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Cancers
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Association of Helicobacter pylori with Gastric Cancer
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Association of Helicobacter pylori with Gastric Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Infectious Agents and Cancer".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 6189

Special Issue Editors

Prof. Dr. Markus Gerhard

E-Mail Website
Guest Editor
Institute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany
Interests: mechanisms of host-pathogen interaction during chronic infection, inflammation and carcinogenesis
Dr. Raquel Mejias-Luque

E-Mail Website
Guest Editor
Institute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany
Interests: mechanisms of host-pathogen interaction during chronic infection, inflammation and carcinogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

With more than 1 million new cases worldwide in 2020, gastric cancer represents the 5th most common cancer and the 4th most common cause of cancer-related death. Although gastric cancer is a very heterogeneous malignant disease, infection with Helicobacter pylori still represents the major risk factor for its development. This is mainly due to the ability of the bacterium to manipulate the host’s immune response and alter epithelial cell homeostasis. Therefore, the study of the molecular mechanisms by which H. pylori induces gastric pathology is extremely important to understand gastric cancer development and identify novel therapeutic strategies to prevent it.

We are pleased to invite you to contribute to the Special Issue “Association of Helicobacter pylori with Gastric Cancer”. In this Special Issue, we will focus on the identification of the mechanisms of infection, alterations of immune and epithelial cell responses, as well as changes in microbiota induced by infection to better understand the contribution of H. pylori infection to gastric carcinogenesis. Original research articles and reviews are welcome.

We look forward to receiving your contributions.

Prof. Dr. Markus Gerhard
Dr. Raquel Mejias-Luque
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • gastric cancer
  • Helicobacter pylori

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Published Papers (3 papers)

