Su1214 - Emergence of Map-Like Redness is a Risk Factor for the Development of Gastric Cancer after H. Pylori Eradication

Abstract Eradication of Helicobacter pylori colonization has been reported to affect the progression of gastric cancer. A comprehensive literature search was performed from 1997 to 2017 using electronic databases. All randomized controlled trials (RCTs) and nonrandomized controlled trials (non-RCT) evaluated the effect of H. pylori eradication on development of gastric cancer. Four RCTs and 9 non-RCTs were included (n = 40,740 participants; 321,269 person-years). Overall, H. pylori eradication therapy was associated with a significantly reduced risk of gastric cancer (incidence rate ratio (IRR) = 0.52, 95% confidence interval (CI): 0.41, 0.65). Results of mixed-effect Poisson regression meta-analysis were similar to those of traditional meta-analyses. In stratified analyses, the IRRs were 0.59 (95% CI: 0.41, 0.86) in RCTs and 0.48 (95% CI: 0.36, 0.64) in non-RCTs. The IRRs were 0.45 (95% CI: 0.34, 0.61) in patients and 0.63 (95% CI: 0.44, 0.90) in the general population. Moreover, the relative risk reduction was approximately 77% on the development of noncardiac gastric cancer with H. pylori eradication therapy in China. Attributable risk percentage and population attributable risk percentage for Chinese patients were 77.08% and 75.33%, respectively, and for Japanese patients were 57.80% and 45.99%, respectively. H. pylori eradication therapy reduces the risk of noncardiac gastric cancer development. The findings indicate the importance of early intervention with H. pylori eradication therapy from the perspective of epidemiology.

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The Rationale and Efficacy of Primary and Secondary Prevention in Adenocarcinomas of the Upper Gastrointestinal Tract

Digestive Diseases ◽

10.1159/000499706 ◽

2019 ◽

Vol 37 (5) ◽

pp. 381-393 ◽

Cited By ~ 1

Author(s):

Jan Bornschein ◽

Elizabeth L. Bird-Lieberman ◽

Peter Malfertheiner

Keyword(s):

Gastric Cancer ◽

Risk Factor ◽

Secondary Prevention ◽

Dietary Factors ◽

Oesophageal Adenocarcinoma ◽

Neoplastic Progression ◽

Treatment Techniques ◽

Risk Of Progression ◽

H Pylori ◽

Definition Of

While the primary risk factor for oesophageal adenocarcinoma (OAC) and its precursor lesion Barrett’s oesophagus (BO) is gastro-oesophageal reflux, the infection with Helicobacter pylori (H. pylori) is the dominant risk factor for gastric cancer. Reduction of reflux by dietary measures and proton pump inhibitors has some merits in OAC prevention, and the chemopreventive effect of Aspirin and statins is being widely investigated; however, improved outcome in OAC occurs primarily as the result of secondary prevention. Early detection of neoplastic lesions in Barrett’s metaplasia can be achieved by surveillance endoscopies. Novel endoscopic imaging modalities carry similar importance as the endoscopic treatment techniques as without detection of early lesions, therapy cannot be applied. Minimally invasive approaches are currently being investigated to identify patients with BO who are at particular risk of neoplastic progression. While dietary factors also play an important role in the prevention of gastric cancer and chemoprevention seems to be promising, the most beneficial effect has been shown for the eradication of H. pylori infection, which results in at least a one third reduction of gastric cancer risk. This effect can be further improved if the eradication takes place prior to the development of pre-neoplastic gastric conditions such as mucosal atrophy or intestinal metaplasia (IM). The definition of the “point of no return”, after which eradication is less effective, is of high importance, although H. pylori eradication can still be beneficial even at more advance stages of mucosal changes. For this reason, patients with advanced atrophy and IM should undergo endoscopic surveillance in the same way as patients with BO. There is also need for development of non-invasive tests to identify patients at high risk of progression to gastric cancer to improve outcome of these surveillance approaches.

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The uninvited guests of our microbiome: Helicobacter pylori and Epstein-Barr virus and their role in gastric cancerogenesis

Postępy Higieny i Medycyny Doświadczalnej ◽

10.2478/ahem-2021-0008 ◽

2021 ◽

Vol 75 (1) ◽

pp. 611-619

Author(s):

Magdalena Dzikowiec ◽

Dorota Pastuszak-Lewandoska

Keyword(s):

