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Study: Fat fuels triple negative breast cancer

Roughly one in five tumors fuel themselves using fat, rather than hormones, demanding doctors to pursue a different form of treatment.
By Stephen Feller   |   March 7, 2016 at 2:50 PM

SAN FRANCISCO, March 7 (UPI) -- A drug that disrupts the ability of certain breast tumors to use fat as an energy source was found to successfully treat cancer in mice, according to a new study.

Researchers at the University of California San Francisco found the drug etomixir, developed to treat heart failure, to stop the growth of triple-negative breast cancer implanted in mice, suggesting a more effective method for battling the disease.

Roughly 20 percent of breast cancer is triple-negative -- not using estrogen, progesterone or human epidermal growth factor receptor 2 to grow -- so hormonal therapies don't work and often chemotherapy is effective for only a short time, making the finding important for some patients.

Etomixir, which prevents cells from processing fat into energy, was developed to treat heart failure but clinical trials with the drug were stopped because of adverse side effects. Recent studies, however, have shown the drug to have promise with prostate and pancreatic cancer.

Previously, researchers at the University of California San Francisco found 90 percent of triple-negative breast cancers produce excessive amounts of the oncogene MYC, which drives tumor development.

For the new study, published in the journal Nature Medicine, the researchers used mass spectrometry to identify fatty acid oxidation metabolites on the surface of cancer cells, which shows the cells could be using fat to create energy.

Working with mice, human tumor tissue, and tumor cells grown in the lab, the researchers found etomoxir stopped the production of adenosine triphosphate, or ATP, the precursor product cells create from fat and sugar to make energy.

In mice with transplanted tumors, those with high levels MYC slowed their growth significantly when treated with etomoxir, while those lower in expression of the gene did not respond as strongly.

"This is very promising, but there is quite a bit more research to do before we can try this approach in humans," Dr. Andrei Goga, a professor of cell and tissue biology at the University of California San Francisco, said in a press release. "Our goal is to try to identify fatty acid oxidation inhibitors and to ascertain which are likely to be most efficacious against these cancers, with the goal of bringing one to the clinic. It may be possible to repurpose drugs that already have been developed."

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