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Kidney Cancer Progression Inhibited by Everolimus Drug

by Rajshri on May 18 2008 11:21 AM

Researchers at Memorial Sloan-Kettering Cancer Centre have revealed that experimental targeted therapy everolimus (RAD001) has the potential to delay cancer progression in patients with metastatic kidney cancer.

The study led by Dr Robert Motzer, an attending physician at Memorial Sloan-Kettering Cancer Centre (MSKCC) revealed that Everolimus, a once-daily oral therapy may inhibit cancer progression in kidney.

"This study has given us a new and clearly useful tool for treating renal cell tumours, and everolimus is an important step forward in terms of disease management and quality of life for patients living with this disease," said Dr. Motzer.

The drug targets mTOR protein, which acts as a central regulator of tumour cell division, cell metabolism, and blood vessel growth.

The researchers conducted the study on more than 400 patients with the disease that had progressed with currently available targeted therapies sunitinib and/or sorafenib. They were randomly given everolimus or placebo.

The findings revealed that after six months, 26 percent of patients in the everolimus group had disease that had not progressed, compared to only 2 percent of the placebo group.

The average difference in progression free survival was four months for everolimus, compared to 1.9 months for the placebo group.

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"For almost 20 years, we made no headway in the management of advanced kidney cancer," said Dr. Motzer.

"Recently, the identification of several new angiogenesis- targeted agents has provided us with new treatment options and an improved outlook for patients with advanced kidney cancer.

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"Based on the results of this trial, everolimus could become another tool in our armamentarium and, in the future, kidney cancer is likely to be managed as a chronic disease with these types of treatment advances," he added.

The findings will be presented on May 31 at the annual meeting of the American Society for Clinical Oncology.

Source-ANI
RAS/C


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