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A new study on mice reveals that drug-resistant melanoma tumors shrink when treatment is interrupted, or given a "holiday", suggesting that changing the dose pattern of cancer drug treatment could be a simple way to extend survival in human patients with late-stage disease.

The research, published in Nature, showed tumors not only became resistant to vemurafenib, but also became dependent on the drug to survive. Once the drug was withdrawn for a two week 'drug holiday', the tumors began to shrink.

The drug can slow the progress of a tumor in the short-term, but it soon becomes ineffective with deadly consequences.

The tumors gain resistance by changing the chemistry of the inside of a cell. However, the researchers showed this process left the cancer cells dependent on the drug - like an addict.

Efim Guzik, professor of cancer biology at University of California, San Francisco, said: "Remarkably, intermittent dosing with vemurafenib prolonged the lives of mice with drug-resistant melanoma tumors.

"By seeking to understand the mechanisms of drug resistance, we have also found a way to enhance the durability of the drug response."

The research raises the possibility that so-called "drug holidays" could extend vemurafenib's effectiveness in humans, although clinical trials have yet to be conducted.

Professor Richard Marais, Director of Cancer Research UK's Paterson Institute at the University of Manchester, was part of a Cancer Research UK-funded team that discovered the BRAF faults in melanoma. He described vemurafenib as "an exciting drug and one of the success stories of cancer research".

"It's not a cure for melanoma but can give people valuable extra months," he added.

More than 12,800 people in the UK are diagnosed with melanoma skin cancer every year and around 2,200 die from the disease.