Analysis of the Expression of Cathepsin S in Gastric Adenocarcinoma and in Helicobacter Pylori Infection

Abstract Background: recent experimental studies have shown a potential link between cathepsin S (CTTS) and gastric cancer progression. Herein, we aimed to evaluate the expression of CTTS in gastric adenocarcinoma.Methods: Cross-sectional study that included two groups, gastric adenocarcinoma (n=42) and gastritis (n=50). The gastritis group was then subdivided into H. pylori positive (n=25) x negative (n=25). Gastric tissue samples were analyzed in order to determine the CTTS expression through immunohistochemistry. Results: In patients with gastritis, the age ranged from 18 to 78 years. Among them, 34% were male, and 66% were female. In patients with gastric cancer, the age ranged from 37 to 85 years. Among them, 50% were male, and 50% were female. When comparing the expression of CTTS between the two groups, only 16% of the gastritis samples had an expression higher than 25%. On the other hand, among patients with gastric adenocarcinoma, 19% had expression between 25-50%, 14.3% between 51-75%, and 26.2% had expressions higher than 75% (p < 0.001). CTTS expression was significantly higher in patients with positive test for H. pylori: 87.5% x 38.5% (p<0.001). There was no statistically significant association between the positivity of CTTS and the clinical-pathological variables, including tumor staging, histological type, angiolymphatic invasion, recurrence, current status and death.Conclusion: CTTS has a higher expression in samples of gastric adenocarcinoma. Patients with gastritis by H. pylori also show a higher expression of CTTS compared with patients with negative results for this bacterium.

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Dangerous Liaison: Helicobacter pylori, Ganglionitis, and Myenteric Gastric Neurons: A Histopathological Study

Analytical Cellular Pathology ◽

10.1155/2019/3085181 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9

Author(s):

Liana Sticlaru ◽

Florica Stăniceanu ◽

Mirela Cioplea ◽

Luciana Nichita ◽

Alexandra Bastian ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Cancer Progression ◽

Myenteric Plexus ◽

Morphological Changes ◽

Neuronal Cell ◽

Histopathological Study ◽

Tissue Samples ◽

H Pylori ◽

The Impact

Chronic inflammation induced by Helicobacter pylori (H. pylori) infection plays a major role in development of gastric cancer. However, recent findings suggested that progression of inflammation and neoplastic transformation in H. pylori infection are more complex than previously believed and could involve different factors that modulate gastric microenvironment and influence host-pathogen interaction. Among these factors, gastric myenteric plexus and its potential adaptive changes in H. pylori infection received little attention. This study is aimed at identifying the impact of H. pylori-associated gastritis on number and morphology of nerve cells in the stomach. The distribution of density, inflammation, and programmed cell death in neurons was immunohistochemically assessed in full-thickness archival tissue samples obtained from 40 patients with H. pylori infection who underwent surgery for gastric cancer and were compared with findings on samples collected from 40 age- and sex-matched subjects without bacteria. Overall, significant differences were noted between H. pylori-positive and H. pylori-negative patients. The analysis of tissue specimens obtained from those with infection revealed higher density and larger surface of the myenteric nervous plexus, as well as a significant increase in the number of gastric neuronal cell bodies and glial cells compared to controls. A predominant CD3-immunoreactive T cell infiltrate confined to the myenteric plexus was observed in infected subjects. The presence of mature B lymphocytes, plasma cells, and eosinophils was also noted, but to a lesser extent, within the ganglia. Myenteric ganglionitis was associated with degeneration and neuronal loss. Our results represent the first histopathological evidence supporting the hypothesis that H. pylori-induced gastric inflammation may induce morphological changes in myenteric gastric ganglia. These findings could help gain understanding of some still unclear aspects of pathogenesis of H. pylori infection, with the possibility of having broader implications for gastric cancer progression.

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TEAD4 modulated LncRNA MNX1-AS1 contributes to gastric cancer progression partly through suppressing BTG2 and activating BCL2

Molecular Cancer ◽

10.1186/s12943-019-1104-1 ◽

2020 ◽

Vol 19 (1) ◽

Cited By ~ 12

Author(s):

You Shuai ◽

Zhonghua Ma ◽

Weitao Liu ◽

Tao Yu ◽

Changsheng Yan ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Progression ◽

Molecular Mechanisms ◽

Mechanistic Model ◽

Ectopic Expression ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Tissue Samples ◽

