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 discovery of BRAF mutations has led to development of targeted therapies to inhibit its function. One of the standard treatment options for melanoma over the last ten years has been to simultaneously target both BRAF mutations and MEK. These two genes are part of the MAPK signalling pathway, which, in cancer, is rewired for uncontrolled growth. Targeting two different critical points in the same domino chain helps slow or stop cancer growth.
The findings are important because altBRAFs were thought to be made through alternative splicing, which is when cells use the same gene to synthesise different proteins. The discovery that genomic deletions, and not splicing, are the cause means a shift away from previous proposals for using drugs that target splicing as a therapeutic strategy.
Even more surprisingly, further analyses revealed that genomic deletions might be a more widespread mechanism of oncogenesis and resistance than previously thought. Though uncommon, researchers found evidence of altBRAFs in melanomas with a normal-functioning BRAF gene, as well as in other types of cancer including non-small cell lung cancer, breast cancer, kidney cancer and prostate cancer.
"Having the opportunity to approach this research with both a clinician's perspective and a scientist's curiosity has been invaluable. It allowed us to uncover not just how melanomas resist treatment but also how this knowledge could lead to more effective therapies for patients. This fusion of clinical insight and scientific investigation is crucial for making real progress in our fight against cancer," concludes Dr. Aya Moreno.
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