Researchers at the National Cancer Center Japan have identified a new gut bacteria strain called YB328 that enhances the effectiveness of certain anticancer drugs, particularly immune checkpoint inhibitors.

YB328 was found to improve the performance of immune checkpoint inhibitors, which are drugs that help the immune system target cancer cells, potentially increasing their response rates.

Current immunotherapy drugs like Opdivo and Keytruda have a response rate of about 20%, meaning most patients do not benefit from these treatments.

The gut microbiome has long been suspected to influence the disparity in immunotherapy effectiveness, with less than half of patients seeing benefits.

Research shows that only around 20% of patients experience long-term success with checkpoint inhibitors, and gut bacteria play a significant role in determining treatment response.

Patients who respond well to immunotherapy tend to have higher levels of the Ruminococcaceae family of bacteria, which correlates with increased T cells in tumors and longer-lasting effects.

Stool samples from 50 cancer patients revealed that responders had a higher ratio of YB328 bacteria, linking this microbe to better treatment outcomes.

In mouse experiments, combining YB328 with checkpoint inhibitors led to tumor shrinkage, and using YB328 with stool from non-responders improved drug efficacy.

Mice treated with YB328 showed reduced tumor sizes compared to those given microbes from non-responding patients, demonstrating the bacterium’s potential in enhancing therapy.

Hiroyoshi Nishikawa from the Cancer Immunology division suggested that administering YB328 could improve outcomes for non-responders and further boost responses in responders.

YB328 activates immune cells, including dendritic cells, which migrate to tumor sites and enhance T-cell activation, providing a mechanism for its efficacy.

The study, published in Nature, underscores the critical role of the gut microbiome—comprising over 100 trillion bacteria—in influencing human health and cancer treatment responses.