Reporter Assays

Abstract Background Gastric cancer (GC) is the third leading cause of cancer-related mortality globally. Long noncoding RNAs (lncRNAs) are dysregulated in obvious malignancies including GC and exploring the regulatory mechanisms underlying their expression is an attractive research area. However, these molecular mechanisms require further clarification, especially upstream mechanisms. Methods LncRNA MNX1-AS1 expression in GC tissue samples was investigated via microarray analysis and further determined in a cohort of GC tissues via quantitative reverse transcription polymerase chain reaction (qRT-PCR) assays. Cell proliferation and flow cytometry assays were performed to confirm the roles of MNX1-AS1 in GC proliferation, cell cycle regulation, and apoptosis. The influence of MNX1-AS1 on GC cell migration and invasion was explored with Transwell assays. A xenograft tumour model was established to verify the effects of MNX1-AS1 on in vivo tumourigenesis. The TEAD4-involved upstream regulatory mechanism of MNX1-AS1 was explored through ChIP and luciferase reporter assays. The mechanistic model of MNX1-AS1 in regulating gene expression was further detected by subcellular fractionation, FISH, RIP, ChIP and luciferase reporter assays. Results It was found that MNX1-AS1 displayed obvious upregulation in GC tissue samples and cell lines, and ectopic expression of MNX1-AS1 predicted poor clinical outcomes for patients with GC. Overexpressed MNX1-AS1 expression promoted proliferation, migration and invasion of GC cells markedly, whereas decreased MNX1-AS1 expression elicited the opposite effects. Consistent with the in vitro results, MNX1-AS1 depletion effectively inhibited the growth of xenograft tumour in vivo. Mechanistically, TEAD4 directly bound the promoter region of MNX1-AS1 and stimulated the transcription of MNX1-AS1. Furthermore, MNX1-AS1 can sponge miR-6785-5p to upregulate the expression of BCL2 in GC cells. Meanwhile, MNX1-AS1 suppressed the transcription of BTG2 by recruiting polycomb repressive complex 2 to BTG2 promoter regions. Conclusions Our findings demonstrate that MNX1-AS1 may be able to serve as a prognostic indicator in GC patients and that TEAD4-activatd MNX1-AS1 can promote GC progression through EZH2/BTG2 and miR-6785-5p/BCL2 axes, implicating it as a novel and potent target for the treatment of GC.

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Clinicopathological and Endoscopic Features of Raspberry-Shaped Gastric Cancer in Helicobacter pylori-Uninfected Patients

Digestion ◽

10.1159/000511907 ◽

2020 ◽

pp. 1-8

Author(s):

Noboru Yatagai ◽

Hiroya Ueyama ◽

Muneo Ikemura ◽

Ryota Uchida ◽

Hisanori Utsunomiya ◽

...

Keyword(s):

Gastric Cancer ◽

Gastric Adenocarcinoma ◽

Submucosal Tumor ◽

Clinicopathological Characteristics ◽

Fundic Gland ◽

Histopathological Classification ◽

Histological Characteristics ◽

Greater Curvature ◽

H Pylori ◽

Tumor Shape

Background: Gastric adenocarcinoma of foveolar type (GA-FV) is a raspberry-shaped gastric cancer (RSGC) and garners much attention as H. pylori (Hp)-uninfected gastric cancer. However, the classification and clinicopathological and endoscopic features of RSGCs in Hp-uninfected patients are poorly defined. We designed a new histopathological classification of RSGC and compared them via endoscopic and clinicopathological characteristics. Summary: From 996 patients with early gastric cancers resected by endoscopy in our hospital, we studied 24 RSGC lesions from 21 (2.4%) Hp-uninfected patients. RSGCs were classified into 3 histological types as follows: GA-FV (n = 19), gastric adenocarcinoma of fundic gland type (GA-FG, n = 2), and gastric adenocarcinoma of fundic gland mucosa type (GA-FGM, n = 3). Most of the lesions were found at the greater curvature of the upper or middle third of the stomach. GA-FV lesions were homogeneously reddish and frequently accompanied with a whitish area around the tumor and an irregular microvascular (MV) pattern; these features were confirmed histopathologically by the presence of homogeneous neoplastic foveolar epithelium with foveolar hyperplasia around the tumors. GA-FG lesions might be heterogeneously reddish with a submucosal tumor shape and regular MV pattern; these were confirmed by the presence of covered or mixed nonneoplastic epithelium on deeper regions of tumors. GA-FGM lesions might be homogeneously reddish and occasionally had a submucosal tumor shape and irregular MV pattern; these were confirmed by the presence of homogeneous neoplastic foveolar epithelium on deeper regions of the tumors. Key Messages: RSGCs in Hp-uninfected patients are classified into 3 histopathological types. For accurate diagnosis of RSGCs, it may be necessary to fully understand endoscopic features of these lesions based on these histological characteristics and to take a precise biopsy.

