Association of the Helicobacter pylori cagA, vacA, and iceA genotypes with chronic follicular gastritis in a Colombian population at high risk for gastric cancer

Carlosama-Rosero, Yeison Harvey; Bolaños-Bravo, H.; Sierra‐Torres, Carlos H.; Rosero, E.A.

doi:10.1016/j.rgmxen.2018.03.012

Cited by 3 publications

(3 citation statements)

References 28 publications

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“…In several prior studies conducted around the world, cagA, vacAs1, and vacAm1 genes, are considered to play a role in pathogenicity and linked to gastric cancer [14,36,37].…”

Section: Helicobacter Pylori Epidemiology and Other Factorsmentioning

confidence: 99%

A Genetic and Immunohistochemical Analysis of Helicobacter pylori Phenotypes and p27 Expression in Adenocarcinoma Patients in Jordan

Al-Sheboul

Mohammad

Shboul

et al. 2023

J Epidemiol Glob Health

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Stomach (gastric) cancer is one of the most prevalent and deadly cancers worldwide and most gastric cancers are adenocarcinomas. Based on prior research, there is an association between Helicobacter pylori (H. pylori) infection together with the frequency of duodenal ulcer, distal gastric adenocarcinoma, mucosa-associated lymphoid tissue (MALT) lymphoma, and antral gastritis. Helicobacter pylori virulence and toxicity factors have been identified before that significantly influence the clinical outcomes of H. pylori infection and gastric adenocarcinoma. However, it remains unclear exactly how different strains of H. pylori affect gastric adenocarcinoma. Current research suggests this involves tumor suppressor genes, like p27 but also H. pylori toxic virulence proteins. Therefore, we quantified known H. pylori genotypes within adenocarcinoma patients to establish the prevalence of known toxins that include cytotoxin-associated gene A (cagA) as well as vacuolating cytotoxin A (vacA) within patients of variable adenocarcinoma diagnosis. This analysis used gastrectomy samples validated for DNA viability. The incidence of H. pylori in adenocarcinoma patients in Jordan was established to be 54.5% positive (ureA gene positive) with cagA genotype occurrence at 57.1%, but also in this population study vacA gene ratios found to be 24.7%:22.1%:14.3%:14.3%. (vacAs1:vacAs2:vacAm1:vacAm2). Using immunohistochemistry (IHC), we confirmed with statistical significance that p27 was dysregulated and suppressed, within nearly all H. pylori vacA genotypes. In addition, within 24.6% of H. pylori samples analyzed was a different bacterial genotype, and curiously that p27 protein expression was retained in 12% of tested adenocarcinoma H. pylori samples. This is suggestive that p27 could be used as a prognostic indicator but also that an unknown genotype could be contributing to the regulatory effects of p27 protein within this bacterial and cellular environment that may include other virulence factors and unknown immune system regulatory changes.

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“…In several prior studies conducted around the world, cagA, vacAs1, and vacAm1 genes, are considered to play a role in pathogenicity and linked to gastric cancer [14,36,37].…”

Section: Helicobacter Pylori Epidemiology and Other Factorsmentioning

confidence: 99%

A Genetic and Immunohistochemical Analysis of Helicobacter pylori Phenotypes and p27 Expression in Adenocarcinoma Patients in Jordan

Al-Sheboul

Mohammad

Shboul

et al. 2023

J Epidemiol Glob Health

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“…Therefore, characterizing the toxicity of H. Pylori in specific carcinomas will further knowledge of microbial toxicity within clinically vulnerable patients. In several prior studies conducted around the world, cagA , vacA s1, and vacA m1 genes, have been thought to play a role in pathogenicity and are linked to gastric cancer [12–14]. The geographic distribution of H. pylori strains varies; for instance, the most common strains in East Asia carry the cagA , vacA s1, and vacA m1 genes [15].…”

Section: Introductionmentioning

confidence: 99%

“…In several prior studies conducted around the world, cagA, vacA s1, and vacA m1 genes, have been thought to play a role in pathogenicity and are linked to gastric cancer [12][13][14]. The geographic distribution of H. pylori strains varies; for instance, the most common strains in East Asia carry the cagA, vacAs1, and vacAm1 genes [15].…”

Section: Introductionmentioning

confidence: 99%

A Genetic and Immunohistochemical Analysis ofH. PyloriPhenotypes and p27 expression in Adenocarcinoma Patients in Jordan