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Research

24 pages, 5257 KiB  
Article
Study of Helicobacter pylori Isolated from a High-Gastric-Cancer-Risk Population: Unveiling the Comprehensive Analysis of Virulence-Associated Genes including Secretion Systems, and Genome-Wide Association Study
by Batsaikhan Saruuljavkhlan, Ricky Indra Alfaray, Khasag Oyuntsetseg, Boldbaatar Gantuya, Ayush Khangai, Namsrai Renchinsengee, Takashi Matsumoto, Junko Akada, Dashdorj Azzaya, Duger Davaadorj and Yoshio Yamaoka
Cancers 2023, 15(18), 4528; https://doi.org/10.3390/cancers15184528 - 12 Sep 2023
Cited by 2 | Viewed by 1914
Abstract
Background: The prevalence of gastric cancer in Mongolia, in East Asia, remains the highest in the world. However, most Helicobacter pylori strains in Mongolia have a less virulent Western-type CagA. We aimed to determine how H. pylori genomic variation affected gastric diseases, especially [...] Read more.
Background: The prevalence of gastric cancer in Mongolia, in East Asia, remains the highest in the world. However, most Helicobacter pylori strains in Mongolia have a less virulent Western-type CagA. We aimed to determine how H. pylori genomic variation affected gastric diseases, especially gastric cancer, based on comprehensive genome analysis. Methods: We identified a set of 274 virulence-associated genes in H. pylori, including virulence factor and outer membrane protein (OMP) genes, the type four secretion system gene cluster, and 13 well-known virulence gene genotypes in 223 H. pylori strains and their associations with gastric cancer and other gastric diseases. We conducted a genome-wide association study on 158 H. pylori strains (15 gastric cancer and 143 non-gastric cancer strains). Results: Out of 274 genes, we found 13 genes were variable depending on disease outcome, especially iron regulating OMP genes. H. pylori strains from Mongolia were divided into two main subgroups: subgroup (Sg1) with high risk and Sg2 with low risk for gastric cancer. The general characteristics of Sg1 strains are that they possess more virulence genotype genes. We found nine non-synonymous single nucleotide polymorphisms in seven genes that are linked with gastric cancer strains. Conclusions: Highly virulent H. pylori strains may adapt through host-influenced genomic variations, potentially impacting gastric carcinogenesis. Full article
(This article belongs to the Special Issue Association of Helicobacter pylori with Gastric Cancer)
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12 pages, 1935 KiB  
Article
Increased IL-17A Serum Levels and Gastric Th17 Cells in Helicobacter pylori-Infected Patients with Gastric Premalignant Lesions
by Chiara Della Bella, Sofia D’Elios, Sara Coletta, Marisa Benagiano, Annalisa Azzurri, Fabio Cianchi, Marina de Bernard and Mario Milco D’Elios
Cancers 2023, 15(6), 1662; https://doi.org/10.3390/cancers15061662 - 8 Mar 2023
Cited by 5 | Viewed by 1801
Abstract
Background: Helicobacter pylori infection is characterized by an inflammatory infiltrate that might be an important antecedent of gastric cancer. The purpose of this study was to evaluate whether interleukin (IL)-17 inflammation is elicited by gastric T cells in Helicobacter pylori patients with [...] Read more.
Background: Helicobacter pylori infection is characterized by an inflammatory infiltrate that might be an important antecedent of gastric cancer. The purpose of this study was to evaluate whether interleukin (IL)-17 inflammation is elicited by gastric T cells in Helicobacter pylori patients with gastric intestinal metaplasia and dysplasia (IM/DYS). We also investigated the serum IL-17A levels in Helicobacter pylori patients with gastric intestinal metaplasia and dysplasia, and patients with Helicobacter pylori non-atrophic gastritis (NAG). Methods: the IL-17 cytokine profile of gastric T cells was investigated in six patients with IM/DYS and Helicobacter pylori infection. Serum IL-17A levels were measured in 45 Helicobacter pylori-infected IM/DYS patients, 45 Helicobacter pylori-infected patients without IM/DYS and in 45 healthy controls (HC). Results: gastric T cells from all IM/DYS patients with Helicobacter pylori were able to proliferate in response to Helicobacter pylori and to produce IL-17A. The Luminex analysis revealed that IL-17A levels were significantly increased in Helicobacter pylori IM/DYS patients compared to healthy controls and to Helicobacter pylori gastritis patients without IM/DYS (452.34 ± 369.13 pg/mL, 246.82 ± 156.06 pg/mL, 169.26 ± 73.82 pg/mL, respectively; p < 0.01, p < 0.05). Conclusions: the results obtained indicate that Helicobacter pylori is able to drive gastric IL-17 inflammation in IM/DYS Helicobacter pylori-infected patients, and that IL-17A serum levels are significantly increased in Helicobacter pylori-infected patients with IM/DYS. Full article
(This article belongs to the Special Issue Association of Helicobacter pylori with Gastric Cancer)
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18 pages, 6033 KiB  
Article
Aberrant Methylation of Somatostatin Receptor 2 Gene Is Initiated in Aged Gastric Mucosa Infected with Helicobacter pylori and Consequential Gene Silencing Is Associated with Establishment of Inflammatory Microenvironment In Vitro Study
by Hee-Jin Kim, Jong-Lyul Park, Byoung-Ha Yoon, Keeok Haam, Haejeong Heo, Jong-Hwan Kim, Seon-Young Kim, Mirang Kim, Woo-Ho Kim, Sang-Il Lee, Kyu-Sang Song, Kwang-Sung Ahn and Yong Sung Kim
Cancers 2022, 14(24), 6183; https://doi.org/10.3390/cancers14246183 - 14 Dec 2022
Cited by 1 | Viewed by 1740
Abstract
The loss-of-function variants are thought to be associated with inflammation in the stomach. We here aimed to evaluate the extent and role of methylation at the SSTR2 promoter in inflammation and gastric tumor formation. A whole-genome bisulfite sequencing analysis revealed that the SSTR2 [...] Read more.
The loss-of-function variants are thought to be associated with inflammation in the stomach. We here aimed to evaluate the extent and role of methylation at the SSTR2 promoter in inflammation and gastric tumor formation. A whole-genome bisulfite sequencing analysis revealed that the SSTR2 promoter was significantly hypermethylated in gastric tumors, dysplasia, and intestinal metaplasia compared to non-tumor tissues from patients with gastric cancer. Using public data, we confirmed SSTR2 promoter methylation in primary gastric tumors and intestinal metaplasia, and even aged gastric mucosae infected with Helicobacter pylori, suggesting that aberrant methylation is initiated in normal gastric mucosa. The loss-of-function of SSTR2 in SNU638 cell-induced cell proliferation in vitro, while stable transfection of SSTR2 in AGS and MKN74 cells inhibited cell proliferation and tumorigenesis in vitro and in vivo. As revealed by a comparison of target genes differentially expressed in these cells with hallmark molecular signatures, inflammation-related pathways were distinctly induced in SSTR2-KO SNU638 cell. By contrast, inflammation-related pathways were inhibited in AGS and MKN74 cells ectopically expressing SSTR2. Collectively, we propose that SSTR2 silencing upon promoter methylation is initiated in aged gastric mucosae infected with H. pylori and promotes the establishment of an inflammatory microenvironment via the intrinsic pathway. These findings provide novel insights into the initiation of gastric carcinogenesis. Full article
(This article belongs to the Special Issue Association of Helicobacter pylori with Gastric Cancer)
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