Researchers observed that removing the amino acid tryptophan from the diet slowed the growth of liver tumors in mice. The findings were reported in Nature Communications, a respected journal in medical science. This study adds another piece to the ongoing effort to understand how liver cancer develops and how it might be restrained through diet and targeted therapies.
Hepatocellular carcinoma remains a major global health challenge, ranking among the leading causes of cancer-related deaths. Even with advances in treatment, survival rates stay modest, with only a limited portion of patients living beyond five years after diagnosis.
The study describes a link between tumor progression and the amino acid tryptophan, which the body converts into a compound called indole-3-pyruvate, or I3P. This metabolic route appears to support the growth of liver cancer cells in the experimental model used in the research.
To test the idea, researchers fed mice with liver tumors a diet devoid of tryptophan. The result was a noticeable slowdown in tumor expansion, and there were no obvious adverse effects on overall health in the animals. While tryptophan is relatively uncommon in some protein sources, caution is advised when translating these findings to humans. Additional studies are needed to determine whether avoiding tryptophan could be safe and effective for people dealing with cancer.
Common foods that supply tryptophan include turkey, red meat, pork, chicken, dairy products, soy products such as tofu and edamame, quinoa, oats, and various fish. These items are widely consumed in North American diets, so any dietary guidance must balance nutrition and individual health needs, avoiding unintended consequences and ensuring adequate intake of other essential nutrients.
Beyond dietary adjustments, researchers are exploring the potential of drugs that target the I3P pathway as a possible cancer therapy. By interrupting this metabolic step, there may be a way to curb tumor growth without relying solely on dietary modification, offering a complementary strategy alongside existing treatments.
Earlier work by other scientists showed that antibiotic treatment could influence cancer development in mouse models, illustrating how gut microbiota and related metabolic processes might intersect with tumor biology. This broader context helps explain why metabolic pathways linked to tryptophan and I3P are of growing interest in cancer research. Nature Communications