			Home About us Contact

H. Pylori Genotypes (h + pylori_genotype)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

CDKN2A promoter methylation is related to the tumor location and histological subtype and associated with Helicobacter pylori flaA(+) strains in gastric adenocarcinomas

APMIS, Issue 4 2010
MARKÊNIA KÉLIA SANTOS ALVES
Alves MKS, Lima VP, Ferrasi AC, Rodrigues MA, de Moura Campos Pardini MI, Rabenhorst SHB. CDKN2A promoter methylation is related to the tumor location and histological subtype and associated with Helicobacter pylori flaA(+) strains in gastric adenocarcinomas. APMIS 2010; 118: 297,307. Promoter hypermethylation of CDKN2A (p16INK4A protein) is the main mechanism of gene inactivation. However, its association with Helicobacter pylori infection is a controversial issue. Therefore, we examined a series of gastric adenocarcinomas to assess the association between p16INK4A inactivation and H. pylori genotype (vacA, cagA, cagE, virB11 and flaA) according to the location and histological subtype of the tumors. p16INK4A expression and CDKN2A promoter methylation were found in 77 gastric adenocarcinoma samples by immunohistochemistry and methylation-specific PCR, respectively. Helicobacter pylori infection and genotype were determined by PCR. A strong negative correlation between immunostaining and CDKN2A promoter region methylation was found. In diffuse subtype tumors, the inactivation of p16INK4A by promoter methylation was unique in noncardia tumors (p = 0.022). In addition, H. pylori -bearing flaA was associated with non-methylation tumors (p = 0.008) and H. pylori strain bearing cagA or vacAs1m1 genes but without flaA was associated with methylated tumors (p = 0.022 and 0.003, respectively). Inactivation of p16INK4A in intestinal and diffuse subtypes showed distinct carcinogenic pathways, depending on the tumor location. Moreover, the process of methylation of the CDKN2A promoter seems to depend on the H. pylori genotype. The present data suggest that there is a differential influence and relevance of H. pylori genotype in gastric cancer development. [source]

Relationships between cagA, vacA, and iceA genotypes of Helicobacter pylori and DNA damage in the gastric mucosa

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2004
Marcelo S.P. Ladeira
Abstract Helicobacter pylori (H. pylori) is believed to predispose carriers to gastric cancer by inducing chronic inflammation. The inflammatory processes may result in the generation of reactive oxygen and nitrogen species that damage DNA. In this study, we investigated the relationships between DNA damage in the gastric mucosa and cagA, vacA, and iceA genotypes of H. pylori. The study was conducted with biopsies from the gastric antrum and corpus of 98 H. pylori -infected and 26 uninfected control patients. H. pylori genotypes were determined by PCR and DNA damage was measured in gastric mucosal cells by the Comet assay (single cell gel electrophoresis). All patients were nonsmokers, not abusing alcohol, and not using prescription or recreational drugs. Levels of DNA damage were significantly higher (P < 0.0001) in the H. pylori -infected patients than in uninfected patients. In comparison with the level of DNA damage in the uninfected controls, the extent of DNA damage in both the antrum (OR = 8.45; 95% CI = 2.33,37.72) and the corpus (OR = 6.55; 95% CI = 2.52,17.72) was related to infection by cagA+/vacAs1m1 and iceA1 strains. The results indicate that the genotype of H. pylori is related to the amount of DNA damage in the gastric mucosa. These genotypes could serve as biomarkers for the risk of extensive DNA damage and possibly gastric cancer. Environ. Mol. Mutagen. 44:91,98, 2004. © 2004 Wiley-Liss, Inc. [source]

Molecular Epidemiology and Outcome of Helicobacter pylori Infection in Thailand: a Cultural Cross Roads

HELICOBACTER, Issue 5 2004
Ratha-Korn Vilaichone
ABSTRACT Background., Thailand is at the cultural cross roads between East and South Asia. It has been suggested that this is also the region where the predominant Helicobacter pylori (H. pylori) genotype changes from East Asian to South Asian. Methods., We compared the molecular epidemiology and outcome of H. pylori infections among different ethnic groups in Thailand (Thai, Thai-Chinese and Chinese). H. pylori isolates were genotyped by polymerase chain reaction based on cagA, cag right end junction and vacA genotypes. Results., Ninety-eight isolates from 38 ethnic Thai, 20 ethnic Chinese and 40 Thai-Chinese were categorized into East Asian (45%), South/Central Asian (26%), Western (1%) or mixed type (29%). The East Asian genotype was the most common among Chinese (85%) and Thai-Chinese (55%) (p < .01 compared to ethnic Thai). The ethnicity of the mother among mixed Thai-Chinese marriages predicted the genotype of the child's H. pylori (e.g. when the mother was Chinese, 84% had East Asian type vs. 29% when the mother was Thai) (p < .001). Gastric cancer was common among ethnic Chinese with East Asian genotype (e.g. all Chinese with gastric cancer or peptic ulcer disease had East Asian genotype, whereas only 40% of Chinese with gastritis had this genotype). Conclusions., Immigration, intermarriage and the variety of H. pylori genotypes in Thailand suggest that Thailand is an ideal site for epidemiological studies attempting to relate H. pylori genotypes and host factors to outcome. Our data also support the hypothesis that the primary caretaker of the children is most likely the source of the infection. [source]

Different Helicobacter pylori Strains Colonize the Antral and Duodenal Mucosa of Duodenal Ulcer Patients

HELICOBACTER, Issue 2 2000
Ann-Catrin E. Thoreson
Background. We have investigated the possibility that the same patients may be colonized by Helicobacter pylori strains of different genotypes or phenotypes in the antrum as compared to in the duodenum. The strains were typed for DNA fingerprints, different lipopolysaccharides (LPS), and Lewis antigen expression on the O,side chains of LPS. Materials and Methods. Polymerase chain reaction (PCR) amplifications using primer sequences (i.e., the Enterobacterial Repetitive Intergenic Consensus [ERIC]) and randomly amplified polymorphic DNA (RAPD) elements were performed to asses chromosomal DNA diversity between H. pylori strains. The expression of different LPS types and Lewis antigens in the various H. pylori isolates were determined by whole bacterial enzyme-linked immunosorbent assays using monoclonal antibodies. Results. Duodenal ulcer patients had different H. pylori genotypes in the duodenum as compared to in the antrum as shown by ERIC-PCR (44%) and by RAPD-PCR (75%). Different DNA patterns were found among the strains that were isolated from various regions of the duodenum in 4 of 16 patients (25%) as shown by ERIC-PCR and in 8 of 16 patients (50%) as shown by RAPD-PCR. Sixty-three percent of the duodenal ulcer patients had H. pylori strains with a different Lewis antigen phenotype in the duodenum as compared to in the antrum, and 3 of 16 patients (19%) had strains with different Lewis antigens expressed by strains from different duodenal biopsies from the same patient. Conclusion. The results suggest that a mixed population of different H. pylori strains with marked variation, both genotypically and phenotypically, colonize the same patient. [source]