Relation of h. pylori to gastric cancer

Introduction: Helicobacter Pylori (H. Pylori) is a gram negative bacterium spiraled in the gastric epithelium. This bacterium is responsible for triggering benign inflammatory processes and is considered a carcinogenic agent. Methodology: This is a bibliographic review based on the analysis of published works, evaluating the relationship between H.Pylori and the development of gastric cancer based on keywords indexed in the DECs (described in science and health): “Helicobacter Pylori” “Cancer” “Stomach” “Gastric cancer” and information from INCA (National Cancer Institute). Result and Discussions: Helicobacter Pyloriinfection is associated with gastric neoplasms in which adenocarcinomas are the most prevalent, with more than 90% of cases. The diagnosis is made through EDA (Upper Digestive Endoscopy) with biopsy of the lesions and has a sensitivity of 97%. The treatment of H. pylori in the patient diagnosed with gastric cancer depends on the type of neoplasia. Conclusion: The relationship between H.Pylori and neoplastic processes is evident. Therefore, proper diagnosis and treatment in all carriers of the bacterium is essential in order to reduce the risk of developing gastric cancer.

The correlation between lncRNAs and Helicobacter pylori in gastric cancer

Pathogens and Disease ◽

10.1093/femspd/ftaa004 ◽

2019 ◽

Vol 77 (9) ◽

Author(s):

Narges Dastmalchi ◽

Seyed Mahdi Banan Khojasteh ◽

Mirsaed Miri Nargesi ◽

Reza Safaralizadeh

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Molecular Mechanisms ◽

Gastrointestinal Diseases ◽

Mechanisms Of Action ◽

Molecular Pathways ◽

Gastric Diseases ◽

Non Coding Rnas ◽

H Pylori ◽

ABSTRACT Helicobacter pylori infection performs a key role in gastric tumorigenesis. Long non-coding RNAs (lncRNAs) have demonstrated a great potential to be regarded as effective malignancy biomarkers for various gastrointestinal diseases including gastric cancer (GC). The present review highlights the relationship between lncRNAs and H. pylori in GC. Several studies have examined not only the involvement of lncRNAs in H. pylori-associated GC progression but also their molecular mechanisms of action. Among the pertinent studies, some have addressed the effects of H. pylori infection on modulatory networks of lncRNAs, while others have evaluated the effects of changes in the expression level of lncRNAs in H. pylori-associated gastric diseases, especially GC. The relationship between lncRNAs and H. pylori was found to be modulated by various molecular pathways.

Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

International Journal of Molecular Sciences ◽

10.3390/ijms22094823 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4823

Author(s):

María Fernanda González ◽

Paula Díaz ◽

Alejandra Sandoval-Bórquez ◽

Daniela Herrera ◽

Andrew F. G. Quest

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Outer Membrane ◽

Extracellular Vesicles ◽

Membrane Vesicles ◽

Outer Membrane Vesicles ◽

Host Cells ◽

Gastric Epithelium ◽

Infected Cells ◽

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

Helicobacter Pylori Induce Gastric Upset

Journal of Medical Research and Surgery ◽

10.52916/jmrs214055 ◽

2021 ◽

pp. 1-1

Author(s):

