Health & Science: New pre-clinical research has identified a possible connection between fructose, a common dietary sugar, and the spread of aggressive ovarian cancer, providing scientists with new clues about how cancer cells can become more capable of metastasizing. The findings were published in Nature Aging and are based primarily on laboratory and animal studies, meaning they do not yet establish that eating sugar directly causes ovarian cancer to spread in people.
Researchers from the Wistar Institute investigated high-grade serous ovarian cancer (HGSOC), one of the most aggressive forms of ovarian cancer. The team found that some cancer cells that survive chemotherapy can remain biologically active even when they are no longer rapidly dividing. These surviving cells can release signals that influence neighboring cancer cells and make them more capable of spreading.
One of the important signals identified in the research was fructose. Scientists found evidence that fructose can support metabolic changes in ovarian cancer cells that promote their ability to disseminate, or spread, within the body.
In experiments involving mice, researchers provided glucose or fructose through drinking water and examined the development of tumor nodules. The experiments showed that fructose and the metabolic processes used to break it down were associated with increased tumor dissemination. Researchers also investigated the enzyme ketohexokinase (KHK), which plays a central role in fructose metabolism.
The findings suggest that fructose may function as more than simply an energy source in this setting. It may also act as part of a communication system within the tumor environment, helping surviving cancer cells influence other tumor cells.
This is particularly significant because ovarian cancer often spreads within the abdominal cavity before it is detected. Once cancer cells migrate away from the original tumor and establish new growths, treatment becomes considerably more difficult.
The study also focused on what happens after chemotherapy. Cancer treatment can eliminate many tumor cells, but some cells may survive treatment and enter a state in which they stop actively dividing while continuing to release biological signals. Researchers found that these surviving cells could alter the surrounding environment in ways that support metastatic behavior.
The research raises questions about whether controlling fructose metabolism could eventually become part of a strategy for preventing or slowing ovarian cancer spread. Scientists say the findings could potentially lead to new treatment targets, particularly therapies aimed at disrupting the metabolic pathways that cancer cells use to become more invasive.
However, it is important to distinguish pre-clinical evidence from proven effects in humans. The current findings do not show that eating normal amounts of fruit or other foods containing naturally occurring sugars causes ovarian cancer to metastasize. More research, including studies in humans, will be needed before scientists can determine how the findings translate into dietary recommendations or treatments.
The results add to a growing body of research showing that cancer metabolism is highly complex. Tumors can use nutrients available in their surrounding environment and can alter their metabolism as they grow, respond to treatment or spread to other parts of the body.
Researchers are increasingly studying the tumor microenvironment—the network of cancer cells, immune cells, blood vessels and chemical signals surrounding a tumor—to understand why some cancers become resistant to treatment and metastasize.
The new ovarian cancer findings also come amid broader research into the relationship between dietary sugars and cancer progression. Other pre-clinical work has found that combinations of glucose and fructose can promote metastatic behavior in advanced colorectal cancer, although that research involved a different cancer type and should not be directly applied to ovarian cancer.
For now, scientists say the ovarian cancer findings should be viewed as an important research lead rather than proof that dietary sugar causes cancer spread. Future studies will need to determine whether the metabolic pathway identified in the experiments can be safely targeted and whether reducing or altering fructose metabolism can actually improve outcomes for patients.
The research nevertheless provides a new perspective on ovarian cancer progression and highlights how understanding the way tumor cells use nutrients could eventually contribute to new approaches for preventing metastasis and improving cancer treatment.
