Drugs in a curative chemotherapy regimen are independently effective and resisted by different mechanisms, so cancer cells have little chance of surviving all drugs, and this benefit occurs without synergistic interactions.

TNFAIP2 was found to interact with IQGAP1 and Integrin β4, which activates RAC1 through TNFAIP2 and IQGAP1 and confers DNA damage-related drug resistance in triple-negative breast cancer.

Data-driven systems biology models of signaling predict cellular response to untested perturbations and can nominate drug combinations to overcome drug resistance in cancer cells.

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.

SOX2 causes resistance to anti-EGFR therapies in EGFR-mutant lung cancer.

Mutagenesis studies identified an androgen receptor mutation that converts enzalutamide-a drug recently approved for the treatment of advanced prostate cancer-into an androgen receptor agonist, and modeling studies informed the design of novel drugs that are effective against the mutant receptor.

Experimental and clinical models identify an effective add-on therapy for drug resistant estrogen receptor positive advanced breast cancer.

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.

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.

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