Genomic gains in ovarian cancer can promote cisplatin resistance via a FAK, Wnt/beta-catenin and Myc signaling pathway supporting pluripotency genes and tumorspheres that can acquire FAK dependence for survival.

Mutations conferring resistance to Escherichia coli against the chemotherapy drug gemcitabine can have opposite effects on bacterial drug degradation and therefore can increase or decrease the chemotherapy load on neighboring cancer cells.

Bacterial evolutionary adaptation to two chemotherapy drugs can lead to changes in bacterial metabolism and impact drug toxicity in a worm host.

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

Lineage resolved single-cell RNA-seq of mammary carcinoma models uncovers a metabolic vulnerability of taxane-resistant clones.

Overlaying single cell readouts of cell cycle and apoptosis onto a multidimensional analysis of pulsed cisplatin signalling dynamics reveals targetable mechanisms of platinum resistance in lung adenocarcinoma.

Retention of Caspase-8 confers a selective advantage to glioblastoma and represents a novel therapeutic target.

Inhibiting the RiBi pathway impedes both EMT and MET processes, enhancing chemotherapy efficacy and presenting a novel avenue to tackle advanced breast cancer treatment resistance.

Oncoprotein BCL6 confers tumor adaptive resistance to genotoxic stress through the IFN-BCL6-PTEN axis in solid tumors and presents a promising combinational target for chemo-sensitization.

A model based on empirical parameter estimates predicts that arresting cancer cell growth by less than 1% per day will produce optimal outcomes in preventing life-threatening cancers, and that such preventive measures are generally more successful than post-diagnostic interventions.