BackgroundThe vacA, cagA and babA2 genotypes of Helicobacter pylori are associated with gastric pathology. The objectives were to determine the frequency of infection and distribution of the vacA, cagA and babA2 genotypes of H. pylori in patients with gastric ulcer, chronic gastritis and gastric cancer, and to evaluate the association of virulent genotypes with diagnosis.MethodsWe studied 921 patients with symptoms of dyspepsia or with presumptive diagnosis of gastric cancer. The DNA of H. pylori and the vacA, cagA and babA2 genes was detected by PCR in total DNA from gastric biopsies. The association of H. pylori and of its cagA, vacA and babA2 genotypes with diagnosis was determined by calculating the odds ratio (OR).ResultsChronic gastritis was confirmed in 767 patients, gastric ulcer in 115 and cancer in 39. The prevalence of H. pylori was 47.8, 49.6 and 61.5% in those groups, respectively. H. pylori was more frequent in the surrounding tissue (69.2%) than in the tumor (53.8%). The vacA s1m1 genotype predominated in the three groups (45.2, 61.4 and 83.3%, respectively). H. pylori was associated with cancer (ORadjusted = 2.08; 95% CI 1.05–4.13; p = 0.035) but not with ulcer (ORadjusted = 1.07; 95% CI 0.71–1.61; p = 0.728). The s1m1 genotype was associated with ulcer and cancer (ORadjusted = 2.02; 95% CI 1.12–3.62; p = 0.019 and ORadjusted = 6.58; 95% CI 2.15–20.08; p = 0.001, respectively). babA2 was associated with gastric cancer, and cagA was not associated with the diagnosis.ConclusionsIn population from Southern Mexico, H. pylori and the s1m1 genotype were associated with gastric cancer and the s1m1/cagA+/babA2+ strains predominated in tumor and adjacent tissue.

The chronic inflammation and damage to the gastric epithelium induced by Helicobacter pylori (H. pylori) are the main risk factors for gastric cancer development. Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) induce chronic inflammation and have been found in gastric tumors. The objectives this observational study were to determine the frequency of multiple infections by Helicobacter pylori, Epstein-Barr virus (EBV) and human cytomegalovirus (HCMV) and to relate the infection by EBV and HCMV with H. pylori vacA/cagA genotypes in patients with chronic gastritis or gastric cancer. DNA from H. pylori, EBV and HCMV was detected by PCR in biopsies from 106 Mexican patients with chronic gastritis and 32 from gastric cancer. The cagA status and the vacA genotypes of H. pylori were determined by PCR. In chronic gastritis and gastric cancer EBV was found in 69.8% and 87.5%, HCMV in 52.8% and 53.1%, and H. pylori in 48.1% and 40.6%, respectively. In chronic gastritis, 53% of H. pylori+ patients were EBV+ and 33% were both EBV+/HCMV+; in gastric cancer, 92.3% of H. pylori-infected individuals were EBV+ and 46.1% were EVB+/HCMV+. All the intestinal- and mixed-type tumors and the 83.3% of diffuse-type tumors were EBV+. No significant differences were found between single infections or coinfections with the diagnosis or the cancer type. The H. pylori genotypes were not related to EBV or HCMV infection. The frequency of dual infections by H. pylori, EBV and HCMV is higher in patients from southwest Mexico than other populations. It is likely that these pathogens act synergistically to induce inflammation and gastric cancer.

Background: Helicobacter pylori (H. pylori) is the main risk factor for the development of chronic gastritis, gastric ulcer, and gastric cancer. In H. pylori-infected individuals, the clinical result is dependent on various factors, among which are bacterial components, the immune response, and environmental influence. Aims: To compare IFN-␥ expression with the H. pylori vacA and cagA genotypes in patients with chronic gastritis and patients with gastric cancer. Methods: Ninety-five patients diagnosed with chronic gastritis and 20 with gastric cancer were included in the study. Three gastric biopsies were taken; one was used for the molecular detection and genotyping of H. pylori; another was fixed in absolute alcohol and histologic sections were made for determining IFN-␥ expression through immunohistochemistry.ଝ Please cite this article as: Martínez-Carrillo DN, Atrisco-Morales J, Hernández-Pando R, Reyes-Navarrete S, Betancourt-Linares R, Cruzdel Carmen I, et al. Diversidad de los genotipos vacA y cagA de Helicobacter pylori y expresión de interferón gamma en pacientes con gastritis crónica y cáncer gástrico. Revista de Gastroenterología de México. 2014;79:220---228.Diversidad de los genotipos vacA y cagA de Helicobacter pylori y expresión de interferón gamma en pacientes con gastritis crónica y cáncer gástrico ResumenAntecedentes: El H. pylori es el principal factor de riesgo para el desarrollo de gastritis crónica, úlcera gástrica y cáncer gástrico. El resultado clínico en infectados por esta bacteria depende de varios factores, entre ellos los componentes bacterianos, la respuesta inmune, y la influencia del medio ambiente. Objetivo: Comparar la expresión de IFN-␥ con los genotipos vacA y cagA de H. pylori en pacientes con gastritis crónica y cáncer gástrico. Pacientes y métodos: Se incluyeron 95 pacientes con diagnóstico de gastritis crónica y 20 con cáncer gástrico. Se tomaron 3 biopsias gástricas, una se utilizó para la identificación molecular y genotipificación de H. pylori. Otra fue fijada en alcohol absoluto y realizaron cortes histológicos para determinar la expresión de IFN-␥ por inmunohistoquímica. Resultados: No se encontraron diferencias en las células que expresaron IFN-␥ entre pacientes con gastritis crónica (mediana del porcentaje de células positivas: 82.6% en pacientes sin H. pylori y 82% en personas infectadas) y cáncer gástrico (70.5% en pacientes H. pylorinegativos y 78.5% en infectados). En pacientes con gastritis crónica infectados por H. pylori vacAs2m2/cagA − la expresión de IFN-␥ fue del 69%, en pacientes con H. pylori vacAs1m2/cagA − fue de 86.5%, en vacAs1m1/cagA − del 86.5%, y en vacAs1m1/cagA + del 82%. En cáncer se encontraron datos similares. Conclusión: La expresión de INF-␥ varía dependiendo del genotipo vacA y cagA de H. pylori, pero no de acuerdo a la presencia de gastritis crónica o cáncer gástrico.

IFN-γ expression varied depending on the H. pylori vacA and cagA genotype, but not in accordance with the presence of chronic gastritis or gastric cancer.

In women, serum levels of CTSB, GKN2, LIPF, LIPFG, AZGP1, TOP2A and PGA4 are proposed as predictive markers of gastric cancer. It is unknown whether GKN1 expression varies with the sex of patients with chronic gastritis or gastric cancer. We studied 36 patients with histopathological diagnosis of chronic gastritis from the state of Guerrero, Mexico. PCR was performed for H. pylori detection and GKN1 expression was determined by RT-qPCR and western blot. GKN1 mRNA expression was significantly lower in patients with chronic follicular gastritis than in those with chronic chemical gastritis (p = 0.00071). The mRNA and protein level of expression of GKN1 were significantly lower in women with chronic follicular gastritis than in men with the same condition (p = 0.0279 and p = 0.0014, respectively); the lowest levels of GKN1 were detected in women with H. pylori-positive follicular gastritis (p = 0.0175 and p = 0.0111, respectively). Through a bioinformatic analysis, estrogen response elements were identified in the GKN1 promoter.