Cleavage of a membrane-bound transcription factor by the chemotherapeutic reagent doxorubicin can block the proliferation of tumor cells.

The inhibition of EPAC1, a cAMP-binding protein, appears as a potential therapeutic strategy to limit doxorubicin-induced cardiotoxicity without interfering with its antitumoral activity.

Breast cancer resistant to either doxorubicin or epirubicin relies on distinct primary metabolic processes, which can be targeted to reduce cancer progression.

Genetic variants that modulate transcriptomic response to doxorubicin in human iPSC-derived cardiomyocytes are predictive of cardiac damage and in vivo sensitivity to anthracycline cardiotoxicity.

Inflammasome-mediated inflammation is critically involved in bone loss caused by doxorubicin.

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.

Biochemical approaches and cellular experiments show a novel effect of METTL3 on homologous recombination repair and chemotherapeutic response via the m6A-YTHDC1-dependent regulation of the EGF/RAD51 axis.

Editors' Summary: This Replication Study did not reproduce those experiments in the original paper that it attempted to reproduce.

Disruption of the intracellular vimentin network upon cellular stress results in enhanced cell surface vimentin on human osteoarthritic chondrocytes and might represent a novel membrane-associated marker of stress-induced premature senescence.