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He C.-Y.,Shenyang University | He C.-Y.,Key Laboratory of Cancer Control in Liaoning Province | Sun L.-P.,Shenyang University | Sun L.-P.,Key Laboratory of Cancer Control in Liaoning Province | And 8 more authors.
Journal of Gastroenterology and Hepatology (Australia) | Year: 2011

Background and Aim: Serum pepsinogen II (sPGII) is underutilized and considered an inconspicuous biomarker in clinical practice. We refocused on this neglected but novel biomarker and conducted the present study, aiming to elucidate the normal level of sPGII in healthy Chinese patients and to investigate the clinical utility of sPGII for gastric disease screening. Methods: In 2008-2009, a total of 2022 participants from northern China were selected and enrolled in the study. sPGII and Helicobacter pylori (H. pylori)-immunoglobulin G were measured with ELISA. Results: sPGII showed a normal value of 6.6microg/L in a total of 466 patients with endoscopically- and histologically-normal stomachs. A small sex difference was observed: the average value of sPGII was 7microg/L and 6microg/L in males and females, respectively (P<0.001). In the differentiation between healthy and diseased (endoscopically-diseased stomach or gastritis/atrophic gastritis in endoscopic biopsies) stomach mucosae, the best sPGII cut-off value was 8.25microg/L (sensitivity 70.6%, specificity 70.8%). In screening the H. pylori seropositivity, the optimum cut-off sPGII value was 10.25microg/L (sensitivity 71.6%, specificity 70.1%). Conclusions: We demonstrated that the mean values of sPGII in a healthy Chinese population are 7microg/L and 6microg/L for males and females, respectively. sPGII significantly increases in diseased and H. pylori-infected stomach, and the best sPGII cut-off value is 8.25microg/L in the differentiation between patients with healthy and diseased stomach mucosae. Furthermore, Chinese patients with sPGII greater than 10.25microg/L are at greater risk of various H. pylori-related gastropathies, and are therefore prior candidates for gastro-protection therapy. © 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd.

Duan Z.,Liaoning Medical University | Duan Z.,Key Laboratory of Cancer Control in Liaoning province | He C.,Liaoning Medical University | He C.,Key Laboratory of Cancer Control in Liaoning province | And 12 more authors.
Gene | Year: 2012

Genetic variations in excision repair cross-complementing group 5 (ERCC5) might influence individual vulnerability to gastric cancer (GC). We investigated effects of two putatively functional polymorphisms in ERCC5 promoter region, rs751402 (+. 25A. >. G) and rs2296147 (+. 202C. >. T), and their potential interaction with environment factors on the risk of developing GC. We performed a sex- and age-matched case-control design with 400 GC cases and 400 healthy controls for rs751402 and 403 GC cases and 403 healthy controls for rs2296147. Our results showed that rs751402 were associated with increased GC risk (AA vs. GG: OR = 1.99, 95%CI: 1.20-3.31, P = 0.008; AG + AA vs. GG: OR = 1.41, 95%CI: 1.07-1.86, P = 0.016), and rs2296147 was also associated with increased cancer risk (CC vs. TT: OR = 2.17, 95%CI: 1.04-4.54, P = 0.039; CC vs. CT + TT: OR = 2.26, 95%CI: 1.09-4.69, P = 0.028). In a stratified analysis, rs751402 (AG + AA vs. GG: OR = 1.44, 95%CI: 1.02-2.02, P = 0.037) and rs2296147 (CC vs. CT + TT: OR = 2.33, 95%CI: 1.00-5.44, P = 0.050) were also found to be associated with diffuse-type GC risk. The most common GT haplotype (rs751402-rs2296147) showed protective effect for GC development (OR = 0.73, 95%CI: 0.58-0.91, P = 0.005), and especially for diffuse-type GC (OR = 0.68, 95%CI: 0.52-0.90, P = 0.006). Genetic effects on increased GC risk seemed to be enhanced by Helicobacter pylori infection, smoking and alcohol drinking, with corresponding adjusted ORs of 4.57, 2.42 and 2.50 for the rs751402 AG/AA variants, and of 5.32, 3.20 and 6.87 for the rs2296147 CC variant, but their interaction effects on GC risk didn't reach statistically significance. ERCC5 rs751402 and rs2296147 polymorphisms might alter the risk of developing GC and especially the diffuse subtype. Further validation of our results in larger populations and additional studies evaluating their function impact are required. © 2012 Elsevier B.V.

Zhu Y.,Liaoning Medical University | Zhu Y.,Key Laboratory of Cancer Control in Liaoning Province | Zhu Y.,West Virginia University | Zhu Y.,The Tumor Hospital of Liaoning Province | And 16 more authors.
FEMS Microbiology Letters | Year: 2015

Though Helicobacter pylori (H. pylori) has been classified as class I carcinogen, key virulence factor(s) generated by H. pylori that causes gastric cancer remains to be fully determined. Here, we show that deletion of peptidyl-prolyl cis-trans isomerase(PPIase) prevented H. pylori from stimulating human gastric epithelial cell (AGS) proliferation. Consistent with this observation, ectopic expression of H. pylori PPIase promoted AGS cell proliferation and anchorage-independent growth. To gain insight into the biochemical mechanism of PPIase-induced effect, early signal events involved in mitogenic signaling pathways were evaluated. Expression of H. pylori PPIase caused an increase in basal as well as EGF-stimulated phosphorylation of ERK and EGF receptor at Tyr1086. Treatment with MEK inhibitor completely blocked PPIase-induced cell proliferation. Our results suggest that H. pylori PPIase has the potential to activate mitogenic signaling pathway and to promote transformation of gastric epithelial cells. H. pylori PPIase may represent a novel target for therapeutic management of gastric cancer patients. © FEMS 2015.

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