Abstract
The global cancer burden of new cases of various types rose with millions of death in 2018. Based on the data extracted by GLOBOCAN 2018, gastric cancer (GC) is the third leading cause of mortality related to cancer across the globe. Carcinogenic or oncogenic infections associated with Helicobacter pylori (Hp) are regarded as one of the essential risk factors for GC development. It contributes to the increased production of cytokines that cause inflammation prior to their growth in the host cells. Hp infections and specific types of polymorphisms within the host cells encoding cytokines are significant contributors to the hostʼs increased susceptibility in terms of the development of GC. Against the backdrop of such an observation is that only a small portion of the cells infected can become malignant. The diversities are a consequence of the differences in the pathogenic pathway of the Hp, susceptibility of the host, environmental conditions, and interplay between these factors. It is evident that hosts carrying cytokine genes with high inflammatory levels and polymorphism tend to exhibit an increased risk of development of GC, with special emphasis being placed on the host cytokines gene polymorphisms.
Highlights
Helicobacter is one of the genera of enteric microbes and has been known to reside within humansgastric epithelial tissue. e genus contains various species of Gram-negative bacteria, including oncogenic Helicobacter pylori (Hp), which is one of the primary causes of gastric cancer (GC) [1, 2]. e stomach of the enteric system is the most suitable anatomical niche for colonization of Hp, which results in the development of chronic gastritis, ulcerative colitis, and the malignant transformation of the gastric mucosa with the inclusion of the mucosal-associated lymphoid tissue (MALT) lymphoma [3]. e oncogenic effects of this pathogen account for more than 75% of gastric malignancy [4]
Stomach cancer is regarded as one of the most common malignancies and one of the leading contributors to deaths related to cancer across the world [7, 8], with more than 50% of the worlds total cases being exhibited in eastern Asia and majorly in China [9]. e reasons behind the reductions in such enormous levels of mortalities related to GC are not fully documented, even though researchers have attributed the decline to the alteration of the lifestyle and dietary factors and steps towards the adoption of healthy
Hp is characteristic in terms of its genetic diversity across the species [22, 23], nucleotide sequence diversity of the individual genes associated with the high rates of mutation, and high level of recombination across the species [24, 25]. e strains from different human hosts are distinct in many aspects, including the sequences of the specific genes, as they exhibit variations in the contents of the genes and the organization of chromosomes. e primary genome of Hp is comprised of 1,100 genes that are exhibited in all strains, with each of the strains comprising of other hundreds of additional genes that are not currently present on the universal basis
Summary
Helicobacter is one of the genera of enteric microbes and has been known to reside within humansgastric epithelial tissue. e genus contains various species of Gram-negative bacteria, including oncogenic Helicobacter pylori (Hp), which is one of the primary causes of gastric cancer (GC) [1, 2]. e stomach of the enteric system is the most suitable anatomical niche for colonization of Hp, which results in the development of chronic gastritis, ulcerative colitis, and the malignant transformation of the gastric mucosa with the inclusion of the mucosal-associated lymphoid tissue (MALT) lymphoma [3]. e oncogenic effects of this pathogen account for more than 75% of gastric malignancy [4]. E stomach of the enteric system is the most suitable anatomical niche for colonization of Hp, which results in the development of chronic gastritis, ulcerative colitis, and the malignant transformation of the gastric mucosa with the inclusion of the mucosal-associated lymphoid tissue (MALT) lymphoma [3]. Hp-induced persistent chronic inflammation has been reported to be linked with epithelial dysplasia, and this precancerous stage further developed into GC following the oncogenic cascades [13, 14]. From the observation that Hp relies on the gastric mucosa of the host cell as an opportunistic pathogen, whenever it gets the opportunity to transform the epithelial cells, it depends on the oncogenic cascades targeting dysregulation of specific cytokines to cause cancer (Figure 1). Hp-induced generation of reacting free radical species tends to promote malignant transformation of inflamed gastric epithelia [17]. E combined effect of hypergastrinemia, inflammasomes, pathobionts, and exogenous and endogenous oxidative stresses, including the host-derived oncogenic factors, tends to trigger tumorigenesis [16, 17, 19,20,21]. ese multifactorial disorders forced the cellular genome to perform aberrant regulation of the cell cycle, leading to the genetic and epigenetic alteration that results in malignant transformations
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