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Genetic ‘switch’ could slow spread of cancer in patients with high-fat diets

In a set of papers published in the journals Nature Genetics and Nature Communications, researchers at Harvard Medical School and the Cancer Center at Beth Israel Deaconess Medical Center have shed new light on the genetic mechanisms that promote [prostate tumor] metastasis in a mouse model and implicated the typical Western high-fat diet as a key environmental factor driving metastasis.

Epidemiological data links dietary fats (and obesity) to many types of cancer, and rates of cancer deaths from metastatic cancers including prostate cancer are much higher in the United States than in nations where lower fat diets are more common.

In tumors that lacked both PTEN and PML tumor suppressing genes, the cells’ fat-production machinery was running amok.

“It was as though we’d found the tumors’ lipogenic, or fat production, switch,” said Pandolfi. “The implication is, if there’s a switch, maybe there’s a drug with which we can block this switch and maybe we can prevent metastasis or even cure metastatic prostate cancer,” he added.

[P]hysicians could soon be able to screen their early-stage prostate cancer patients for those whose tumors lack both PTEN and PML tumor suppressing genes, putting them at increased risk for progressing to metastatic disease. These patients may be helped by starving these tumors of fat either with the fat-blocking drug or through diet.

Read full, original post: Flip the Switch – Changes in fat metabolism may promote prostate cancer metastasis

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