That study, published in 2013, was the first to prove that bacterial DNA can impact carcinogenesis. Acute myeloid leukemia showed the highest integration of bacterial DNA, but gastric adenocarcinoma was a close second. Most of the species were of the Proteobacteria lineages (83%), with a third of that represented by Pseudomonas, particularly P. fluorescens and P. aeruginosa. Both of those species have been shown to promote gastric tumorigenesis in rats. All of the DNA integrations occurred in five genes; four of these are already known to be upregulated in gastric cancer (PLOS Comp Biol. 2013;9[6]:e1003107).
Interestingly, only a few of the sample reads turned up DNA integration with H. pylori.
This reduction in gastric microbial diversity could be an important key to H. pylori’s relation to gastric cancer, Dr. Peek said. He examined this in residents of two towns in Colombia, South America: Tumaco, where the risk of gastric cancer is low, and Tuquerres, where it’s 25 times higher (Sci Rep. 2016. doi:10.1038/srep18594).
What was different was the gastric microbiome of residents. Those living in low-risk Tumaco had much more microbial diversity: 361 varieties, compared with 194 in Tuquerres. And 16 of these groups – representative of what’s usually considered a healthy microbiome – were absent in the high-risk subjects. But Tuquerres residents had two bacteria that weren’t found in Tumaco residents, including Leptorichia wadei, which has been associated with necrotizing enterocolitis.
There was no difference, however, in the prevalence of H. pylori between these high- and low-risk groups.
These new findings illustrate an increasingly complicated interplay of bacteria and gastric cancer, Dr. Peek said. But they also provide a new direction for research.
“We have a framework now where we can move forward and try to understand how some of these other strains impact gastric cancer risk,” he said.
Dr. Peek had no relevant financial disclosures.
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