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Melanoma’s safe haven targeted for shut-down

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In a new research published in Cancer Cell recently, it is revealed that melanoma cells become drug resistant with the help of the safe haven provided by the surrounding healthy cells. About 50% of the melanomas occur due to a mutation in a gene called BRAF. Typically, drugs called BRAF inhibitors that targets the faulty genes are used to treat these melanomas. However, the problem is these cancers soon develop a resistance to these targeted treatments.

In their research, scientists at the Francis Crick Institute, funded by Cancer Research UK, and at the Cancer Research UK Manchester Institute have discovered that a side effect of BRAF inhibitors which eventually makes the cancer cell drug resistant. It is found that BRAF inhibitors prompt healthy cells to form a ‘safe haven’ shielding melanoma cells from cancer drugs. So even though some cancer cells are destroyed, the protected cancer cells survive – and the disease rebound in a form that is untreatable with fatal consequences.

The scientists experimented on mice and in sample from patients' tumors. Their study showed that the shield of cells that surround melanoma cells turn on a parallel set of cell signals that helps them survive. The researchers also found a way to overcome the resistance to BRAF inhibitors. By adding a second experimental drug that blocks this alternative route by targeting a protein called FAK, the resistance to BRAF inhibitors can be overcome. In their lab study it was found that this combination of two drugs increased the cancer cell death and slowed cell growth in the samples. Also, it stopped tumors from growing bigger in mice.

This treatment method is still not dubbed as a cure, but by adding a second targeted therapy could improve treatment by overcoming the cancer's resistance to drug. It can also extend the time before the cancer can strike back. FAK inhibitors are being tested in early stage cancer trials. However, it will take some years before we know how effective they are along with BRAF inhibitors.

Francis Crick Institute based study author Dr. Erik Sahai said skin cancers are caused by a faulty BRAF gene that typically out-smarts the targeted drugs after a few months of treatment. He is of the opinion that understanding why it happens is a crucial to improving the treatment. With this study, they now know how melanoma cells exploit their neighboring cells to survive in the presence of targeted drugs. Since, it is now known that the safe haven is triggered as a response to the same drugs used for treating this class of melanoma, steps to improve the treatment process can be taken.

Richard Marais, who is a co-author in this study and also the director of the Cancer Research UK Manchester Institute at the University of Manchester, said that understanding the complex behavior of melanoma cells is vital to improving survival. Now that this study has revealed what is stopping the best drugs from working in this deadly skin cancer, the next step is to see if adding a second drug is safe and effective in patients.

Nell Barrie, Cancer Research UK’s senior science information manager opined that this research has showed some crucial details and has helped in  understanding how melanoma cells develop resistance to drugs and how it can be tackled head on. The researchers have worked through the issue with meticulous care to show not just how this happens, but how we can tackle the problem.

The survival rates of melanoma cancer are improving since the last 40 years. However, there is still so much to do and this research is a step in the right direction.

Suffering from melanoma and losing hope on life? Try this guide to help cure the disease yourself!