A research team at Emory University in the United States analyzed the mechanism of breast cancer chemotherapy. The research team confirmed this using breast cancer cell models and animal models, including connective tissue cells, cancer cells, and non-cancerous cells found in breast and other tissues.
The research team administered docetaxel, one of the anticancer drugs, to breast cancer cell models and animal models at appropriate concentrations. As a result, at low doses, stromal cells were damaged and cancer cells were not damaged. The treatment induced cancer cells to re-enter the cell cycle. Stromal cells function to induce cell differentiation, expression of function, and apoptosis.
The research team analyzed that this was because stromal cells were damaged by docetaxel administration, increasing the level of interleukin 6, an inflammatory indicator, and releasing G-CSF, which promotes neutrophil production. These values are two major cell signals in the human body and had the effect of awakening dormant cancer cells.
The research team stated that when determining chemotherapy response, not only the cancer cells themselves but also the effects of surrounding cells, including stromal cells, should be considered. It was emphasized that high levels of interleukin 6 in the blood should be recognized as a biomarker that increases the risk of early recurrence in breast cancer patients receiving chemotherapy.
Meanwhile, the results of this study were recently published in ‘PLOS Biology.’
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