Journal of Molecular Oncology Research

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Rapid Communication - Journal of Molecular Oncology Research (2022) Volume 6, Issue 7

The interaction of Helicobacter pylori with cancer immunomodulatory stromal cells: Modern knowledge into gastric cancer pathogenesis.

Amirhossen Sahebkar*

Department of Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

*Corresponding Author:
Amirhossen Sahebkar
Department of Applied Biomedical Research Center
Mashhad University of Medical Sciences, Mashhad, Iran

Received: 29-June-2022, Manuscript No. AAMOR-22-69683; Editor assigned: 01-July-2022, Pre QC No. AAMOR-22-69683(PQ); Reviewed: 15-July-2022, QC No. AAMOR-22-69683; Revised: 22-July-2022; AAMOR-22-69683(R); Published: 29-July-2022, DOI: 10.35841/aamor-6.7.132

Citation: Sahebkar A. The interaction of Helicobacter pylori with cancer immunomodulatory stromal cells: Modern knowledge into gastric cancer pathogenesis. J Mol Oncol Res. 2022;6(7):132

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Gastric cancer is the fourth most common cause of cancer-linked passings within the world. Gastric tumor cells have organic characteristics such as fast expansion, tall invasiveness, and sedate resistance, which result in repeat and destitute survival. Helicobacter pylori (H. pylori) has been proposed as a first-class carcinogen for gastric cancer agreeing to the 1994 world wellbeing organization (WHO) classification. One of the vital instruments by which H. pylori influences the gastric environment and advances carcinogenesis is activating irritation. H. pylori actuates an fiery reaction and a plenty of distinctive flag transduction forms, driving to gastric mucosal unsettling influence, incessant gastritis, and a multi-step complex pathway that starts carcinogenesis. It appears irrefutable that the interaction between different cell sorts, counting resistant cells, gastric epithelium, organs, and stem cells, is crucial for the movement and advancement of carcinogenesis concerning H. pylori. The intelligent of H. pylori with encompassing cells play a key part in cancer movement


Cancer-associated fibroblasts, Helicobacter pylori, Tumor-associated macrophages, Myeloid-derived suppressor


Gastric cancer is the fourth most common cause of cancer- associated passings all over the world. Ninety percent of all stomach tumors are decided to be threatening. In spite of the fact that the predominance of gastric cancer has been declining over the past a few a long time, it is still a critical healthcare issue. In spite of specialized headways in medicines, counting focused on treatment, adjuvant chemotherapy, radiotherapy, and progressed surgical strategies, patients still encounter cancer metastasis and repeat [1]. Gastric tumor cells have a few natural characteristics, such as quick multiplication, tall invasiveness, and anti-apoptotic properties, which ordinarily result in repeat and destitute survival. Furthermore, in a few cases, helpful resection isn't conceivable due to the intrusive nature of gastric cancer. The forecast of progressed and metastatic gastric cancer with both broad lymph hub intrusion and metastasis is destitute, while early discovery of gastric cancer is related with great survival.

As Rudolf Virchow depicted numerous a long time prior, the tumor microenvironment is accepted to play a urgent part within the improvement of tumors [2]. Aggravation within the tumor microenvironment impacts numerous harm highlights, counting the development and survival of tumor cells, metastasis, and angiogenesis. The relationship between cancer and irritation can result from two pathways: an natural pathway, decided by hereditary changes, such as oncogenes, that lead to neoplasia and aggravation; and an outward pathway, actuated by incendiary leukocytes within the setting of unremitting contaminations and tireless incendiary conditions, such as Helicobacter pylori (H. pylori) contamination as well as incendiary bowel infection (IBD), which increment cancer hazard.

There are a few hazard components for gastric cancer, counting H. pylori contamination, hereditary have, and natural factors. The degree to which H. pylori disease is recognized as a chance calculate for gastric adenocarcinoma can shift enormously over different populaces with moderately comparative rates H. pylori contamination. The interaction between H. pylori strains and the different gastric microbiota complexes is one of the plausible causes of these contrasts. Most H. pylori strains can adjust the gastric environment and consequently influence the territory of inhabitant microbes to raise the chance of gastric carcinogenicity. The stomach highlights a particular microbiota of five primary phylae, counting Proteobacteria, Firmicutes, Actinobacteria, Bacteroidetes, and Fusobacteria. Most discoveries illustrate that H. pylori-positive and -negative microbiota are primarily ruled by the same phyla, yet with distinctive relative rates. The transcendent phyla within the pediatric populace were moreover Proteobacteria, Firmicutes, Bacteroides, and Actinobacteria. Be that as it may, the relative extents contrasted between H. pylori-positive and negative children
. In another ponder, H. pylori-positive people appeared critical concentrations of Proteobacteria, Spirochetes, and Acidobacteria, but Actinoculitis, Bacteroidetes and Firmicutis were distinguished as it were to a constrained degree. Subsequently, the association of H. pylori in gastric clutters may well be intervened by the gastric microbiota composed of as it were 3 species of commensal gastric and intestinal microbiota (Clostridium, Bacteroides, and Lactobacillus) in combination with H. pylori disease which was adequate to fortify gastric neoplasia in germ-free mice. It can be concluded that these genera are expanded within the stomachs of patients with premalignant and harmful injuries [3].

Past investigate has appeared that the microbiota may either contribute to pernicious impacts by creating carcinogenic nitrosamines beneath hypochlorhydria conditions or appear useful impacts by moving forward the mending of gastric ulcers, decreasing the emission of pro-inflammatory cytokines, or inactivating H. pylori colonization. An examination of patients at assorted histologic stages of gastric carcinogenesis uncovered an converse relationship between H. pylori plenitude and microbial differing qualities in non-cancer gastric biopsies, but gastric cancer was related with a lower differences compared to other tests with comparative H. pylori plenitude, while anti-microbial treatment turned around the distinction [4]. Children with H. pylori disease are more likely to have helminth contaminations and have been appeared to have a lower chance of survival for gastric adenocarcinoma.

A later think about inspected gastric biopsy examples some time recently, and one year after H. pylori annihilation. It was illustrated that Roseburia and Sphingomonas were diminished in people with inveterate irritation one year after H. pylori destruction. The event and perseverance of gastric decay and intestinal metaplasia one year after H. pylori annihilation were related with a cluster of verbal microscopic organisms that included Peptostreptococcus, Parvimonas, Streptococcus, Granulicatella, and Rothia. This consider bolsters the suspicion that the nearness of H. pylori gives distinctive microbiome specialties that contribute to the advancement of gastric cancer [5].


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