High fuel diet may increase risk of prostate cancer
Obesity is linked to prostate cancer, scientists know, but it’s not clear why. On Monday, researchers reported a surprising connection.
When prostate cancers lose a particular gene, they become tiny fat factories, a team at Beth Israel Deaconess Medical Center in Boston reported in a paper published in ‘Nature Genetics’.
Then the cancers spread from the prostate, often with deadly effect. Prostate cancers that have not lost that gene also can spread, or metastasise — in mice, at least — but only if they have a ready source of fat from the diet.
That finding suggests that dietary fat can substitute for the loss of the gene, fueling prostate cancer. Moreover, the investigators found, an obesity drug that blocks fat production can make metastatic prostate cancers regress in mice and prevent them from spreading.
“What this paper suggests is that fat or high-fat diets promote more aggressive prostate cancer,” said Cory Abate-Shen, interim director of the Herbert Irving Comprehensive Cancer Center at Columbia University.
Now the scientists are planning a clinical trial in men with prostate cancer to see if the obesity drug may be an effective treatment for this cancer. The American Cancer Society estimates that prostate cancer will be diagnosed in about 1,65,000 American men this year.
Geneticists knew prostate cancers often start when a protective gene, PTEN, shuts down. But the tumours in men that lose only PTEN tend to languish, rarely spreading beyond the prostate and rarely becoming lethal.
The cancers change if a second gene, called PML, also shuts down. Suddenly, indolent cells become cancers that spread and kill. But why?
In the new study, researchers found that when PML was lost, cancerous cells — in petri dishes and in mice — started churning out fat, which may protect the cells from certain toxic molecules. But the fat also may help the cancers spread, the researchers suggested.
Dr Pier Paolo Pandolfi, director of the Cancer Center and Cancer Research Institute at Beth Israel Deaconess and lead author of the new study, along with his colleagues, are planning a clinical trial with fatostatin to treat prostate cancer in humans. They also wonder if low-fat diets might help and what kinds of dietary fat might fuel prostate cancers.
The cancers change if a second gene, called PML, also shuts down. Suddenly, indolent cells become cancers that spread and kill. But why?
In the new study, researchers found that when PML was lost, cancerous cells — in petri dishes and in mice — started churning out fat, which may protect the cells from certain toxic molecules. But the fat also may help the cancers spread, the researchers suggested.
Dr Pier Paolo Pandolfi, director of the Cancer Center and Cancer Research Institute at Beth Israel Deaconess and lead author of the new study, along with his colleagues, are planning a clinical trial with fatostatin to treat prostate cancer in humans. They also wonder if low-fat diets might help and what kinds of dietary fat might fuel prostate cancers.
