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.

A study that models the evolution of drug resistance in tumors reveals that drugs are more effective when given in combination than sequentially, and that cure is much more likely when the drugs target different pathways.

The functional relevance of stem cell niche perturbation in sarcomagenesis is defined and the mouse model presented provides a rationale for the use of combination therapy for the treatment of genetically heterogeneous sarcomas.

Tregs form an "immunosuppressive ring" around solid tumors that is broken down during adoptive cell therapy and cyclophosphamide combination immunotherapy.

In two independent cohorts, NNRTI-based cART regimens are associated with significantly lower cell-associated HIV RNA levels than PI-based regimens, suggesting more potent suppression of residual virus replication by NNRTI-based regimens.

Fibrolamellar carcinoma results from a genetic lesion that produces the DNAJ-PKAc fusion kinase, which is recruited into macromolecular complexes and is sensitive to combinations of signal transduction inhibitor drugs.

Combined EGFR and SOS1 inhibition synergize to inhibit NSCLC spheroid growth.

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.

Libraries of patient-derived tumor organoids are a reliable and scalable model system that can help identify and optimize targeted therapies in a pre-clinical setting.

Downregulation of mitochondrial activity by immunosuppressive tumor-derived soluble factors leads to systemic unresponsiveness to the PD-1 blockade therapy.