Association Between Helicobacter pylori and Gastric Carcinoma

Abstract

Gastric carcinoma is the third leading cause of cancer mortality worldwide. In 2018, the incidence of gastric carcinoma worldwide was over 1,000,000 new cases, with approximately 783,000 deaths. The rate of new cases is noticeably increased in Eastern Asia. Helicobacter pylori is responsible for the increased incidence of gastric cancer. In the year 2015, H. pylori had an approximate prevalence of 4.4 billion positive cases worldwide, with the most positive cases found within the region of Africa, Latin America and the Caribbean, and of Asia. H. pylori is known to have multiple strains which allow it to survive in the host cell epithelium chronically. Research has shown many factors which play a significant role in developing infection and thereafter its progression to gastric carcinoma. After H. pylori colonizes the gastric mucosa, its effects can be potentiated by virulence factors, host factors, and environmental factors. H. pylori contains virulence factors that aid in the adhesion, translocation, inflammation, and infectivity of the host gastric epithelium. It alters the functions of the host immune response and cytokines, utilizing these factors to invade and persist in the gastric epithelium for a long period of time. The human body will identify H. pylori to be foreign and will exacerbate an inflammatory response in an effort to eradicate the bacterium. Consequently, this will cause H. pylori to induce a serious infection which may progress to cancer. In this review, we will discuss the various factors involved in the infectious process of H. pylori and how they help the infection progress to gastric carcinoma. This will allow us to better understand and modulate treatments to effectively eradicate this bacterium before it triggers the body into developing cancer.

Feeding Fiber-Bound Polyphenol Ingredients at Different Levels Modulates Colonic Postbiotics to Improve Gut Health in Dogs

“…Like hesperidin, ponciretin has shown anticancer and anti-inflammatory effects, with cytotoxic effects on a colon cancer cell line in vitro [ 27 ] and attenuating colitis in mice by the anti-inflammatory effects of suppressing NF-κB activation and correcting the imbalance of Th17/Treg cells [ 33 , 34 ]. In addition, ponciretin can inhibit the growth of Helicobacter pylori [ 35 ], a bacterium implicated in gastritis, stomach ulcers, and lymphomas of the gastrointestinal tract [ 36 ].…”

Clinicopathological Study of Helicobactor Pylori Infection and Gastric Carcinoma at a Tertiary Care Hospital in Kathmandu

“…Zhang et a1 13 reported that H. pylori infects more than half of the world's population and the infection is usually acquired in childhood and remains for life long. Similarly, Tiwari et al 14 mentioned that younger patients (less than 45 years) from the Indian sub-continent infected with H. pylori have higher risk of developing gastric carcinoma while, Thapa et al 4 found the common age group for the H. pylori infection in both the sexes is between 61-70 years and the infection is highly prevalent in distal gastric carcinoma.…”

“…3 The invasion and colonization of the gastric mucosa by H. pylori is strengthened by host factors, environmental factors and virulence factors like adhesion, translocation, and inflammation of the host gastric epithelium which changes the normal host immune response and cytokines to remain in the gastric epithelium for an extended period of time. 4 The human immune system identifies H. pylori as a foreign particle and provokes the inflammatory response to eradicate the bacterium from the body which induces the serious infection and may further progress to cancer. 5 The chronic infection with H. pylori bacteria is the most important risk factor for the development of non-cardia gastric cancer and lower grade B-cell mucosa associated lymphoid tissue (MALT) lymphoma estimating 6,60,000 cancer cases in the year 2008 attributed to H. pylori and corresponding to 5.2% of the total burden from all cancers globally.…”

Helicobacter pylori-Induced Progranulin Promotes the Progression of the Gastric Epithelial Cell Cycle by Regulating CDK4

“…Eradication of H. pylori reduces the incidence of gastric cancer [ 48 , 49 ]. Current research has shown that a variety of virulence factors produced by H. pylori , for instance, CagA, VacA, HtrA, Baba, Saba, and oipa, can help it attach to gastric epithelial cells, cause the host immune system to release various pro-inflammatory cytokines and chemokines and activate multiple signal pathways, such as the NF-κB, Wnt/β-catenin, and PI3K/Akt/mTOR pathways, which affect cell proliferation and differentiation, and promote the transformation of normal gastric epithelial cells into cancer cells [ 50 , 51 ]. In this study, we demonstrated that H. pylori increased the proliferative activity of gastric epithelial cells in a certain range, and the increased activity was positively correlated with the number of bacteria loaded.…”