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Initially strong responses to BRAF inhibitor treatment are inevitably dulled by development of drug resistance in the cancer cells. Earlier studies have identified how melanoma cells themselves adapt to BRAF inhibition; now, in two recent studies, investigators identify mechanisms by which drug sensitivity is reduced and show that stromal cells in the tumor microenvironment also have a pivotal role in developing resistance.
Wilson and colleagues studied soluble growth factors that enable many cancer cells to overcome inhibition by targeted kinase inhibitors. They found that hepatocyte growth factor (HGF) signaling (long known to regulate tumor invasion, angiogenesis, and metastasis through its receptor c-MET) reduced sensitivity to the BRAF …