Regulation of chemo-sensitivity in ovarian cancer via a stroma dependent glutathione pathway.

The primary chemotherapeutic agents for epithelial ovarian cancer are platinum-based drugs, which are commonly used in combination with a taxane regimen. These treatments are generally effective at achieving remission, but the remission is often followed by a relapse and acquired resistance to chemotherapy. In order to overcome these barriers of drug resistance, it is important to understand the underlying mechanisms regulating the development of drug-resistant tumors. Tumors evolve through interactions with the surrounding microenvironment, which are comprised of a complex mixture of cells including fibroblasts and immune cells. In ovarian cancer, fibroblasts can make up a significant component of the primary tumor. While fibroblasts are known to influence the behavior of cancer cells directly through secretion of growth factors, and extracellular matrix (ECM) proteins, the interactions between fibroblasts and immune cells are less understood. In a recently published study from Cell, Wang and colleagues present intriguing work characterizing the role of fibroblast and T cells in modulating platinum resistance in ovarian cancer. Here, we briefly summarize and comment on their findings in relation to the tumor microenvironment and chemoresistance.