Researchers Genetic Evidence For Treating Lung Disease

This free press release first time scientists Jefferson ‘s Kimmel Cancer Center show that the loss of tumor suppressor protein caveolin-1 (CAV-1) causes mitochondrial oxidative stress in the stromal micro-environment, the process that feeds the cancer cells are more common in breast cancer .

“We now have genetic testing in mitochondrial oxidative stress is important to guide the growth of the tumor,” says researcher Michael P. Lisanti. “That means we need to create anti-cancer drugs, in particular, the objective of such oxidative stress.


And antioxidants have already been there in the market as food supplements, such as N-acetyl cysteine,” he said.The study researchers used a genetically tractable model of Jefferson human cancer associated fibroblasts using sh-RNA target knockdown approach. Without the Cav-1 protein.

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The researchers found that oxidative stress in cancer in fibroblasts leads to mitochondrial dysfunction in fibroblasts of the stroma.In this context. Oxidative stress and autophagy result (producing recycled nutrients) in the tumor microenvironment act as metabolic energy or “food” to “fuel” tumor growth, researchers suggest that loss of Cav -1 increases mitochondrial oxidative stress in the tumor stroma.

Thereby increasing both volume and mass of tumor cells and four times without any increase in tumor angiogenesis.”This study provides genetic evidence necessary for the reduction of oxidative stress in the body decreases tumor growth,” said Lisanti.These results were published online Feb. 15 issue of Cancer Biology and Therapy.

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