it to resist the impact of activating ESR1 mutations in breast cancer.

A drug used in hormone replacement therapy can target estrogen receptors that have become resistant to breast cancer treatments.

miR-34a prevents inflammation-induced colonic regeneration from oncogenesis by simultaneously targeting processes in both immune and epithelial cells, including T helper 17 cell differentiation, recruitment, and IL-17 induced epithelial proliferation.

Lineage specifiers FoxA1 and FoxA2 control lung cancer growth and identity by activating gastric differentiation and suppressing squamous cell carcinoma transdifferentiation.

Cancer cells driven by mutations in KRAS or EGFR are dependent on DUSP6 to prevent ERK-induced cell death, creating a novel vulnerability for targeted therapy.