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

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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Relationship of Anti-Lewis x and Anti-Lewis y Antibodies in Serum Samples from Gastric Cancer and Chronic Gastritis Patients toHelicobacter pylori-Mediated Autoimmunity

Infection and Immunity ◽

10.1128/iai.69.8.4774-4781.2001 ◽

2001 ◽

Vol 69 (8) ◽

pp. 4774-4781 ◽

Cited By ~ 25

Author(s):

Michael A. Heneghan ◽

Ciaran F. McCarthy ◽

Daiva Janulaityte ◽

Anthony P. Moran

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Antibody Production ◽

Enzyme Linked Immunosorbent Assay ◽

Serum Samples ◽

Lewis Y ◽

H Pylori ◽

Negative Controls ◽

Relationship Of

ABSTRACT Lewis (Le) antigens have been implicated in the pathogenesis of atrophic gastritis and gastric cancer in the setting ofHelicobacter pylori infection, and H. pylori-induced anti-Le antibodies have been described that cross-react with the gastric mucosa of both mice and humans. The aim of this study was to examine the presence of anti-Le antibodies in patients with H. pylori infection and gastric cancer and to examine the relationships between anti-Le antibody production, bacterial Le expression, gastric histopathology, and host Le erythrocyte phenotype. Anti-Le antibody production and H. pylori Le expression were determined by enzyme-linked immunosorbent assay, erythrocyte Le phenotype was examined by agglutination assays, and histology was scored blindly. Significant levels of anti-Lex antibody (P < 0.0001, T = 76.4, DF = 5) and anti-Ley antibody (P < 0.0001, T = 73.05, DF = 5) were found in the sera of patients with gastric cancer and other H. pylori-associated pathology compared with H. pylori-negative controls. Following incubation of patient sera with synthetic Le glycoconjugates, anti-Lex and -Ley autoantibody binding was abolished. The degree of the anti-Lex and -Leyantibody response was unrelated to the host Le phenotype but was significantly associated with the bacterial expression of Lex (r = 0.863,r 2 = 0.745, P < 0.0001) and Ley (r = 0.796,r 2 = 0.634, P < 0.0001), respectively. Collectively, these data suggest that anti-Le antibodies are present in most patients with H. pyloriinfection, including those with gastric cancer, that variability exists in the strength of the anti-Le response, and that this response is independent of the host Le phenotype but related to the bacterial Le phenotype.

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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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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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Los genes como marcadores de riesgo en cáncer gástrico: revisión de estudios en población colombiana

Respuestas ◽

10.22463/0122820x.383 ◽

2013 ◽

Vol 18 (2) ◽

pp. 61-73

Author(s):

Claudia Marcela Yáñez-Gutiérrez

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gene Polymorphisms ◽

Genetic Factors ◽

Human Gene ◽

Risk Markers ◽

Different Populations ◽

H Pylori ◽

Cáncer Gástrico

El objetivo de esta revisión, fue identificar el rol de los genes como marcadores de riesgo en cáncer gástrico (CG) en población colombiana. Se revisaron publicaciones de investigaciones realizadas en los últimos diez años, utilizando las bases MEDLINE y LILACS y complementando la pesquisa con la bibliografía relevante de los artículos. Se encontraron estudios en busca de asociación de CG con polimorfismos de varios genes humanos involucrados en la respuesta inmune, la desintoxicación y el supresor p53. En Colombia al igual que en otros países, las evidencias de asociación de polimorfismos genéticos con CG son aún controversiales, debido a la variación de los resultados que arrojan los estudios en las diferentes poblaciones. El genoma de las cepas de Helicobacter pylori que infectan población colombiana también ha sido investigado en búsqueda de polimorfismos de virulencia. El genotipo cagA/vacAs1m1 identificado como citotóxico en esta bacteria, mostró en la mayoría de las investigaciones, asociación con CG. La evidencia de asociación de CG con factores genéticos en población colombiana no es concluyente. Está lejos aún, la identificación de marcadores genéticos que permitan predecir el riesgo a desarrollar CG. A pesar de ello, algunos polimorfismos de genes humanos como los de IL-1 o los de algunas enzimas desintoxicantes, así como los genes cagA y vacA de Helicobacter pylori podrían ser candidatos a futuros marcadores de riesgo en esta neoplasia.Palabras clave: cáncer gástrico, riesgo, genotipo, Colombia. ABSTRACT The objective of this review was to identify the role of genes as risk markers in gastric cancer (GC) in Colombian population studies. The study reviewed research publications in the last ten years, using the MEDLINE and LILACS, as well as various literature research of relevant articles. Searching studies found GC association with several human gene polymorphisms involved in the immune response, detoxification and suppressor p53. In Colombia, as in other countries, the evidence of the association of genetic polymorphisms with GC are still controversial because of the variation in results that studies in different populations. The genome of Helicobacter pylori strains that infect Colombian population has also been investigated in search of polymorphisms of virulence. cagA/ vacAs1m1 genotype identified as cytotoxic in this bacterium, demonstrated most of the research associated with GC. Evidence of association of GC with Colombian population genetic factors was inconclusive. It is yet to be determined the exact identification of genetic markers that can predict the risk of developing GC. However, some human gene polymorphisms as IL-1 or some detoxifying enzymes and the vacA and cagA of H. pylori could be candidates for future risk markers in these tumors.Keywords: gastric cancer, risk, genotype, Colombia

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

Gastroenterology ◽

10.1016/s0016-5085(18)31914-0 ◽

2018 ◽

Vol 154 (6) ◽

pp. S-504-S-505

Author(s):

Tomoari Kamada ◽

Ken Haruma ◽

Noriaki Manabe ◽

Jiro Hata ◽

Akiko Shiotani ◽

...

Keyword(s):

Gastric Cancer ◽

Risk Factor ◽

H Pylori ◽

Development Of 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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