Fat cells may fuel aggressive breast cancers: Study

A new study suggests that some breast cancers may "feed" on nearby fat cells, offering scientists a potential pathway to treating one of the deadliest forms of the disease, according to American media.

The research published Wednesday in Nature Communications focused on triple-negative breast cancer, which accounts for about 15% of cases and is more common in Black women and women under the age of 40, NBC News reported.

The cancer is notoriously aggressive, with higher recurrence rates and fewer treatment options.

Lead author Jeremy Williams, a postdoctoral scholar at the University of California, San Francisco, said the team found that tumor cells appear to draw energy from fat cells by inserting "a straw-like structure" into them and extracting lipids, according to NBC News.

"Aggressive cancer cells can co-opt different nutrient sources to help them grow, including by stimulating fat cells in the breast to release their lipids," said Williams. "In the future, new treatments might starve the tumor cells by preventing their access to lipids from neighboring cells."

'A new way cancer grows and feeds itself'

Experiments on human tissue and mouse models showed that when researchers blocked tumor cells' ability to form the structures, known as gap junctions, tumor growth stopped.

"Knocking out a single gene impaired the formation and progression of the tumor," said Williams.

Experts not involved in the study called the findings groundbreaking.

"They found a new way cancer grows and feeds itself," said Justin Balko, professor of cancer research at Vanderbilt University Medical Center.

Columbia University oncologist, Julia McGuinness, added that it is "suggesting one pathway to treat aggressive cancers for which we don’t have any good therapies."

McGuinness noted the study’s broader implications. "Slimming down could be protective," she said, highlighting that obesity is already linked to poorer outcomes for women with breast cancer.

While researchers caution that more work is needed to confirm the mechanism in humans, several existing drugs that block gap junction formation are already in early clinical trials for other uses, raising hopes that a new treatment avenue may be closer than expected.