
Taking frequent breaks from medication may help patients with skin cancer live for longer, studies in mice have shown.
Researchers in California and Switzerland found that melanomas that develop a resistance to anti-cancer drug Zelboraf (vemurafenib), developed by Plexxicon and Roche, also become addicted to the drug and thrive on it to survive.
They found that withdrawing the medicine caused tumours to shrink.
The study, published in the journal Nature, showed that mice continuously treated with vemurafenib all died of drug-resistant disease within about 100 days, while all the mice treated with vemurafenib but with regular "drug holidays" all lived past 100 days.
University of California, San Francisco cancer biology professor and study co-lead researcher Dr Martin McMahon said; "Vemurafenib has revolutionised treatment of a specific subset of melanoma expressing mutated BRAF, but its long-term effectiveness is diminished by the development of drug resistance.
"By seeking to understand the mechanisms of drug resistance, we have also found a way to enhance the durability of the drug response via intermittent dosing."
In 2011, the US Food and Drug Administration approved the drug vemurafenib for patients with late-stage melanoma with mutations in BRAF after clinical trials showed a significant increase in survival for participants.
But while the drug causes tumours to shrink initially, most people on vemurafenib suffer cancer recurrence with a drug-resistant form of melanoma.
Scientists at the UCSF, Novartis Institutes for Biomedical Research and University Hospital Zurich discovered that melanoma cells become drug resistant by making more of the BRAF protein, the very target of the drug itself.
They found that, if by becoming resistant to vemurafenib’s anti-cancer potency, a melanoma also becomes addicted to it, then drug-resistant tumours may shrink when the vemurafenib is removed.
Melanoma is the most aggressive type of skin cancer. In 2012, 9,180 people in the US died from the disease, according to the National Cancer Institute.
Image: Martin McMahon, professor of cancer biology at the University of California, San Francisco. Image: Courtesy of UCSF.