Fructose Signals Ovarian Cancer Spread in Study
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- The Wistar Institute study, published in Nature Aging, found chemotherapy-surviving ovarian cancer cells release fructose that acts as a chemical message to neighboring cancer cells, increasing their ability to spread.
- First author Aidan Cole and colleagues used a preclinical model to show it is the molecules these surviving cells release — not the cells themselves — that drive metastasis, which accounts for roughly 90% of ovarian cancer deaths.
- High dietary fructose, at levels comparable to sugary drinks, promoted cancer spread even without chemotherapy, and high-fructose corn syrup accounts for ~8-20% of daily calorie intake in some Americans.
- Fructose lowers cholesterol production inside neighboring cancer cells via a CRISPR-identified pathway, weakening the cell-to-cell bonds that function as a biological glue and enabling cells to detach and migrate.
- Statins, taken by 39 million Americans, also weakened connections between cancer cells in the study; researchers are now investigating whether cholesterol-lowering drugs interfere with chemotherapy effectiveness.
- Senior author Katherine Aird emphasized findings are not yet tested in patients and are not a reason to stop statins, but flagged the relevance for postmenopausal women — the demographic most affected by ovarian cancer and often already prescribed statins.
- The Wistar team is planning follow-up studies to test whether the same fructose-related pathway drives metastasis in pancreatic, colon, and liver cancers, which also spread within the torso.
Why it matters: With 39 million Americans taking statins and ovarian cancer most common in postmenopausal women — many of whom already take cholesterol-lowering drugs — the finding opens a concrete clinical question about whether statins interfere with chemotherapy, even as researchers urge patients not to change medications without evidence from patient trials.