Brown

Mohammad

Shboul

et al. 2022

Preprint

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Gastric cancer is one of the most prevalent malignant cancers worldwide and specifically, adenocarcinoma. Based on prior research, there is an association between Helicobacter pylori (H. pylori) infection and the frequency of duodenal ulcer, distal gastric adenocarcinoma, mucosa-associated lymphoid tissue lymphoma, and antral gastritis. H. pylori virulence and toxicity factors have been identified that significantly influence the clinical outcomes of H. pylori infection and gastric adenocarcinoma. However, it is unclear exactly how different strains of H. pylori infection affect gastric adenocarcinoma. Current research suggests this involves tumor suppressor genes, like p27, but also H. Pylori toxic proteins. Therefore, we quantified known H. Pylori genotypes within adenocarcinoma patients to establish the prevalence of known toxins that include cytotoxin-associated gene A (cagA) and vacuolating cytotoxin A (vacA) within patients of variable diagnosis. This analysis used gastrectomy samples which were validated for DNA viability. The incidence of H. Pylori in adenocarcinoma patients in Jordan was established to be 54.5% positive (ureA gene) with cagA genotype occurrence at 57.1% but also vacA gene ratios 24.7%:22.1%: 14.3%:14.3%. (vacAs1:vacAs2: vacAm1:vacAm2). It is statistically significant that p27 was dysregulated and suppressed within nearly all H. Pylori vacA genotypes but also that according to our analysis that 24.6% of H. Pylori samples analyzed had an unknown novel genotype and curiously that p27 protein expression was retained in only 12% of tested adenocarcinoma H. Pylori samples which is suggestive that p27 could be used as a prognostic indicator but also that an un-known yet genotype as yet not characterized could be contributing to the regulation of p27 protein within this cellular environment.

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Astaxanthin Inhibits Matrix Metalloproteinase Expression by Suppressing PI3K/AKT/mTOR Activation in Helicobacter pylori-Infected Gastric Epithelial Cells

2022

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Helicobacter pylori (H. pylori) increases production of reactive oxygen species (ROS) and activates signaling pathways associated with gastric cell invasion, which are mediated by matrix metalloproteinases (MMPs). We previously demonstrated that H. pylori activated mitogen-activated protein kinase (MAPK) and increased expression of MMP-10 in gastric epithelial cells. MMPs degrade the extracellular matrix, enhancing tumor invasion and cancer progression. The signaling pathway of phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase B (AKT)/mammalian target of rapamycin (mTOR) is associated with MMP expression. ROS activates PIK3/AKT/mTOR signaling in cancer. Astaxanthin, a xanthophyll carotenoid, shows antioxidant activity by reducing ROS levels in gastric epithelial cells infected with H. pylori. This study aimed to determine whether astaxanthin inhibits MMP expression, cell invasion, and migration by reducing the PI3K/AKT/mTOR signaling in H. pylori-infected gastric epithelial AGS cells. H. pylori induced PIK3/AKT/mTOR and NF-κB activation, decreased IκBα, and induced MMP (MMP-7 and -10) expression, the invasive phenotype, and migration in AGS cells. Astaxanthin suppressed these H. pylori-induced alterations in AGS cells. Specific inhibitors of PI3K, AKT, and mTOR reversed the H. pylori-stimulated NF-κB activation and decreased IκBα levels in the cells. In conclusion, astaxanthin suppressed MMP expression, cell invasion, and migration via inhibition of PI3K/AKT/mTOR/NF-κB signaling in H. pylori-stimulated gastric epithelial AGS cells.

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Association of the Helicobacter pylori cagA, vacA, and iceA genotypes with chronic follicular gastritis in a Colombian population at high risk for gastric cancer

Cited by 3 publications

References 28 publications

A Genetic and Immunohistochemical Analysis of Helicobacter pylori Phenotypes and p27 Expression in Adenocarcinoma Patients in Jordan

A Genetic and Immunohistochemical Analysis of Helicobacter pylori Phenotypes and p27 Expression in Adenocarcinoma Patients in Jordan

A Genetic and Immunohistochemical Analysis ofH. PyloriPhenotypes and p27 expression in Adenocarcinoma Patients in Jordan

Astaxanthin Inhibits Matrix Metalloproteinase Expression by Suppressing PI3K/AKT/mTOR Activation in Helicobacter pylori-Infected Gastric Epithelial Cells

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