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Genetic Polymorphisms of CXCL8 (−251) Are Associated with the Susceptibility of Helicobacter pylori Infection Increased the Risk of Inflammation and Gastric Cancer in Thai Gastroduodenal Patients

Iranian Journal of Allergy Asthma and Immunology ◽

10.18502/ijaai.v18i4.1417 ◽

2019 ◽

Cited By ~ 1

Author(s):

Wongwarut Boonyanugomol ◽

Kamolchanok Rukseree ◽

Worrarat Kongkasame ◽

Prasit Palittapongarnpim ◽

Seung-Chul Baik ◽

...

Keyword(s):

Gene Expression ◽

Gastric Cancer ◽

Helicobacter Pylori ◽

Cancer Progression ◽

Chemokine Receptor ◽

Gene Polymorphisms ◽

Inflammatory Responses ◽

Increased Risk ◽

Cxc Chemokine ◽

H Pylori

CXC Chemokine Ligand 8 (CXCL8) plays an important role in gastric inflammation and in the progression of gastric cancer induced by Helicobacter pylori (H. pylori) infection. The association of CXCL8, CXC Chemokine Receptor 1 (CXCR1), and CXC Chemokine Receptor 2 (CXCR2) polymorphisms with H. pylori infection and gastric cancer progression needs to be investigated in a population within an enigma area consisting of multiple ethnicities, such as Thailand. To analyze the relative risk of H. pylori infection and gastric cancer among Thai gastroduodenal patients, gene polymorphisms in CXCL8 (promoter region -251) and in CXCR1 and CXCR2 (receptors for CXCL8) were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and allele specific-PCR (AS-PCR). We also determined the presence of cytotoxin-associated gene A (cagA) in Thai patients with H. pylori infection. Correlation between the CXCL8 (-251) polymorphism and CXCL8 gene expression was evaluated by quantitative reverse transcriptase-PCR (qRT-PCR). We found a significant association between the T/A and A/A genotypes of CXCL8 (-251) with H. pylori infection. However, no significant correlation was found between the CXCR1 (+2607) and CXCR2 (+1208) gene polymorphisms with H. pylori infection among Thai gastroduodenal subjects. Within the H. pylori-infected group of Thai gastroduodenal patients, no significant differences in cagA were observed. In addition, the A/A genotype of CXCL8 (-251) significantly correlated with the risk of gastric cancer and correlated with higher CXCL8 gene expression levels in Thai gastroduodenal patients. These results suggest that CXCL8 (-251) polymorphisms are associated with H. pylori infection, an increased risk of stronger inflammatory responses, and gastric cancer in Thai gastroduodenal patients.

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Two Distinct Etiologies of Gastric Cancer: Infection and Autoimmunity

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.752346 ◽

2021 ◽

Vol 9 ◽

Author(s):

Stella G. Hoft ◽

Christine N. Noto ◽

Richard J. DiPaolo

Keyword(s):

Gastric Cancer ◽

T Cells ◽

Gastric Adenocarcinoma ◽

Inflammatory Diseases ◽

The United States ◽

Autoimmune Gastritis ◽

Gastric Disease ◽

Increased Risk ◽

H Pylori ◽

Gastrointestinal Ulceration

Gastric cancer is a leading cause of mortality worldwide. The risk of developing gastric adenocarcinoma, which comprises >90% of gastric cancers, is multifactorial, but most associated with Helicobacter pylori infection. Autoimmune gastritis is a chronic autoinflammatory syndrome where self-reactive immune cells are activated by gastric epithelial cell autoantigens. This cause of gastritis is more so associated with the development of neuroendocrine tumors. However, in both autoimmune and infection-induced gastritis, high risk metaplastic lesions develop within the gastric mucosa. This warrants concern for carcinogenesis in both inflammatory settings. There are many similarities and differences in disease progression between these two etiologies of chronic gastritis. Both diseases have an increased risk of gastric adenocarcinoma development, but each have their own unique comorbidities. Autoimmune gastritis is a primary cause of pernicious anemia, whereas chronic infection typically causes gastrointestinal ulceration. Both immune responses are driven by T cells, primarily CD4+ T cells of the IFN-γ producing, Th1 phenotype. Neutrophilic infiltrates help clear H. pylori infection, but neutrophils are not necessarily recruited in the autoimmune setting. There have also been hypotheses that infection with H. pylori initiates autoimmune gastritis, but the literature is far from definitive with evidence of infection-independent autoimmune gastric disease. Gastric cancer incidence is increasing among young women in the United States, a population at higher risk of developing autoimmune disease, and H. pylori infection rates are falling. Therefore, a better understanding of these two chronic inflammatory diseases is needed to identify their roles in initiating gastric cancer.

