A team of UK scientists has made the discovery that drugs that target a fault in a protein called BRAF could actually fuel the progression of cancer in some cases.
The findings of the study, which was jointly funded by Cancer Research UK, the Institute of Cancer Research (ICR) and the Wellcome Trust, are published in Cell.
Malignant melanoma is the most deadly form of skin cancer and is difficult to treat successfully once it has spread to other organs.
The BRAF gene is faulty in about half of malignant melanomas and many other cancers, making it a suitable drug target.
Drugs that block BRAF function in cells are already showing positive results in early clinical trials in melanoma patients in the US.
Hot on the post earlier today about anti-angiogenic drugs causing accelerated tumour invasion when used in the short term, this article on BRAF inhibition was also timely and relevant. One BRAF inhibitor in development, sorafenib (Nexavar) also inhibits VEGF.
The consequence of the CRUK research is that patients need to be carefully screened before deciding upon therapy. Those without a faulty RAS gene could be better candidates for BRAF therapy and those with may encourage the cancer to grow. This may provide a good biomarker in diseases such as melanoma.
The findings give new insights into how the drugs work, and ultimately, how the underlying biology affects tumourigenesis and growth.