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Roche’s Zelboraf for Melanoma Spurs Other Skin Cancer’s Growth, Study Says
Roche Holding AG (ROG)’s melanoma drug Zelboraf speeds growth of another type of skin cancer, researchers said today in a study underscoring the need to test the medicine in combination with a second treatment.
Scientists at the Institute of Cancer Research analyzed DNA in 21 tissue samples from Zelboraf patients who developed cutaneous squamous-cell carcinoma. About 60 percent of the samples had one of two known cancer-causing gene mutations not targeted by the drug, they said in an article published in the New England Journal of Medicine today.
About 15 percent to 30 percent of melanoma patients treated with Zelboraf and other so-called BRAF inhibitors develop non- melanoma skin cancers, the researchers said. The drugs speeds squamous-cell carcinoma in patients who would probably have gotten the cancer anyway, they said.
“It’s acting as an accelerator of the inevitable in patients that are already predisposed to the disease,” said Richard Marais, a professor of molecular oncology at the London- based institute.
Combining Zelboraf with a second type of drug may stem the effect, said Marais, a co-author of the study, in a telephone interview. Using a type of medicine known as a MEK inhibitor to attack the same pathway that stimulates cell growth appeared to block development of the second type of tumor in mice, the researchers said.
Roche began testing Zelboraf, which works by blocking a protein that fuels tumor growth in about half of patients with advanced forms of melanoma, together with a MEK inhibitor known as GDC-0973 in the BRIM7 patient trial last year. The Basel, Switzerland-based drugmaker helped sponsor the institute’s research.
U.S. regulators approved Zelboraf for sale in August. The European Medicines Agency recommended the drug be approved last month. Roche is awaiting a final decision from the European Commission.
To contact the reporter on this story: Naomi Kresge in London at nkresge@bloomberg.net
To contact the editor responsible for this story: Phil Serafino at pserafino@bloomberg.net
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