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.
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.
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.
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.
A simulation study is used to demonstrate how mistakes in identifying the experimental unit and the unit of analysis can lead to incorrect analyses and inappropriate inferences when reporting research studies.