Browse our latest Cancer Biology articles

Classification of MET mutations allows a better understanding of sensitivity and resistance to targeted therapies used in cancer.

Integrated analyses of acute myeloid leukemia genetics and epigenetics demonstrate that epigenetic evolution occurs in a convergent manner in the absence of DNA mutations at relapse post-chemotherapy.

Genetic and biochemical approaches reveal that mammalian cells possess a novel DDI2 and transcription-independent pathway for the rapid recovery of proteasome activity after clinically relevant pulse treatment with proteasome inhibitors.

High-resolution NMR data and precise kinase activity assays on Abelson kinase bearing mutations in its αI-helix identify the αI-helix parts involved in disassembly of Abelson’s regulatory core and kinase activation.

DePARylation is essential for cell survival and thus poly(ADP-ribose) glycohydrolase (PARG) expression correlates with cytotoxicity induced by PARG inhibition, which will benefit the development of PARG inhibitors for cancer treatment.

Results show that STAT3 and KRAS jointly regulate oncogenic dependency of mutant KRAS cancer cells.

Multifaceted properties of the water-soluble derivative of antibiotic heliomycin enable it to offer greater antitumor value than its parent compound by inhibiting the tNOX-NAD⁺-SIRT1 axis to induce apoptosis.

Acute myeloid leukemia-specific predictive logic models reveal new therapeutic targets involved in cancer resistance mechanisms paving the way for personalized precision medicine.

Osteocytes, sensing mechanical stimulation generated by exercise, inhibit the proliferation of non-small cell lung cancer cells and sustain their dormancy by releasing small extracellular vesicles containing tumor-suppressive micro-RNAs.

A microfluidic device induces doxorubicin-resistant polyaneuploid cancer cells from triple negative breast cancer cells, revealing NUPR1/HDAC11 axis dysfunction drives chemoresistance, increasing tumor heterogeneity and impacting clinical outcomes.