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Helicobacter pylori Variations Linked to Increased Stomach Cancer Risk, Study Finds



According to findings made by Japanese researchers, individuals who also have an infection with the bacterium Helicobacter pylori have a much higher risk of developing stomach cancer than those who do not.

The study, which was published on Thursday in the New England Journal of Medicine, may aid in the creation of individualized genomic medicine to treat stomach cancer.

Stomach, or gastric, disease is the fourth driving reason for malignant growth passing around the world. A pathogenic CDH1 gene hereditary variant is one of the genetic risk factors. H. pylori infection is just one of the environmental risk factors. Because of the high virulence of H. pylori, countries in East Asia have a higher incidence of stomach cancer.

For cancer prevention, surveillance, and treatment selection, pathogenic variant testing is now common. However, there are no large-scale case-control studies on stomach cancer. These kinds of studies compare a group of people who have a disease to a similar group of people who don’t. Using a large case-control study of Japanese participants, the researchers wanted to see how pathogenic variants interact with environmental factors like H. pylori to change the risk of stomach cancer.

The team used genomic analysis to look for 27 genes associated with hereditary tumors in DNA samples from over 11,000 participants with stomach cancer and 44,000 participants without stomach cancer to determine whether the participants were carriers of pathogenic variants. Nine genes were found to have a strong connection to the risk of stomach cancer in their analysis.

The scientists then, at that point, broke down the communication between the pathogenic variations in the nine qualities and H. pylori, still up in the air by persistent history. They discovered that when a pathogenic variant and H. pylori infection were present together, the risk of stomach cancer was significantly higher than when either factor was present alone. Four of the nine genes were particularly intriguing because they encode proteins that typically aid in DNA repair. These pathogenic variations might worsen the harm done by H. pylori contamination, which prompts malignant growth by advancing DNA twofold strand breaks and weakening stomach cell DNA. The risk of developing gastric cancer appears to be significantly raised when this damage is combined with genetic variants that prevent normal damage repair.

Since the predominance of H. pylori contamination is high, and its annihilation troublesome, evaluating for pathogenic variations can assist with figuring out who ought to be focused on for mediations. It is still a top priority to eliminate H. pylori and lower the risk of stomach cancer by testing for and eliminating the infection, regardless of whether individuals carry the pathogenic variants. This study is part of a larger effort to learn how genetic and environmental factors interact to better prevent and treat cancer.

Yukihide Momozawa, a co-author and researcher at the Riken Center for Integrative Medical Sciences, stated in a statement, “Our study will contribute to medical practice guidelines on gastric cancer and pathogenic variants, and is expected to contribute to establishing a tailor-made genomic medicine system, including improved diagnostic accuracy, development of therapies targeting causative genes, and more appropriate preventive measures for gastric cancer.”

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