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  • 1
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; Germany ; POPULATION ; RISK ; GENE ; GENES ; NITRIC-OXIDE SYNTHASE ; INFECTION ; CARCINOGENESIS ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; NO ; PROMOTER ; RATES ; VARIABILITY ; HELICOBACTER-PYLORI ; INTERFERON-GAMMA ; inflammation ; ONCOLOGY ; RE ; SNPs ; GRADE ; HELICOBACTER-PYLORI INFECTION ; USA ; nitric oxide synthase ; cyclooxygenase ; PROMOTER VARIANT ; Helicobacter pylori ; HIGH-RISK POPULATION ; VENEZUELA ; NUCLEOTIDE ; ANTRUM ; gastric premalignant lesions ; interferon gamma ; VACA
    Abstract: Chronic inflammation induced by Helicobacter pylori is a key process in gastric carcinogenesis. We hypothesized that genetic polymorphisms in important mediators of H. pylori-induced inflammation may influence the risk of developing various grades of precancerous lesions. We studied the associations between single nucleotide polymorphisms (SNPs) in cyclooxygenase 1 and 2 (PTGS1 and PTGS2), inducible nitric oxide synthase (NOS2A), interferon gamma (IFNG) and its receptor (IFNGR1), and risk of gastric precancerous lesions in a Venezuelan population characterized by high rates of H. pylori infection. We found no association of precancerous lesions with SNPs in PTGS1 and in IFNG. A nonsynonymous SNP of NOS2A (Ser608Leu) and an SNP located in the promoter of IFNGR1 (C-56T) were associated with higher risk of atrophic gastritis [odds ratio (OR)= 1.37, 95% confidence interval (CI)=1.01-1.86, and OR=1.49, 95% CI=1.01-2.19, respectively]. Two SNPs; of PTGS2 were associated with risk of dysplasia (OR = 1.60, 95% CI = 1.01 -2.54, and OR = 0.66, 95% CI = 0.43-0.99). We conclude that genetic variability in the genes we studied does not play a major role in the early stages of gastric carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 18287876
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  • 2
    Keywords: BLOOD ; Germany ; HEPATOCELLULAR-CARCINOMA ; GENOME ; LINES ; DNA ; CELL-LINES ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; AMPLIFICATION ; ASSAY ; PLASMA ; SNP ; LINE ; PCR ; cell lines ; STANDARD ; SERUM ; SINGLE ; RE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; RESOURCE ; EXTRACTION ; PRIMER ; LEVEL ; ASSAYS ; RESOURCES ; MULTIPLE DISPLACEMENT AMPLIFICATION ; ROLLING-CIRCLE AMPLIFICATION
    Abstract: While DNA of good quality and sufficient amount can be obtained easily from whole blood, buccal swabs, surgical specimens, or cell lines, these DNA-rich sources are not always available. This is particularly the case in studies for which biological specimens were collected when genotyping assays were not widely available. In those studies, serum or plasma is often the only source of DNA. Newly developed whole genome amplification (WGA) methods, based on phi 29 polymerase, may play a significant role in recovering DNA in such instances. We tested a total of 528 plasma samples kept in storage at -40 degrees C for approximately 10 years for 8 single nucleotide polymorphisms (SNPs) using the 5' exonuclease (TaqMan (R)) assay. These specimens yielded undetectable levels of DNA following extraction with an affinity column but produced an average 52.7 mu g (standard deviation of 31.2 mu g) of DNA when column-extracted DNA was used as a template for WGA. This increased the genotyping success rate from 54% to 93%. There were only 3 disagreements out of 364 paired gehotyping results for pre- and post-WGA DNAs, indicating an error rate of 0.82%. These results are encouraging for expanding the use of poor DNA resources in genotyping studies
    Type of Publication: Journal article published
    PubMed ID: 16235563
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  • 3
    Keywords: CANCER ; carcinoma ; DIAGNOSIS ; FOLLOW-UP ; RISK ; GENE ; GENES ; ACCURACY ; DNA ; INFECTION ; MARKER ; CARCINOGENESIS ; ASSOCIATION ; POLYMORPHISMS ; VARIANTS ; TRIAL ; LESIONS ; PROGRESSION ; EXPERIENCE ; DIFFERENCE ; RATES ; POLYMERASE-CHAIN-REACTION ; STOMACH ; INDIVIDUALS ; CHAIN-REACTION ; chemoprevention ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; BIOPSY ; CHAIN ; ONCOLOGY ; REGRESSION ; RE ; VARIANT ; INCREASE ; polymerase chain reaction ; gastric cancer ; development ; INTERVAL ; methods ; GENOTYPE ; TESTS ; STRAINS ; USA ; odds ratio ; SPECIMENS ; Helicobacter pylori ; BIOPSIES ; LOGISTIC-REGRESSION ; CAGA ; gastric ; HIGH-RISK POPULATION ; VENEZUELA
    Abstract: Background Helicobacter pylori infection is associated with the development of gastric cancer. Although infection with an H. pylori strain containing the cytotoxin-associated (cag A) gene (a marker for a pathogenicity island) may increase the risk of atrophic gastritis and gastric cancer, the relationship of variants in pathogenic H. pylori genes to the severity and progression of precancerous lesions is not well defined. Methods Gastric biopsy specimens were obtained at enrollment from 2145 participants in a chemoprevention trial in Tachira State, Venezuela, and examined histologically to determine the severity of precancerous lesions. The presence of H. pylori DNA in gastric biopsies and the strain type according to presence or absence of the cagA gene were detected by polymerase chain reaction and specific probes. The relationship between H. pylori DNA and histologic diagnosis was analyzed by polytomous logistic regression. Rates of progression and regression of precancerous lesions were determined from biopsies from additional annual gastroscopies (mean follow-up = 3.5 years). All statistical tests were two-sided. Results At enrollment, there was a strong association between cagA-positive H. pylori infection and the severity of gastric precancerous lesions, but cagA-negative H. pylori was associated only with chronic gastritis. Using individuals with normal mucosa or superficial gastritis as control subjects, the odds ratio for dysplasia was 15.5 (95% confidence interval [CI] = 6.42 to 37.2) in cagA-positive individuals compared with uninfected individuals and 0.90 (95% CI = 0.37 to 2.17) for individuals infected with cagA-negative H. pylori compared with uninfected individuals. Individuals infected with cagA-positive H. pylori appeared more likely to experience progression (and less likely to experience regression) of precancerous lesions than those infected with cagA-negative H. pylori, but the differences did not attain statistical significance. Conclusions This large epidemiologic study shows a strong relationship between the presence of H. pylori DNA in gastric biopsies and the severity of precancerous lesions that is specific to cagA-positive strains. The association between H. pylori and gastric carcinoma may have been previously underestimated due to the poor accuracy of serologic H. pylori markers and lack of discrimination by cagA genotype
    Type of Publication: Journal article published
    PubMed ID: 17728213
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