scholarly journals Helicobacter pylori; a Way to Gastric Cancer?

2021 ◽  
Author(s):  
Norma Sánchez-Zauco ◽  
Erandi Pérez-Figueroa ◽  
Carmen Maldonado-Bernal
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Inflammatory Responses ◽  
Salt Intake ◽  
Clinical Symptoms ◽  
Nucleotide Polymorphisms ◽  
Stomach Pain ◽  
High Salt Intake ◽  
Patient Prognosis ◽  
Development Of Gastric Cancer

Gastric cancer is one of the types of cancer that is associated with Helicobacter pylori infection. The infection starts in childhood, and 50–90% of the population in the world is infected. The clinical symptoms can be stomach pain, gastritis, atrophy gastric, and only 2–3% of the infected population developed gastric cancer. The majority of gastric cancers are adenocarcinomas. From Lauren’s histological classification, gastric cancer is divided into two large groups: intestinal and diffuse. The cells that gives rise to them are different and the epidemiologic features and diagnosis are different according to gender and age; however; the survival rate is approximately of 5-years. Surgery is the only radical treatment, but the adjuvant treatment is chemotherapy and radiotherapy which unfortunately lead to only a modest survival benefit. On this review, we describe the major risk factors associated with the bacteria: cagPAI, CagA, VacA, HOPs, as well as host immune and inflammatory responses: immune cells, Toll-like receptors, cytokines, immune signal pathway, genetic predisposition, such as single nucleotide polymorphisms (SNP’s) and environmental factors: age, high salt intake, diets low in fruit and vegetables, alcohol intake, and tobacco use. Finally, we included the interaction of all factors for the development of gastric cancer. Knowing and understanding the role of all factors in the development of gastric cancer will allow the implementation of better therapies and improve patient prognosis.

scholarly journals Eradication Treatment of Helicobacter pylori Infection: Its Importance and Possible Relationship in Preventing the Development of Gastric Cancer

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Bruna Maria Roesler ◽  
Sandra Cecília Botelho Costa ◽  
José Murilo Robilotta Zeitune
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Genetic Factors ◽  
Salt Intake ◽  
Mucosal Damage ◽  
Bacterial Virulence ◽  
Host Genetic ◽  
H Pylori ◽  
Host Genetic Factors ◽  
Development Of Gastric Cancer

Helicobacter pylori is the most important carcinogen for gastric adenocarcinoma. Bacterial virulence factors are essential players in modulating the immune response involved in the initiation of carcinogenesis in the stomach; host genetic factors contribute to the regulation of the inflammatory response and to the aggravation of mucosal damage. In terms of environmental factors, salt intake and smoking contribute to the development of lesions. Various therapeutic schemes are proposed to eradicate H. pylori infection, which could potentially prevent gastric cancer, offering the greatest benefit if performed before premalignant changes of the gastric mucosa have occurred.

scholarly journals The influence of cytokine gene polymorphisms on the risk of developing gastric cancer in patients with Helicobacter pylori infection

2015 ◽  
Vol 49 (3) ◽  
pp. 256-264 ◽  
Author(s):  
David Stubljar ◽  
Samo Jeverica ◽  
Tomislav Jukic ◽  
Miha Skvarc ◽  
Tadeja Pintar ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Chronic Gastritis ◽  
Gene Polymorphisms ◽  
Inflammatory Responses ◽  
Control Group ◽  
Nucleotide Polymorphisms ◽  
Slovenian Population ◽  
Significant Difference ◽  
H Pylori

Abstract Background. Helicobacter pylori infection is the main cause of gastric cancer. The disease progression is influenced by the host inflammatory responses, and cytokine single nucleotide polymorphisms (SNPs) may have a role in the course of the disease. The aim of our study was to investigate proinflammatory cytokine polymorphisms, previously associated with the development of gastric cancer, in a Slovenian population. Patients and methods. In total 318 patients and controls were selected for the study and divided into three groups: (i) patients with gastric cancer (n = 58), (ii) patients with chronic gastritis (n = 60) and (iii) healthy control group (n = 200). H. pylori infection in patient groups was determined by serology, histology and culture. Four proinflammatory gene polymorphisms were determined (IL-1β, IL-1rα, TNF-α, TLR-4) in all subjects. Results. We found a statistically significant difference between males and females for the groups (p = 0.025). Odds ratio (OR) for gastric cancer risk for females was 0.557 (95% confidence interval [CI]: 0.233―1.329) and for chronic gastritis 2.073 (95% CI: 1.005―4.277). IL-1B-511*T/T homozygous allele for cancer group had OR = 2.349 (95% CI: 0.583―9.462), heterozygous IL-1B-511*T had OR = 1.470 (95% CI: 0.583―3.709) and heterozygotes in TNF-A-308 genotype for chronic gastritis had OR = 1.402 (95% CI: 0.626―3.139). Other alleles had OR less than 1. Conclusions. We could not prove association between gastric cancer and chronic gastritis due to H. pylori in any cytokine SNPs studied in Slovenian population. Other SNPs might be responsible besides infection with H. pylori for the progression from atrophy to neoplastic transformation.

scholarly journals 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

2019 ◽  
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.  

Evaluation of the Epidemiologic Efficacy of Eradicating Helicobacter pylori on Development of Gastric Cancer

2019 ◽  
Vol 41 (1) ◽  
pp. 97-108 ◽  
Author(s):  
Fujiao Duan ◽  
Chunhua Song ◽  
Jintao Zhang ◽  
Peng Wang ◽  
Hua Ye ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Population Attributable Risk ◽  
Eradication Therapy ◽  
Attributable Risk ◽  
Chinese Patients ◽  
Controlled Trials ◽  
Mixed Effect ◽  
H Pylori ◽  
Development Of Gastric Cancer

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.

scholarly journals New Biology to New Treatment of Helicobacter pylori-Induced Gastric Cancer

2016 ◽  
Vol 34 (5) ◽  
pp. 510-516 ◽  
Author(s):  
Richard M. Peek Jr.
Keyword(s):  
Gastric Cancer ◽  
Salt Intake ◽  
Disease Risk ◽  
Host Cells ◽  
Human Populations ◽  
High Salt Intake ◽  
Increased Risk ◽  
New Biology ◽  
New Treatment ◽  
H Pylori

Background:Helicobacter pylori is a bacterial carcinogen that is supposed to have the highest known level of risk for the development of gastric cancer, a disease that claims hundreds of thousands of lives per year. Approximately 89% of the global gastric cancer burden and 5.5% of malignancies worldwide are attributed to H. pylori-induced inflammation and injury. However, only a fraction of colonized persons ever develop neoplasia, and disease risk involves well-choreographed interactions between pathogen and host, which are dependent upon strain-specific bacterial factors, host genotypic traits, and/or environmental conditions. Key Messages: One H. pylori strain-specific virulence determinant that augments the risk for gastric cancer is the cag pathogenicity island, a secretion system that injects the bacterial oncoprotein CagA into host cells. Host polymorphisms within genes that regulate immunity and oncogenesis also heighten the risk for gastric cancer, in conjunction with H. pylori strain-specific constituents. Further, conditions such as iron deficiency and high salt intake can influence H. pylori phenotypes that lower the threshold for disease. Conclusions: Delineation of bacterial, host, and environmental mediators that augment gastric cancer risk has profound ramifications for both physicians and biomedical researchers as such findings will not only focus prevention approaches that target H. pylori-infected human populations at increased risk for stomach cancer, but will also provide mechanistic insights into inflammatory carcinomas that develop beyond the gastric niche.

scholarly journals Gastric xanthelasma: case report

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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