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Leveraging lipid levels to starve liver cancer

takes a nontraditional research approach: He first identifies a disease and then develops translational models to find potential therapeutics. His lab focuses on diseases of the liver. Metabolic dysfunction–associated steatotic liver disease, or MASLD, and metabolic dysfunction–associated steatohepatitis, or MASH, are two of the most common. Only has been approved to treat these conditions, so researchers are pushing to find more and better treatments.

“Understanding how MASLD and MASH can progress to liver cancer is a huge need, especially over the next 15 to 20 years,” Helsley said.

Using human liver tissue samples, Helsley examined lipid levels in the tumor and in matched, nontumor samples. He found that monounsaturated fatty acids, made by the enzyme stearoyl-CoA desaturase, or SCD, accumulate in tumor tissue.

Other researchers are exploring SCD inhibitors as a therapeutic option, but Helsley wants to attack the pathway from the opposite end. His target: CPT1A, the enzyme responsible for breaking down, or oxidizing, monounsaturated fatty acids. His lab found that the CPT1A pathway shuts down in human liver tumors, allowing monosaturated fatty acids, the tumor’s food source, to build up.

Helsley’s plan is to deplete these fatty acids and starve the tumor.

“When the capacity to oxidize monounsaturated fatty acids is turned off, they build up,” Helsley said. “It’s like yin and yang. … If we can figure out a way to exploit that pathway and turn it on, we think we could further prevent tumor growth.”

Helsley will give a talk at the 2025 ASBMB Annual Meeting, April 12–15 in Chicago, titled “The contribution of fatty acid oxidation to diet-induced hepatocellular carcinoma.”