Hazim Abdul Rahman Alhit

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Serum Antibody ◽

Endoscopic Biopsy ◽

Helicobacter Pylori Infection ◽

Gastric Epithelium ◽

Gastric Diseases ◽

Heterogeneous Distribution ◽

Cytotoxin Associated Gene A ◽

Editorial: Helicobacter pylori is a micro-aerophilic, helical-form gramnegative aggressive bacteria. Accordingly, the idiom “Helico” intimates its helical appearance, “bacter” symbolizes bacteria, while “pylori” denotes stomach due to the first and common site of this bacteria living. Further, Marshall B. and Warren R. observed and described it in 1982. Then, the followed investigators studied this bacterium in detail with its consequences and complexities [1]. Gastric upset (Indigestion), dyspepsia: means impaired gastric digestion. Accordingly, the patient complains of upper abdominal pain, heartburn, belching, nausea, even feeling earlier gastric fullness than expected while eating. Furthermore, there are many causes of indigestion like gastroesophageal reflux disease, ulcer disease, gastritis, and even gastric cancer. Hence, unexplained recent onset dyspepsia in older people may need additional examinations. Moreover, one of the common causes is Helicobacter pylori infection, which needs laboratory and endoscopic examination [2]. Argument Many theories investigated the etiology and pathogenesis of Helicobacter pylori infection, concerning chronic or acute gastritis. Hence, gastric upset is the main presentation of both types of gastritis. Evidences The genotype is valuable in determining the dominant Helicobacter pylori strains as the isolates were different genetically plus heterogeneous distribution. Accordingly, the vac and cag markers operate a significant function in defining clinical consequences. These virulence agents are present in a subset of Helicobacter pylori strains isolates like cagA, iceA, vacA, and ureC. Moreover, the cagA causes cytotoxins induction by the gastric epithelial cell as Interleukin 8 [3]. The molecular intercommunication researches exhibit that the act of acarus calamus in hindering biofilm formation in Helicobacter pylori is due to the inhibitory impact of phytobio-active component, β-sitosterol, on the quorum sensing molecules-ToxB, PhnB, DnaA, plus Sip. Consequently, this opinion may suggest the molecular mechanism of Helicobacter pylori in producing the acidrelated complaints and gives a clue to a new therapy [4]. Helicobacter pylori infection causes lncRNA risk impression linked to H. pylori in gastric cancer patients and can prognosticate the prediction of these patients [5]. There was a close relationship between raised serum IgE levels in Helicobacter pylori infected patients [6]. Counterargument The laboratory investigations of Helicobacter pylori infection depend on several factors like the fluctuations of serum antibody titers in a time series, the antigene detection in stool tests, the false-positive results of lab tests, or the manner of endoscopic biopsy collection. Furthermore, other factors like the variations in Cytotoxin-Associated Gene A (CagA) in East Asian patients. Moreover, the gastric nodularity or atrophy, the patient’s age, the severity of the gastric mucosal infection are causes of variations in Helicobacter pylori detection at the time of the investigation [7]. Refutation The significant markers of H. pylori, the presence of the vacuolating cytotoxin (vacA), the cytotoxin-associated gene A (cagA), which induced by the direct communication with gastric epithelium factor antigen (iceA gene), and the presence of urease C gene (ureC). Consequently, all these factors play the principal factors in deciding the gastric consequences of Helicobacter infections. Conclusion Helicobacter pylori induce gastric upset by several mechanisms to form numerous Gastric diseases.

Prevalence of H. pylori Infection in Relatives of Peruvian Patients with Gastric Cancer

Asian Pacific Journal of Cancer Care ◽

10.31557/apjcc.2021.6.1.53-57 ◽

2021 ◽

Vol 6 (1) ◽

pp. 53-57

Author(s):

Miluska Castillo ◽

Luis A. Bernabe ◽

Carlos A. Castaneda ◽

Nancy Suarez ◽

Fernando Barreda ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Tissue Sample ◽

Gastric Tissue ◽

Infection Rates ◽

Urease Test ◽

H Pylori ◽

Objective: The aim of this study was to determine the relationship between Helicobacter pylori (H. pylori) infection in relatives and patients with gastric cancer (GC).Methods: H. pylori infection was evaluated by the breath urease test in 171 relatives and by qPCR technique in gastric tissue of 61 patients (n=45 for GC and n=16 for non-GC). Results: There were included 137 relatives of GC patients and 34 of non-GC. The median age of the relatives of patients with a gastric tissue sample was 39 years (10-86). Infection was found in 60.2% (n=103) relatives. There were no higher H. pylori infection rates in relatives of patients with gastric cancer (62% vs 62.9%, p=0.33), H. pylori infection (60% vs 60%, p=0.96), or metaplasia (58.8% vs 61.8%, p=0.71). Conclusion: The prevalence of infection in relatives of GC patients is high in our population but not associated with H. pylori presence in the paired case.

