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Changes in MAPK signaling allow lung cancer cells to transition between lineages that respond differently to treatment.

Oxaliplatin-resistant colorectal cancer cells exhibit unregulated death receptor 4 expression with increased receptor palmitoylation and translocation into lipid rafts, increasing their sensitivity to apoptosis via TRAIL.

Anti-tumor properties of sub-class of xanthine analogs involve restoration of p53 pathway transcriptome, independent of p53/p73, dependent on ATF3/ATF4 and Noxa in mutated-p53 tumors and the compounds trigger an S-phase checkpoint.

Computational methods reveal how mutations affect the conformational landscape of the kinase domain of EGFR resulting in abnormal signaling and provide a structural framework for ongoing drug discovery efforts on mutant-specific EGFR inhibition.

FLT3-ITD/STAT5A signaling is more sensitive to Dot1L inhibition than the canonical MLL-fusion activated drivers of leukemogenesis, providing a potential therapeutic avenue for one of the most frequent lesions in leukemia.

HOXA9 is a transcriptional maintenance factor for anti-apoptotic genes that accelerate MYC-driven leukemia.

The E2F/Dp transcription factors, which are key cell cycle regulators, can also mediate the regulation of carbohydrate metabolism in larva by controlling both systemic trehalose homeostasis and fat storage.

Erlotinib-resistant AXL overexpressing cells are present in therapy-naive tumors, and expression of AXL in these cells is regulated through a stochastic mechanism centered on the epigenetic regulation of miR-335.

Cellular acidity, capacity for net acid extrusion, and expression of acid-base transporters in human breast carcinomas independently predict variation in proliferative activity, lymph node metastasis, and patient survival.

Topoisomerase 2α DNA breaks induced by G-quadruplex ligands are associated with a topological stress resulting from a transcription-dependent mechanism and counteracted by DNA topoisomerase 1 and factors promoting transcription elongation.