Performance of DNA Methylation on the Molecular Pathogenesis of Helicobacter pylori in Gastric Cancer; targeted therapy approach

Gastric cancer (GC) is a significant cause of cancer mortality which has led to focused ex-ploration of the pathology of GC. The advent of genome-wide analysis methods has made it possible to uncover genetic and epigenetic fluctuation such as abnormal DNA methyla-tion in gene promoter regions that is expected to play a key role in GC. The study of gastric malignancies requires an etiological perspective, and Helicobacter pylori (H. pylori) was identified to play a role in GC. H. pylori infection causes chronic inflammation of the gastric epithelium causing abnormal polyclonal methylation, which might raise the risk of GC. In the last two decades, various pathogenic factors by which H. pylori infection causes GC have been discovered. Abnormal DNA methylation is triggered in several genes, rendering them inactive. In GC, methylation patterns are linked to certain subtypes including micro -satellite instability. Multiple cancer-related processes are more usually changed by abnor-mal DNA methylation than through mutations, according to current general and combined investigations. Furthermore, the amount of acquired abnormal DNA methylation is heavily linked to the chances of developing GC. Therefore, we investigated abnormal DNA meth-ylation in GC and the link between methylation and H. pylori infection.

Automated summary

Gastric cancer is a major cause of cancer mortality, and abnormal DNA methylation in gene promoter regions plays a key role in the development of gastric cancer. Helicobacter pylori infection is identified to be associated with gastric cancer. Abnormal DNA methylation triggers inactivation of multiple genes, and is more common in cancer-related processes than mutations. The extent of abnormal DNA methylation is closely linked to the risk of developing gastric cancer.