Helicobacter pylori Colonization Drives Urokinase Receptor (uPAR) Expression in Murine Gastric Epithelium During Early Pathogenesis

Microorganisms ◽

10.3390/microorganisms8071019 ◽

2020 ◽

Vol 8 (7) ◽

pp. 1019

Author(s):

Warner Alpízar-Alpízar ◽

Mette E. Skindersoe ◽

Lone Rasmussen ◽

Mette C. Kriegbaum ◽

Ib J. Christensen ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Epithelial Cells ◽

Protein Expression ◽

De Novo ◽

Urokinase Receptor ◽

Gastric Epithelium ◽

Upar Expression ◽

(1) Background: Persistent Helicobacter pylori infection is the most important risk factor for gastric cancer. The urokinase receptor (uPAR) is upregulated in lesions harboring cancer invasion and inflammation. Circumstantial evidence tends to correlate H. pylori colonization with increased uPAR expression in the human gastric epithelium, but a direct causative link has not yet been established in vivo; (2) Methods: In a mouse model of H. pylori-induced gastritis, we investigated the temporal emergence of uPAR protein expression in the gastric mucosa in response to H. pylori (SS1 strain) infection; (3) Results: We observed intense uPAR immunoreactivity in foveolar epithelial cells of the gastric corpus due to de novo synthesis, compared to non-infected animals. This uPAR induction represents a very early response, but it increases progressively over time as do infiltrating immune cells. Eradication of H. pylori infection by antimicrobial therapy causes a regression of uPAR expression to its physiological baseline levels. Suppression of the inflammatory response by prostaglandin E2 treatment attenuates uPAR expression. Notwithstanding this relationship, H. pylori does induce uPAR expression in vitro in co-cultures with gastric cancer cell lines; (4) Conclusions: We showed that persistent H. pylori colonization is a necessary event for the emergence of a relatively high uPAR protein expression in murine gastric epithelial cells.

Intrafamilial Infection of Helicobacter Pylori: Abnormal Gastric Epithelial Cells, Pedestal-Rich H. Pylori Adherence, and a Gene Mutation in a Child with Protein-Losing Gastroenteropathy

Medical University ◽

10.2478/medu-2019-0013 ◽

2019 ◽

Vol 2 (3) ◽

pp. 83-99

Author(s):

T.W. Wan ◽

O. Khokhlova ◽

W. Higuchi ◽

I. Protasova ◽

Olga V. Peryanova ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Epithelial Cells ◽

Gene Mutation ◽

Virulence Factor ◽

East Asian ◽

Gastric Epithelium ◽

Gastric Epithelial Cells ◽

Abstract Helicobacter pylori, one of the most prevalent human pathogens, colonizes the gastric mucosa and is associated with gastric diseases, such as gastritis and peptic ulcers, and is also a bacterial risk factor for gastric cancer. Cytotoxin-associated gene A (CagA) protein, a major virulence factor of H. pylori, is phosphorylated in cells at its Glu-Pro-IIe-Tyr-Ala (EPIYA) motif and is considered to trigger gastric cancer. CagA is classified into two forms, Western CagA with EPIYA-ABC and East Asian CagA with EPIYA-ABD, with the latter associated with a high risk of developing gastric cancer. CagA causes morphological transformation of cells, yielding the “hummingbird” phenotype in AGS cells and possibly membranous pedestals in the gastric epithelium, albeit rarely. H. pylori adherence to the gastric mucosa is not yet fully understood. Here, we describe an intrafamilial infection case of H. pylori, focusing on the gastric epithelium, H. pylori adherence, and a gene mutation in a child with protein-losing gastroenteropathy (characterized by excessive loss of plasma proteins into the gastrointestinal tract). H. pylori, which also infected family members (mother and father), was genetically a single clone with the virulence genes of an East Asian type. The patient’ gastric mucosa exhibited some unique features. Endoscopy revealed the presence of protein plugs on the mucosal surface, which were immunoelectrophoretically similar to serum proteins. Electron microscopy revealed abnormal gastric epithelial cells, totally covered with the secretions or possessing small swollen structures and irregular microvilli. The patient’s H. pylori infection was characterized by frequently occurring thick pedestals, formed along adherent H. pylori. The serum protein level returned to normal and the protein plugs disappeared after the successful eradication of H. pylori, albeit with lag periods for healing. He had a mutation in the OCRL1 gene, associated with Dent disease (asymptomatic proteinuria). Thus, in the patient’s gastric mucosa, we found the abnormal gastric epithelial cells, which may be caused by an OCRL1 mutation or H. pylori, and pedestal-rich H. pylori infection, possibly caused by a higher level of action of CagA in the abnormal epithelial cells. The data suggests a novel H. pylori virulence factor associated with “excessive plasma protein release”.

