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Deregulated cell fate specification pathways, including oncogenic Ras, cause activation of JNK-signaling at contact sites with wild type cells, which drives apoptosis and aberrant cell elimination in a contact-dependent manner.

The rational drug design combining the bioassay identified a novel selective androgen receptor (AR) degrader for both AR and AR-VRs and illustrated the synergistic importance of AR antagonism and degradation in advanced prostate cancer treatment.

ELYS, a multifunctional protein with critical roles in the cell cycle, is essential for the vigorous proliferation and survival of difficult-to-treat cancers carrying mutations in the KRAS oncogene, making it a compelling target for novel drug treatments.

Human papillomavirus type 8 E6 promotes alternative end joining by compromising non-homologous end joining and homologous recombination.

Specific tissue environments provide selective pressures that give rise to distinct Ras oncogenic dosage in primary liver tumours and their metastatic-like outgrowths.

HOTAIR is required in an ongoing manner when it regulates epigenetic status and reprograms cancer cell gene expression in promoting breast cancer metastasis.

The dimer destabilizers cause a dimer-to-monomer equilibrium shift favoring the human thymidylate synthase monomer more degradable by the proteasome, thus breaking the long-standing link between inhibition and enhanced expression of the protein to fight cancer drug resistance.

Immunization with NY-ESO-1 S-FLU virus elicits a robust NY-ESO-1-specific CTL response and suppresses the NY-ESO-1-expressing tumour development and spontaneous metastasis.

EZH2/cMET may serve as biomarkers to stratify chondrosarcoma patients for cMET inhibitor treatment.

Dalpiciclib could partially abrogate ER nuclear transportation induced by pyrotinib in HER2+HR+ breast cancer and CALML5 could serve as a potential risk factor in the treatment of HER2+HR+ breast cancer.