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A team of researchers has managed to exploit a vulnerability in melanoma or skin cancer that develops resistance to a targeted therapy, providing a potential new therapeutic strategy to selectively kill the drug-resistant cancer cells.

The study has shown that when cancer cells develop drug resistance, they also acquire a new vulnerability, the Xinhua reported.


The researchers, led by Rene Bernards of the Netherlands Cancer Institute and Oncode Institute in Denmark, exposed this new vulnerability in melanoma that has developed resistance to treatment with a BRAF inhibitor — a targeted therapy that blocks a signalling pathway in the cancer cell through which it gets the message to keep on dividing.

Since more than half of all melanoma patients have a mutation in this BRAF gene, the BRAF-inhibitor stops tumour growth in those patients.

But within a few months, the tumour cell adapts the original signalling pathway and becomes active again, and even hyperactive.

The researchers, however, found that the hyperactive resistant melanoma cells produced large amounts of reactive oxygen species, but cancer cells still sensitive to the drug did not do so.


Representational image, pixabay

The study, published in the journal Cell, found that the abundance of free radicals caused the resistant melanoma cells to stop dividing, but they did not die.

When tested on mice along with an existing drug, vorinostat, which is known to stimulate the production of free oxygen radicals, the researchers saw tumours shrink under the influence of the drug, the report said.

This laid the foundation for a new therapeutic strategy: Treating patients with BRAF-mutated melanoma, as usual, with signal pathway inhibitors.

When the tumour becomes resistant, stop giving those inhibitors and immediately treat the patients with vorinostat to kill the resistant cancer cells.

Also Read: Leukemia Progression in Kids Can be Delayed Through Bone Density Treatment

“It is not a combination drug. It is very important that you first stop the signalling pathway inhibitors because they suppress the free radicals and thus eliminate the effects of vorinostat,” Bernards said. (IANS)


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