The Evolving Epidemiology ofHelicobacter pyloriInfection and Gastric Cancer

Canadian Journal of Gastroenterology ◽

10.1155/2003/692808 ◽

2003 ◽

Vol 17 (suppl b) ◽

pp. 18B-20B ◽

Cited By ~ 20

Author(s):

Jia-Qing Huang ◽

Richard H Hunt

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Meta Analysis ◽

Epidemiological Studies ◽

Increased Risk ◽

H Pylori ◽

The relationship betweenHelicobacter pyloriinfection and the risk of gastric cancer has been well established in the last decade. Four metaanalyses have found that the infection increases the risk of noncardia gastric cancer by 2- to 6-fold compared with noninfected control populations. However, the role ofcagAstrains ofH pyloriin relation to gastric cancer has not been evaluated systematically. We undertook a meta-analysis of epidemiological studies examining the relationship between infection withcagA-positive strains ofH pyloriand the risk of gastric cancer, and found that patients who are seropositive forcagAstrains ofH pyloriare at an increased risk for developing noncardia gastric cancer compared with those withH pyloriinfection alone. Therefore, searching forcagA-positive strains ofH pylorimay help identify populations at a greater risk for developing gastric cancer.

Function of Non-coding RNA in Helicobacter pylori-Infected Gastric Cancer

Frontiers in Molecular Biosciences ◽

10.3389/fmolb.2021.649105 ◽

2021 ◽

Vol 8 ◽

Author(s):

Chao Wang ◽

Yiyang Hu ◽

Huan Yang ◽

Sumin Wang ◽

Bo Zhou ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Tumor Progression ◽

Digestive System ◽

Non Coding Rna ◽

Gastric Cancer Treatment ◽

Multiple Levels ◽

New Perspective ◽

H Pylori ◽

Gastric cancer is a common malignant tumor of the digestive system. Its occurrence and development are the result of a combination of genetic, environmental, and microbial factors. Helicobacter pylori infection is a chronic infection that is closely related to the occurrence of gastric tumorigenesis. Non-coding RNA has been demonstrated to play a very important role in the organism, exerting a prominent role in the carcinogenesis, proliferation, apoptosis, invasion, metastasis, and chemoresistance of tumor progression. H. pylori infection affects the expression of non-coding RNA at multiple levels such as genetic polymorphisms and signaling pathways, thereby promoting or inhibiting tumor progression or chemoresistance. This paper mainly introduces the relationship between H. pylori-infected gastric cancer and non-coding RNA, providing a new perspective for gastric cancer treatment.

Potential Association of EEF1A Dimethylation at Lysine 55 in the Basal Area of Helicobacter Pylori-Eradicated Gastric Mucosa with the Risk of Gastric Cancer: A Retrospective Observational Study

10.21203/rs.3.rs-1072695/v1 ◽

2021 ◽

Author(s):

Yuka Hirashita ◽

Masahide Fukuda ◽

Masaaki Kodama ◽

Yoshiyuki Tsukamoto ◽

Tadayoshi Okimoto ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gastric Mucosa ◽

