Fructose from chemo-surviving cells drives ovarian cancer spread
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- Aidan Cole, Ph.D. and colleagues at The Wistar Institute found in a preclinical model that molecules released by chemotherapy-surviving ovarian cancer cells — not the cells themselves — significantly increased neighboring cells' ability to spread, marking what Cole called the first such demonstration outside a dish.
- Fructose was identified as the key signal, with chemotherapy-surviving cells producing and releasing it to encourage metastasis in nearby tumor cells, according to the Nature Aging study.
- Cholesterol acts as a "biological glue" between cells; a CRISPR screen revealed fructose lowers cholesterol production in neighboring cells, weakening adhesion and enabling cancer cells to detach and move into other areas.
- Dietary fructose at levels comparable to sugary drinks encouraged cancer spread even without chemotherapy in the study, and high fructose corn syrup accounts for roughly 8–20% of daily calories in some Americans — a modifiable risk factor researchers have not yet tested in patients.
- Statins, used by 39 million people in the United States, weakened cancer cell connections on their own in the experiments, and the team is now investigating whether cholesterol-lowering drugs could interfere with chemotherapy in ovarian cancer patients.
- Katherine Aird, Ph.D., senior author, said the findings are not a reason for patients to stop statins and noted that ovarian cancer is most common in postmenopausal women who are often already on the drugs, while follow-up studies will test whether the mechanism applies to pancreatic, colon, and liver cancers.
Why it matters: If confirmed in patients, the mechanism would reframe a widespread dietary component — fructose, present in roughly 8–20% of daily calories for some Americans — as a potential fuel for ovarian cancer metastasis, and would put a spotlight on the 39 million Americans on statins whose cholesterol-lowering treatment could theoretically interact with chemotherapy outcomes.
