Browse our latest Cancer Biology articles

TMEM127 depletion alters membrane dynamics, promoting cell surface accumulation and constitutive activity of growth factor receptors, and ultimately providing a novel paradigm for oncogenesis through aberrant receptor localization and signaling.

Analysis of the action of WDR5 inhibitors in leukemia cells reveals decreased ribosome inventory, impaired protein synthesis, induction of nucleolar stress, and activation of p53 via alternative splicing of MDM4.

N-cadherin and Slit2/3/Robo interactions provide the outward force to drive collective Schwann cell migration during nerve regeneration, identifying a dual role for N-cadherin in both adhesion and repulsion processes during Schwann cell collective migration.

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.