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Genome-Wide Characterization of RNA Editing Sites in Primary Gastric Adenocarcinoma through RNA-seq Data Analysis

International Journal of Genomics ◽

10.1155/2020/6493963 ◽

2020 ◽

Vol 2020 ◽

pp. 1-16

Author(s):

Javad Behroozi ◽

Shirin Shahbazi ◽

Mohammad Reza Bakhtiarizadeh ◽

Habibollah Mahmoodzadeh

Keyword(s):

Gastric Cancer ◽

Rna Editing ◽

Gastric Adenocarcinoma ◽

Cancer Progression ◽

Variant Calling ◽

Distinct Pattern ◽

Rna Seq ◽

Comprehensive Overview ◽

Protein Coding ◽

Cancer Tissues

RNA editing is a posttranscriptional nucleotide modification in humans. Of the various types of RNA editing, the adenosine to inosine substitution is the most widespread in higher eukaryotes, which is mediated by the ADAR family enzymes. Inosine is recognized by the biological machinery as guanosine; therefore, editing could have substantial functional effects throughout the genome. RNA editing could contribute to cancer either by exclusive editing of tumor suppressor/promoting genes or by introducing transcriptomic diversity to promote cancer progression. Here, we provided a comprehensive overview of the RNA editing sites in gastric adenocarcinoma and highlighted some of their possible contributions to gastric cancer. RNA-seq data corresponding to 8 gastric adenocarcinoma and their paired nontumor counterparts were retrieved from the GEO database. After preprocessing and variant calling steps, a stringent filtering pipeline was employed to distinguish potential RNA editing sites from SNPs. The identified potential editing sites were annotated and compared with those in the DARNED database. Totally, 12362 high-confidence adenosine to inosine RNA editing sites were detected across all samples. Of these, 12105 and 257 were known and novel editing events, respectively. These editing sites were unevenly distributed across genomic regions, and nearly half of them were located in 3 ′ UTR. Our results revealed that 4868 editing sites were common in both normal and cancer tissues. From the remaining sites, 3985 and 3509 were exclusive to normal and cancer tissues, respectively. Further analysis revealed a significant number of differentially edited events among these sites, which were located in protein coding genes and microRNAs. Given the distinct pattern of RNA editing in gastric adenocarcinoma and adjacent normal tissue, edited sites have the potential to serve as the diagnostic biomarkers and therapeutic targets in gastric cancer.

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IMMUNOHISTOCHEMICAL EXPRESSION OF HER2 IN ADENOCARCINOMA OF THE STOMACH

Arquivos de Gastroenterologia ◽

10.1590/s0004-28032015000200015 ◽

2015 ◽

Vol 52 (2) ◽

pp. 152-155 ◽

Cited By ~ 5

Author(s):

Diego Michelon DE CARLI ◽

Marta Pires da ROCHA ◽

Luis Carlos Moreira ANTUNES ◽

Renato Borges FAGUNDES

Keyword(s):

Gastric Cancer ◽

Gastric Adenocarcinoma ◽

Immunohistochemical Analysis ◽

Anatomical Site ◽

Her2 Expression ◽

Immunohistochemical Expression ◽

Her2 Gene ◽

Cross Sectional ◽

Dismal Prognosis ◽

Location Methods

Background Worldwide, gastric cancer is the fourth cancer in incidence and the second most common cause of cancer death. Gastric cancer is asymptomatic in the early stages and very often diagnosed at advanced stages, determining a dismal prognosis. Expression of the HER2 gene has been identified in about 20% of gastric cancer cases, and its hyper-expression is associated with poor prognosis. Objective To investigate HER2 immunohistochemical expression in gastric adenocarcinoma and its relationship to the histological type and anatomic location. Methods A cross-sectional retrospective study analyzed the immunohistochemical expression of HER2 in a sample of 48 specimens of gastric cancer. Immunohistochemical analysis were performed using avidin-biotin-peroxidase method with C-erb B2 (clone EP1045Y), as a primary antibody (Biocare Medical, USA). Standardized gastric adenocarcinoma‘s HER2 expression criteria has been used in the analysis of samples. Results There were seven cases with reactivity for HER2. Five were of intestinal-type while two cases were of mixed-type in which the expression occurred in the intestinal component. It was identified a significant association of HER2 expression in the intestinal subtype of gastric adenocarcinoma (P=0.003). Regarding the anatomical site, HER2 was positive in only one (16.6%) of the six proximal cases and six (14.28%) of the 42 distal cases (P=0.88). Conclusion HER2 immunoexpression was identified in 14.6% of the samples, and the expression was significantly associated to Lauren’s intestinal subtype.

