Ovarian cancer is one of the deadliest cancers affecting women because it is often discovered after it has already spread.
Although many patients respond well to platinum-based chemotherapy at first, the disease frequently returns.
In most cases, the returning cancer spreads throughout the abdominal cavity, and this spread, known as metastasis, is responsible for about 90% of ovarian cancer deaths.
A new study from The Wistar Institute has uncovered an unexpected factor that may help explain why this happens.
The research, published in Nature Aging, found that some cancer cells that survive chemotherapy continue to influence nearby cancer cells even though they are no longer actively dividing. Instead of becoming inactive, these surviving cells release chemical signals that make neighboring cancer cells more likely to spread.
The researchers identified one surprising signal: fructose. Fructose is a simple sugar that naturally occurs in fruit but is also found in large amounts in sweetened drinks and foods made with high-fructose corn syrup.
According to the study, fructose produced by chemotherapy-surviving cancer cells acted as a messenger that encouraged nearby cancer cells to become more aggressive.
Lead author Dr. Aidan Cole explained that this is one of the first studies showing that a nutrient can work as a communication signal between cancer cells. The team demonstrated in preclinical models that molecules released by surviving cells, rather than the cells themselves, were enough to increase cancer spread.
The researchers then discovered something even more surprising. High levels of fructose from the diet also appeared to increase the ability of ovarian cancer cells to spread, even without chemotherapy. This finding raises the possibility that nutrition could influence cancer progression, although the researchers stress that this idea has not yet been tested in patients.
The team wanted to understand why fructose had this effect. They found that fructose reduced cholesterol production inside neighboring cancer cells. Cholesterol does much more than affect heart health. Within cells, it helps maintain strong connections between neighboring cells. When cholesterol production falls, these connections weaken, making it easier for cancer cells to separate and spread to other parts of the body.
This finding also raised questions about cholesterol-lowering medicines known as statins. In laboratory experiments, statins also reduced these cell connections. The researchers emphasized that patients should not stop taking statins, but they believe future studies should examine whether these medicines influence chemotherapy outcomes in ovarian cancer.
The scientists also believe this biological process may not be limited to ovarian cancer. They are already investigating whether pancreatic, colon, liver and other cancers that spread inside the abdomen use similar signaling pathways.
The study offers an entirely new way of thinking about cancer recurrence after chemotherapy. Instead of focusing only on the surviving cancer cells, future treatments may also target the chemical messages these cells release.
However, the work was performed in preclinical models, so clinical studies are still needed before dietary advice or treatment recommendations can change. Overall, the publication in Nature Aging opens an exciting new direction for understanding cancer spread and developing future therapies.
The findings are important because they connect cancer biology with metabolism and nutrition in a way that has not been fully appreciated before.
While patients should not change their medications or diet based on this study alone, the research provides strong scientific evidence for further clinical investigation. If confirmed in people, it could eventually influence dietary guidance and the design of combination cancer treatments.
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Source: The Wistar Institute.
