Researchers have discovered one way in which melanoma becomes resistant to a particular form of targeted therapy, and understanding this phenomenon may lead to a new melanoma target or prompt new designs of these treatments, they say. The results were published in the journal Clinical Cancer Research.
When targeted therapies were first approved for the treatment of cancer, they were hailed as a potential "cure" for different types of cancers and an acceptable alternative to chemotherapy, since they were designed to target the mutations responsible for cancer while sparing healthy, unmutated cells. In the case of melanoma, the gene BRAFV600E/K seemed like a particularly promising target, since the gene is mutated in approximately 40 to 50% of all cases of melanoma. However, while patients with these mutations who receive drugs designed to target BRAF mutations do live slightly longer, they often relapse within several months of treatment.
"We once thought targeted therapies could be a 'magic bullet' for cancer treatment, but we've learned over time that this simply is not the case, especially with regard to BRAF inhibitors for melanoma," said Russel E. Kaufman, M.D., president emeritus of The Wistar Institute and lead author of the study. "We felt it was important to examine the tumor microenvironment to provide one possible explanation for why patients become resistant to targeted therapy in order to guide treatment decisions and perhaps arrive at better, more effective therapies."
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