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    Keywords: PATHWAY ; DIFFERENTIATION ; QUERCETIN ; MUTATIONS ; adenocarcinoma ; GASTRIC-CANCER ; WNT ; BETA-CATENIN EXPRESSION ; TUMOR STEM-CELLS ; DYSREGULATION
    Abstract: OBJECTIVES: Risk of pancreatic cancer between Helicobacter pylori infected and noninfected persons is controversial, and therefore a meta-analysis was performed. METHODS: PubMed was searched up to September 2014. Only population-based nested case-control studies comparing the serological prevalence of Helicobacter pylori between pancreatic cancer cases and cancer-free controls were eligible. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) for pancreatic cancer risk between Helicobacter pylori infected and noninfected persons were estimated. RESULTS: Five eligible nested case-control studies were included, with 1446 pancreatic cancer cases and 2235 cancer-free controls. On the whole, the proportion of pancreatic cancer cases among those infected with Helicobacter pylori was not significant different from those noninfected (OR, 0.99; 95% CI, 0.65-1.50; P = 0.96). Likewise, seropositivity of cytotoxin-associated gene A (CagA) showed nonsignificant association with pancreatic cancer (OR, 0.92; 95% CI, 0.65-1.30; P = 0.63). The CagA-positive virulent strains of Helicobacter pylori did not increase the risk of pancreatic cancer (OR, 0.97; 95% CI, 0.50-1.89; P = 0.93). However, CagA-negative nonvirulent strains of Helicobacter pylori had a significant increased risk for pancreatic cancer (OR, 1.47; 95% CI, 1.11-1.96; P = 0.008). CONCLUSIONS: The CagA-negative non-virulent strains of Helicobacter pylori may be a potential risk factor of pancreatic cancer. High-quality prospective large-scaled studies are required for more conclusive results.
    Type of Publication: Journal article published
    PubMed ID: 26390415
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  • 2
    Keywords: RISK ; HUMAN-PAPILLOMAVIRUS ; POLYMERASE-CHAIN-REACTION ; adenocarcinoma ; NASOPHARYNGEAL CARCINOMA ; HELICOBACTER-PYLORI INFECTION ; EBV ; CLINICOPATHOLOGICAL FEATURES ; GASTRODUODENAL DISEASES ; IN-SITU DETECTION
    Abstract: Epstein-Barr virus (EBV) infection is found in a subset of gastric cancers. Previous reviews have exclusively focused on EBV-encoded small RNA (EBER) positivity in gastric cancer tissues, but a comprehensive evaluation of other type of studies is lacking. We searched the PubMed database up to September, 2014, and performed a systematic review. We considered studies comparing EBV nucleic acids positivity in gastric cancer tissue with positivity in either adjacent non-tumor tissue of cancer patients or non-tumor mucosa from healthy individuals, patients with benign gastric diseases, or deceased individuals. We also considered studies comparing EBV antibodies in serum from cancer patients and healthy controls. Selection of potentially eligible studies and data extraction were performed by 2 independent reviewers. Due to the heterogeneity of studies, we did not perform formal meta-analysis. Forty-seven studies (8069 cases and 1840 controls) were identified. EBER positivity determined by in situ hybridization (ISH) was significantly higher in cancer tissues (range 5.0%-17.9%) than in adjacent mucosa from the same patients or biopsies from all control groups (almost 0%). High EBV nuclear antigen-1 (EBNA-1) positivity by PCR was found in gastric cancer tissues, but most were not validated by ISH or adjusted for inflammatory severity and lymphocyte infiltration. Only 4 studies tested for EBV antibodies, with large variation in the seropositivities of different antibodies in both cases and controls, and did not find an association between EBV seropositivity and gastric cancer. In summary, tissue-based ISH methods strongly suggest an association between EBV infection and gastric cancer, but PCR method alone is invalid to confirm such association. Very limited evidence from serological studies and the lack of novel antibodies warrant further investigations to identify potential risk factors of EBV for gastric cancer.
    Type of Publication: Journal article published
    PubMed ID: 25997049
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