This would be quite an interesting paradigm shift from what I understood was the prime reason for therapy drug resistance. It is commonly assumed, in CLL/SLL, that clones are born with different degrees of resistance to drugs and lay in hiding only to emerge after therapy or a time lapse. Speculation has it that there might exist a competition of sorts between clones that often keeps a numerically indolent clone dominating until a frontline chemo based therapy wipes it out, allowing the drug resistant clone(s) to rise to dominance.
This research, using breast cancer, suggests that members of the dominant cancer cell population, having been exposed to chemotherapy, react to chemo stress by creating cancer stem cells from its own ranks with differing phenotypic characteristics.
Quote: "...our study emphasizes cancer cell plasticity as greatly important to the sub-clonal heterogeneity of tumors. Therapy can exacerbate this plasticity, forcing cells into new phenotypic states. I think classifying cancer cells into hierarchical arrangements may need to be dissolved in models of adaptive resistance to chemotherapy"
The research involves breast cancer and the resistance is referred to as from "chemotherapy" so I wonder if the finding of resistance would be applicable to all therapies i.e. immunotherapies (CD20 mAbs like Rituxan, Ofatumumab, Obinutuzumab etc), Kinase inhibitors i.e. (Ibruinib, Idelalisib, Imatinib), deacetylase inhibitors etc.? In CML the chosen therapy of Imatinib aka Gleevec still produces resistant cancer. Curiously to both "mammary carcinoma" and Imatinib relapsed CML patients, Dasatinib, a Src tyrosine kinase inhibitor, has shown efficacy. Dasatinib has been used experimentally in lysing senescent cells in conjunction with Quercetin in mouse studies. Recently posted.
Bottom line: Correctly timed combination of phenotype targeting drugs may be needed to cure our cancers.