Study Finds Fatty Acids as Key Driver of Triple-Negative Tumor Growth - Video

Researchers at the Huntsman Cancer Institute, University of Utah, have found that triple-negative breast cancer (TNBC) uses lipids-or fatty acids-as fuel, making it more aggressive in patients with obesity. The National Cancer Institute-funded study indicates that targeting elevated lipid levels could slow tumor growth and guide safer dietary strategies for patients and survivors.

Lead researcher Dr. Keren Hilgendorf explains that lipids, often overlooked in obesity research, are key building blocks for tumor development. “Breast cancer cells are essentially addicted to lipids,” she said, emphasizing that their abundance in obese individuals may explain higher cancer prevalence and severity.

The team conducted preclinical studies using mouse models on high-fat diets as well as models genetically engineered to have hyperlipidemia-high blood lipid levels-without other obesity-related traits like elevated glucose or insulin. This approach allowed them to isolate the specific impact of lipids on cancer growth. Their findings showed that high lipid availability alone accelerated tumor proliferation, while reducing lipids significantly slowed it, even in the presence of metabolic risk factors.

The results suggest that lipid-lowering medications, already in clinical use for cardiovascular conditions, might be repurposed to suppress certain cancer types. The researchers, however, caution that more testing in human models is needed. They further advise that breast cancer patients avoid high-fat diets such as keto, which might unintentionally feed tumor growth.

The team plans to explore whether lipid-lowering drugs can enhance chemotherapy response and to study the mechanisms through which lipids fuel cancer cell proliferation in breast, ovarian, and colorectal cancers.

Reference: Vieira, R. F. L., et al. (2025). Hyperlipidemia drives tumor growth in a mouse model of obesity-accelerated breast cancer growth. Cancer & Metabolism. doi.org/10.1186/s40170-025-00407-0.