Eradication Therapy ◽

Basal Area ◽

Immunofluorescent Staining ◽

Upper Gastrointestinal Endoscopy ◽

H Pylori ◽

Abstract Background Although eradication therapy for chronic Helicobacter pylori reduces the risk of gastric cancer (GC), its effectiveness is incomplete. Therefore, it is critically important to identify those patients who remain at high risk after H. pylori eradication therapy. Accumulation of protein methylation is strongly implicated in cancer, and a recent study showed that dimethylation of eEF1A lysine 55 (eEF1AK55me2) promotes carcinogenesis in vivo. We aimed to investigate the relationship between eEF1A dimethylation and H. pylori status in gastric mucosa and to reveal potential downstream molecules of eEF1A dimethylation in H. pylori-eradicated mucosa. Methods Records of 115 patients (11 H. pylori-negative, 29 H. pylori-positive, 75 post-eradication patients) who underwent upper gastrointestinal endoscopy were retrospectively reviewed. The eEF1A dimethyl level was evaluated in each functional cell type of gastric mucosa by immunofluorescent staining. We also investigated the relationship between eEF1AK55me2 downregulation by CRISPR/Cas9-mediated deletion of Mettl13, which is known as a dimethyltransferase of eEF1AK55me2. Results The level of eEF1A dimethylation significantly increased in the surface and basal areas of H. pylori-positive mucosa compared with -negative mucosa (surface, p=0.0031; basal, p<0.0001). The eEF1A dimethyl levels in the surface area were significantly reduced by eradication therapy (p=0.005), but those in the basal area were maintained even after eradication therapy. Multivariate analysis revealed that high dimethylation of eEF1A in the basal area of the mucosa was the independent factor related to GC incidence (odds ratio=3.6611, 95% confidence interval=1.0350–12.949, p=0.0441). We also showed the relationship between eEF1A dimethylation and expressions of reprogramming factors Oct4 and Nanog by immunohistochemistry and in vitro genome editing experiments. Conclusions The results indicated that H. pylori infection potently induced eEF1A dimethylation in gastric mucosa. The accumulation of dimethyl-eEF1A in the basal area of the mucosa might contribute to GC risk via regulation of reprograming factors in H. pylori-eradicated gastric mucosa.

What is the Relationship Between Helicobacter Pylori CagA Genotypes and Gastrointestinal Diseases in the Iranian Population? A Systematic Review and Meta-Analysis

10.21203/rs.3.rs-80096/v1 ◽

2020 ◽

Author(s):

Masoud Keikha ◽

Mohsen Karbalaei

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Meta Analysis ◽

Gastrointestinal Diseases ◽

Iranian Population ◽

Cancer Disease ◽

Gastrointestinal Complications ◽

Cytotoxin Associated Gene A ◽

H Pylori ◽

Abstract Background: Helicobacter pylori (H. pylori) is one of the most well-known risk factors for getting the gastric cancer disease. In recent studies, the relationship between its virulence factors, specially CagA (cytotoxin‐associated gene A) toxin and development into the gastrointestinal diseases is taken into consideration. According to review of literature, despite the presence of four motifs A, B, C, and D in CagA toxin, two motifs C and D are more associated with gastrointestinal complications in patients who are infected by H. pylori. Methods: In the present study, we researched about theses ambiguities using a comprehensive meta-analysis study. In this study, we assessed the information of 1762 Iranian patients for potential relationship between all genotypes of cagA gene and gastrointestinal diseases.Results: According to statistical analysis, the abundance of cagA genotypes AB, ABC, ABCC, ABCCC, and ABD in Iranian population is 5.52%, 80.18%, 22.81%, 2.76%, and 0% respectively. In addition, it was determined that there is a significant relationship between cagA genotypes ABCC and ABCCC on the one hand and cagA genotype ABCCC on the other hand with susceptibility to chronic gastritis and gastric cancer respectively.Conclusions: Overall, it can be concluded that the higher number of EPIYA-C copy numbers lead to the higher risk of gastric cancer. According to our results, it seems that the presence of EPIYA-ABCCC motif in strains of H. pylori should be considered as an appropriate marker in preventing the gastric cancer among the Iranian population.