A diet high in fat — such as that typically found in the United States — has long been suspected of fueling prostate cancer growth, and researchers think they have found a way to shut down the destructive mechanism of that fat, a report in Science Daily shows.
Researchers at the Cancer Center at Beth Israel Deaconess Medical Center (BIDMC) set out to determine the genetic mechanisms that promote metastasis — accelerated growth — in prostate cancer. Prostate tumors tend to be slow growing; so slow, men with prostate cancer tend to die with it, not from it. It’s only when prostate tumors metastasize that the disease is fatal.
Dr. Pier Paolo Pandolfi, director of the Cancer Center and Cancer Research Institute at BIDMC knew that historically, data showed dietary fat linked many types of cancer, including prostate cancer. Data show prostate cancer affects only about 10 percent of men in Asian countries; yet that rate climbs to about 40 percent when they immigrate to the United States mirroring the native-born U.S. population. Pandolfi wanted to know if there was a way to block the mechanism behind fat’s ability to hyperdrive prostate cancer.
Scientists know that a tumor-suppressing gene might be key. One such gene, dubbed PTEN, is known to play a major role in prostate cancer. Its absence is linked to metastatic prostate disease, but animal studies suggest the loss of PTEN alone is not enough to trigger progression. Pandolfi and his colleagues sought to identify an additional tumor-suppressing pathway that may work in concert with PTEN to drive metastasis.
Poring through gene data, Pandolfi and his researchers noticed that another tumor suppressor gene, called PML, seemed to be present in non-metastatic prostate tumors, but was absent in about a third of metastatic prostate tumors. And about 20 percent of metastatic prostate tumors lack both the PML and PTEN genes.
What they found surprised all: The metastatic tumors produced huge amounts of lipids, or fats. In tumors that lacked both the PTEN and PML tumor suppressing genes, the cells’ fat-production mechanism appeared to run wild.
“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.”
Such a “switch” already exists. Discovered in 2009, “fatostatin” is currently being investigated for the treatment of obesity. Pandolfi and colleagues tested the molecule in lab mice. “The obesity drug blocked the lipogenesis fantastically and the tumors regressed and didn’t metastasize.”
The findings could result in much better treatments for the disease — and possibly a cure. In the meantime, doctors could soon be able to screen their early-stage prostate cancer patients for those whose tumors lack both the PTEN and PML tumor suppressing genes, which would put them at increased risk for prostate cancer. These patients may be helped with the fat-blocking drug or through diet.
“The data are tremendously actionable, and they surely will convince you to change your lifestyle,” Pandolfi said.
Pandolfi and his researchers published their findings in the journals Nature Genetics and Nature Communications.
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