Gastric Cancer ◽

Epstein Barr Virus ◽

Human Microbiome ◽

Infectious Agents ◽

Gastrointestinal Microbiome ◽

Barr Virus ◽

Epstein Barr ◽

H Pylori ◽

Development Of Gastric Cancer

Abstract It is well established that human body is an ecosystem for numerous microorganisms: bacteria, fungi, eukaryotic parasites, and viruses. They form a “microbiome” that under conditions of homeostasis remains in a friendly mutual relationship with the host. However, the composition and diversity of this microbe community is dynamic and can be changed under the influence of environmental factors, such as diet, antibiotic therapy, lifestyle, and the host’s genotype and immunity. The result of gut microbiome dysbiosis can lead even to cancer. The aim of this review is the description of the healthy gastrointestinal microbiome and the role of two infectious agents: Gram-negative bacteria Helicobacter pylori and Epstein-Barr virus in the development of gastric cancer in terms of gut dysbiosis. H. pylori is the most important pathogen of gastric microbiome with clear impact on its diversity. Coinfection with Epstein-Barr virus causes chronic gastritis, and the inflammatory process is significantly increased. The process of carcinogenesis begins with chronic inflammation that causes atrophic gastritis, intestinal metaplasia, dysplasia, and finally cancer. It has been proven that chronic inflammatory infection caused by infectious agents increases the risk of stomach cancer. Molecular methods that are progressively used to explore the human microbiome provide hope that this knowledge will be used for future diagnoses and therapy in the state of its dysbiosis and in cases of gastric cancer.

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Relação do H. pylori com o desenvolvimento do câncer gástrico: revisão sistemática / Relationship of H. pylori to the development of gastric cancer: a systematic review

Brazilian Journal of Development ◽

10.34117/bjdv7n12-279 ◽

2021 ◽

Vol 7 (12) ◽

pp. 114228-114244

Author(s):

Ariane Roberta Bispo da Costa ◽

Maria Eleonora Feracin da Silva Picoli ◽

Raquel Machado Cavalca Coutinho ◽

Fernando Ananias ◽

Jacqueline Fátima Martins de Almeida Moraes

Keyword(s):

Gastric Cancer ◽

Systematic Review ◽

H Pylori ◽

Relationship Of ◽

Development Of Gastric Cancer ◽

Cáncer Gástrico

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Microbiome signatures in a fast and slow progressing gastric cancer murine model and their contribution to gastric carcinogenesis

10.1101/2020.10.15.341701 ◽

2020 ◽

Author(s):

Prerna Bali ◽

Joanna Coker ◽

Ivonne Lozano-Pope ◽

Karsten Zengler ◽

Marygorret Obonyo

Keyword(s):

Gastric Cancer ◽

Microbial Diversity ◽

Cancer Progression ◽

Double Knockout ◽

Histological Data ◽

H Pylori ◽

Faster Development ◽

Gastric Cancer Progression ◽

Development Of Gastric Cancer

AbstractGastric cancer is the third most common cancer in the world and Helicobacter spp. being one of the main factors responsible for development of cancer. Alongside Helicobacter the microbiota of the stomach mucosa may also play an important role in gastric cancer progression. Previously we had established that MyD88 deficient mice rapidly progressed to neoplasia when infected with H. felis. Thus, in order to assess the role of microbiota in gastric cancer progression we measured the changes in microbial diversity of the stomach in mice with different genotypic backgrounds (Wild type (WT), MyD88 deficient (MyD88−/−), mice deficient in the Toll/IL-1R (TIR) domain-containing adaptor-inducing interferon-β (TRIF, Triflps2), and MyD88 and Trif deficient (MyD88−/− and Trif−/−)double knockout (DKO) mice), both in uninfected and Helicobacter infected mice and its correlation of these changes with gastric cancer progression. We observed that there was an overall reduction in microbial diversity post infection with H. felis across all genotypes. Campylobacterales were observed in all infected mice, with marked reduction in abundance at 3 and 6 months in MyD88−/− mice. This low abundance of H. pylori could facilitate dominance of other organisms of microbiome like Lactobacilliales. A sharp increase in Lactobacilliales in infected MyD88−/− and DKO mice at 3 and 6 months was observed as compared to Trif−/− and WT mice suggesting its possible role in gastric cancer progression. This was further reinforced upon comparison of Lactobacillus ratio with histological data suggesting that Lactobacillales is closely associated with Helicobacter infection and gastric cancer progression. Thus, this study firstly suggests that difference in genotypes could define the stomach microbiome and make it more susceptible to development of gastric cancer upon Helicobacter infections. Secondly the increase in Lactobacillales could contribute to faster development of gastric cancer and serve as a probable bio marker for fast progressing form of gastric cancer.

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Reversal Phenomenon on the Mucosal Borderline Relates to Development of Gastric Cancer after Successful Eradication of H. pylori

Journal of Gastroenterology and Hepatology Research ◽

10.17554/j.issn.2224-3992.2017.06.703 ◽

2017 ◽

Vol 6 (2) ◽

pp. 2333-2338 ◽

Cited By ~ 2

Author(s):

Yoshitaka Nawata ◽

◽

Kazuyoshi Yagi ◽

Megumi Tanaka ◽

Atsuo Nakamura

Keyword(s):

Gastric Cancer ◽

Reversal Phenomenon ◽

H Pylori ◽

Development Of Gastric Cancer

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Gastric xanthelasma: case report

International Surgery Journal ◽

10.18203/2349-2902.isj20200313 ◽

2020 ◽

Vol 7 (2) ◽

pp. 594

Author(s):

Ana C. Almeida ◽

Emília C. Fraga ◽

Cristina P. Camacho ◽

Maria J. Amaral ◽

António Milheiro ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Case Report ◽

