A study has disentangled the mechanisms behind one of the ways melanoma cancer cells develop resistance to treatment. The study found that, in response to some drugs, melanomas can ‘break’ parts of their BRAF gene, which is mutated in 1 in 2 melanomas. This helps the tumor create alternative versions of the protein which lack regions targeted by one BRAF inhibitors, one of the main drugs used to treat this type of cancer, making treatment less effective. The findings pave the way for alternative strategies to treat BRAF-mutated melanoma, which leads to relapse in 50% of patients within a one-year period.
