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INTERNATIONAL CONGRESS OF

CancerGenetics

• The effect of Helicobacter pylori (H. pylori) on Gastric Cancer (GC)

• Zahra Amirkhani,¹ Ali Rezaeian,^2,* Aidin Amini Sefidab,³
  1. Student Research Committee, Larestan University of Medical Sciences, Larestan, Iran.
  2. Student Research Committee, Larestan University of Medical Sciences, Larestan, Iran.
  3. Student Research Committee, Larestan University of Medical Sciences, Larestan, Iran.
  
  
  
• Introduction: Gastric cancer (GC) remains the fifth most common malignant tumor and the third leading cause of cancer death, despite the decline in incidence and mortality worldwide over the past five decades. Helicobacter pylori is the predominant species of the human stomach microbiome, and its proliferation causes a persistent inflammatory reaction. Gastritis caused by H. pylori is the strongest unique risk factor for stomach cancer; however, only a small proportion of infected people develop malignancy. Two distinct histological types of stomach cancer have been described, each with different pathophysiological characteristics. Gastric cancer of the dispersed type usually affects young people and includes neoplastic cells individually that do not form the structure of the glands. The more common form of stomach cancer progresses through a series of histological stages that begin with the transition from normal mucus to chronic superficial gastritis, which then leads to atrophic gastritis and intestinal metaplasia and eventually to dysplasia and adenocarcinoma2. Helicobacter pylori is a microbial species that specifically colonizes the stomach epithelium and is the most common bacterial infection worldwide. The effectiveness of eradicating H. pylori has been proven for GC and Prevention of precancerous lesions in different populations. H. pylori, such as intestinal microbiota dysbiosis, has remained metabolic effects and increased prevalence of antibiotic-resistant pathogens. Previous retrospective studies had reported dysbiosis microbial communities, altered bacterial interactions, and an overreach of intestinal buds in GC and precancerous lesions. Non-H stomach bacteria. pylori may also play an important role in stomach carcinogenesis, although the exact mechanism has not yet been determined. But our goal in this study is to continue to examine the effect of the most common bacterial infection and its conversion to stomach cancer.
• Methods: In this study,15 articles published from 2016 to 2024, which were in the form of original research and systematic review were examined. The study used the keywords Gastric Cancer(GC), New model for Diagnosis of cancer, H.pylori.
• Results: Almost 700,000 people are diagnosed with this malignant cancer every year, and the 5-year survival rate in the United States is <15% 1. Microbial network analysis showed that the presence of H. pylori affects the strength of microbial gastric interactions, which may be associated with GC progression. However, whether H. pylori can act as a bacterial driver and interact with other stomach bacteria that are later involved in the carcinogenic process, still unknown. Until now, studies characterizing changes in the entire micro-gastrointestinal ecosystem on the eradication of H. pylori is limited. Inflammation of the stomach is known to be associated with the risk of disease here, in which gastritis anthral is associated with duodenal ulcer, as well as pangasteritis can lead to ulcers of the stomach and adenocarcinoma. Duodenal ulcer processes as a result of the colonization of the stomach by H. pylori is initially caused by inflammation caused by H. pylori is created. This then leads to a decrease in the number of D cells that produce somatostatin that prevents the release of the stomach. This is known as higher gastric levels in patients with H. pylori is seen positive and therefore increased acid secretion (caused by the stomach) in the stomach body. The next step to increase the risk of duodenal ulcer remains disputed, with this increased acid secretion potentially contributing to the formation of gastric metaplasia in duodenum; this can also be achieved by H. pylori to be colonized to lead to further inflammation and scarring.
• Conclusion: Studies that focus on specific interactions between H. pylori and its host focus can provide models for general patterns that may spread to other malignancies that develop from inflammatory foci in the liver and digestive tract. Most cellular liver cancers are related to chronic hepatitis B and hepatitis C infections, and biliary tract cholangiocarcinoma is strongly associated with chronic inflammation caused by parasites. Chronic esophagitis, pancreatitis and ulcerative colitis each significantly increase the risk of adenocarcinoma at their respective anatomical sites. Focusing on colorectal neoplasia, commonalities between inflammatory-induced stomach cancer and cancers that arise in the context of ulcerative colitis have been reported. It is hoped that in the near future, according to the studies carried out, the progress of this problem and the resulting issues can be prevented.
• Keywords: Gastric Cancer(GC), New model for Diagnosis of cancer, H.pylori