Predictive Marker ◽

Gastric Antrum ◽

Complete Regression ◽

Upper Gi ◽

H Pylori ◽

Single Lesion ◽

Development Of Gastric Cancer

Xanthelasma, also known as Xanthoma or lipid island, is an uncommon gastrointestinal tract (GIT) tumor-like lesion and the stomach is its most frequent location in upper GI lesions, specifically in the gastric antrum, as a single lesion. The pathogenesis appears to be related to healing processes in response to tissue damage provoked by inflammation induced by Helicobacter pylori infection. Many studies have reported that successful H. pylori eradication helps prevent gastric cancer (GC) development. We present a case of a 77 years old patient that showed endoscopic diagnosis of erythematous gastropathy, a gastric antrum xanthelasma and H. Pylori infection. After confirmed H. pylori eradication, the lesion had complete regression. The successful eradication of H. pylori probably led to a total regression of the lesion. Gastric xanthelasma (GX) has been shown to be an independent predictive marker for early GC detection after H. pylori eradication. GX could be a useful marker for predicting the development of gastric cancer.

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THE ASSOCIATION OF THE COMBINATION OF TP53 GENE CODON 72 POLYMORPHISM AND HELICOBACTER PYLORI INFECTION WITH GASTRIC CANCER

Journal of Medicine and Pharmacy ◽

10.34071/jmp.2017.1.7 ◽

2017 ◽

pp. 47-52

Author(s):

Thi Minh Thi Ha ◽

Van Huy Tran ◽

Viet Nhan Nguyen

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Risk Factor ◽

Tp53 Gene ◽

Codon 72 ◽

Codon 72 Polymorphism ◽

Pcr Rflp ◽

Two Factors ◽

Risk Patients ◽

H Pylori

Background: The interaction of environment factor and host factor plays the important role in the pathogenesis of gastric cancer (GC). This study aimed to evaluate the association of the combination of TP53 gene codon 72 polymorphism and the H. pylori infection with GC risk. Patients and methods: 112 patients with GC and 136 patients without GC were extracted DNA from specimens of gastric mucosa, then were determined TP53 gene codon 72 polymorphism by PCR-RFLP and diagnosed H. pylori infection by PCR with ureC gene-specific primers. Results: There was no significant association between TP53 gene codon 72 polymorphism and GC risk, as well as between H. pylori infection and GC risk. The combination of two factors (TP53 gene codon 72 polymorphism and H. pylori infection) was found to be associated with GC risk: The combination of Pro/Pro genotype and H. pylori (+) was the GC risk factor, OR = 2.62 (95%CI: 1.20–5.71) as compared to other combinations. In the group of H. pylori-positive patients, Pro/Pro genotype was the GC risk factor, OR = 2.42 (95%CI: 1.05 – 5.59) as compared to (Arg/Arg + Arg/Pro) group, and OR = 3.48 (95%CI: 1.23 – 9.78) as compared to Arg/Arg genotype. Conclusion: The factors of TP53 gene codon 72 polymorphism and H. pylori infection were not associated with GC risk as assessed separately, but they had the interaction associated with GC risk. Key words: TP53 gene codon 72 polymorphism, Helicobacter pylori, gastric cancer

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Molecular characterization of the stomach microbiota in patients with gastric cancer and in controls

Journal of Medical Microbiology ◽

10.1099/jmm.0.007302-0 ◽

2009 ◽

Vol 58 (4) ◽

pp. 509-516 ◽

Cited By ~ 156

Author(s):

Johan Dicksved ◽

Mathilda Lindberg ◽

Magnus Rosenquist ◽

Helena Enroth ◽

Janet K. Jansson ◽

...

Keyword(s):

Gastric Cancer ◽

Gastric Acid ◽

Rflp Analysis ◽

Rrna Gene ◽

Bacterial Phyla ◽

Increased Risk ◽

H Pylori ◽

Development Of Gastric Cancer

Persistent infection of the gastric mucosa by Helicobacter pylori can initiate an inflammatory cascade that progresses into atrophic gastritis, a condition associated with reduced capacity for secretion of gastric acid and an increased risk of developing gastric cancer. The role of H. pylori as an initiator of inflammation is evident but the mechanism for development into gastric cancer has not yet been proven. A reduced capacity for gastric acid secretion allows survival and proliferation of other microbes that normally are killed by the acidic environment. It has been postulated that some of these species may be involved in the development of gastric cancer; however, their identities are poorly defined. In this study, the gastric microbiota from ten patients with gastric cancer was characterized and compared with that from five dyspeptic controls using the molecular profiling approach terminal restriction fragment length polymorphism (T-RFLP), in combination with 16S rRNA gene cloning and sequencing. T-RFLP analysis revealed a complex bacterial community in the cancer patients that was not significantly different from that in the controls. Sequencing of 140 clones revealed 102 phylotypes, with representatives from five bacterial phyla (Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria and Fusobacteria). The data revealed a relatively low abundance of H. pylori and showed that the gastric cancer microbiota was instead dominated by different species of the genera Streptococcus, Lactobacillus, Veillonella and Prevotella. The respective role of these species in development of gastric cancer remains to be determined.

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