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Transcriptome Analysis of the Inhibitory Effect of Astaxanthin on Helicobacter pylori-Induced Gastric Carcinoma Cell Motility

Marine Drugs ◽

10.3390/md18070365 ◽

2020 ◽

Vol 18 (7) ◽

pp. 365 ◽

Cited By ~ 1

Author(s):

Suhn Hyung Kim ◽

Hyeyoung Kim

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Gastric Carcinoma ◽

Cell Motility ◽

Cancer Progression ◽

Migration And Invasion ◽

Pcr Analysis ◽

Human Gastric Cancer ◽

Gastric Carcinoma Cell ◽

H Pylori

Helicobacter pylori (H. pylori) infection promotes the metastasis of gastric carcinoma cells by modulating signal transduction pathways that regulate cell proliferation, motility, and invasion. Astaxanthin (ASTX), a xanthophyll carotenoid, is known to inhibit cancer cell migration and invasion, however the mechanism of action of ASTX in H. pylori-infected gastric epithelial cells is not well understood. To gain insight into this process, we carried out a comparative RNA sequencing (RNA-Seq) analysis of human gastric cancer AGS (adenocarcinoma gastric) cells as a function of H. pylori infection and ASTX administration. The results were used to identify genes that are differently expressed in response to H. pylori and ASTX. Gene ontology (GO) analysis identified differentially expressed genes (DEGs) to be associated with cell cytoskeleton remodeling, motility, and/or migration. Among the 20 genes identified, those encoding c-MET, PI3KC2, PLCγ1, Cdc42, and ROCK1 were selected for verification by real-time PCR analysis. The verified genes were mapped, using signaling networks contained in the KEGG database, to create a signaling pathway through which ASTX might mitigate the effects of H. pylori-infection. We propose that H. pylori-induced upregulation of the upstream regulator c-MET, and hence, its downstream targets Cdc42 and ROCK1, is suppressed by ASTX. ASTX is also suggested to counteract H. pylori-induced activation of PI3K and PLCγ. In conclusion, ASTX can suppress H. pylori-induced gastric cancer progression by inhibiting cytoskeleton reorganization and reducing cell motility through downregulation of c-MET, EGFR, PI3KC2, PLCγ1, Cdc42, and ROCK1.

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GENDER, AGE, ENDOSCOPIC FINDINGS, UREASE AND HELICOBACTER PYLORI: ALL UNCORRELATED WITHIN A SAMPLE OF A HIGH GASTRIC CANCER PREVALENCE POPULATION IN AMAZON

Arquivos de Gastroenterologia ◽

10.1590/s0004-2803.201900000-50 ◽

2019 ◽

Vol 56 (3) ◽

pp. 264-269

Author(s):

Ariney Costa de MIRANDA ◽

Cássio CALDATO ◽

Mira Nabil SAID ◽

Caio de Souza LEVY ◽

Claudio Eduardo Corrêa TEIXEIRA ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Cross Sectional Study ◽

Upper Gastrointestinal Endoscopy ◽

Histopathological Analysis ◽

Rapid Urease Test ◽

Cross Sectional ◽

Cancer Prevalence ◽

Urease Test ◽

H Pylori

ABSTRACT BACKGROUND: It is widely assumed that gender, age, gastritis and Helicobacter pylori , all have some degree of correlation and, therefore, can synergistically lead to the development of gastric cancer. OBJECTIVE: In this cross-sectional study, we expected to observe the above mentioned correlation in the analysis of medical records of 67 patients of both sexes (female, n=44), mean age ± standard deviation: 41±12 years old, all from Belém (capital of Pará State, Brazilian Amazon), a city historically known as one with the highest gastric cancer prevalence in this country. METHODS: All patients were submitted to upper gastrointestinal endoscopy for gastric biopsy histopathological analysis and rapid urease test. All diagnoses of gastritis were recorded considering its topography, category and the degree of inflammatory activity, being associated or not associated with H. pylori infection. RESULTS: The results show that no statistically relevant associations were found among the prevalences of the observed variables. CONCLUSION: The authors hypothesize that observed risk factors associated to gastric cancer might be lesser synergistic than is usually expected.

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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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