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In addition, patient‑derived matched tumor samples following therapy with kinase inhibitors showed decreased numbers of CSPG4‑positive cells as compared to pre‑therapy tumor samples. Our results indicate that BRAF and MEK inhibition downregulates CSPG4 expression until the cells have developed permanent resistance. Our findings provide the basis for further investigation of the role of CSPG4 in the development of drug‑resistance in melanoma cells.Following the publication of the above paper, an interested reader drew to our attent
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