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More than half of all colorectal cancers are sporadic, or nonhereditary. A key driver in the development of sporadic colorectal cancer is dysbiosis – an imbalance in the type and number of microbes that typically reside in the human gut. A recent study found that colorectal dysbiosis induced epigenetic changes and promoted the development of precancerous lesions in the guts of fecal transplant recipient mice.
The authors of the study transplanted fecal samples from healthy individuals or from individuals with sporadic colorectal cancer into the guts of 136 germ-free mice. Seven and 14 weeks after the transfer, the mice were assessed for dysbiosis, epigenetic changes in their colonic cell DNA, and the presence of aberrant crypt foci (ACF) – precancerous lesions associated with the development of colorectal cancer.
The mice that received fecal transplants from people with colorectal cancer had dysbiosis and exhibited higher numbers of ACF compared to those that received transplants from healthy people. The mice also exhibited hypermethylation of specific genes. Hypermethylation is a type of epigenetic modification of DNA that drives gene expression and is associated with increased risk for developing ACF.
Based on these findings, the study authors then analyzed the blood of 1,000 people who were scheduled for routine colonoscopy, looking for the presence of specific colonic bacteria (dysbiosis) and indications of hypermethylation of the same genes identified in the mice. They found that hypermethylation of these genes correlated with sporadic colorectal cancer incidence, which could potentially serve as a diagnostic marker for the disease.