Helicobacter pylori Infection: A Protective Factor for Esophageal Squamous Cell Carcinoma in a Taiwanese Population

2005 ◽  
Vol 100 (3) ◽  
pp. 588-593 ◽  
Author(s):  
Deng-Chyang Wu ◽  
I-Chen Wu ◽  
Jang-Ming Lee ◽  
Hon-Ki Hsu ◽  
Ein-Long Kao ◽  
...  
2009 ◽  
Vol 136 (5) ◽  
pp. A-749
Author(s):  
Marino Venerito ◽  
Sabine Kohrs ◽  
Thomas Wex ◽  
Klaus Mönkemüller ◽  
Daniel Schubert ◽  
...  

2001 ◽  
Vol 125 (5) ◽  
pp. 520-521 ◽  
Author(s):  
Erdinc Aygenc ◽  
Adin Selcuk ◽  
Serdar Celikkanat ◽  
Cem Ozbek ◽  
Cafer Ozdem

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Huiqin Gao ◽  
Lunan Li ◽  
Chenjing Zhang ◽  
Jiangfeng Tu ◽  
Xiaoge Geng ◽  
...  

Background. Helicobacter pylori is an important carcinogenic factor in gastric cancer. Studies have shown that Helicobacter pylori infection is inversely associated with certain diseases such as esophageal cancer and whose infection appears to have a “protective effect.” At present, the relationship between Helicobacter pylori infection and esophageal cancer remains controversial. This study was designed to investigate the relationship between Helicobacter pylori infection and the risk of esophageal cancer in different regions and ethnicities. Methods. Systematic search of the articles on the relationship between Helicobacter pylori infection and esophageal cancer from the database with the duration time up to December 2018. This systematic review was performed under the MOOSE guidelines. Results. This meta-analysis included 35 studies with 345,886 patients enrolled. There was no significant correlation between Helicobacter pylori infection and esophageal squamous cell carcinoma in the general population (OR: 0.84; 95% CI: 0.64-1.09/OR: 0.74; 95% CI: 0.54-0.97). However, a significant correlation was found in the Middle East (OR: 0.34; 95% CI: 0.22-0.52/95% CI: 0.26-0.44). There was no significant difference in the prevalence of Helicobacter pylori between the case group and the control group in esophageal adenocarcinoma (8.87% vs. 9.67%). The pooled OR was 0.55 (95% CI: 0.43-0.70) or 0.23 (95% CI: 0.15-0.36). When grouped by match or not, the pooled OR of the nonmatching group and the matching group was 0.48/0.21 (95% CI: 0.36-0.65/95% CI: 0.13-0.36) and 0.73/0.71 (95% CI: 0.57-0.92/95% CI: 0.60-0.84), respectively. Conclusion. In the general populations, no significant association was found between Helicobacter pylori infection and the risk of esophageal squamous cell carcinoma. However, lower risk was found in the Middle East. Helicobacter pylori infection may reduce the risk of esophageal adenocarcinoma, but such “protection effect” may be overestimated.


2018 ◽  
Vol 48 (1) ◽  
pp. 251-262 ◽  
Author(s):  
Xian-Zi Yang ◽  
Qing-Jun He ◽  
Tian-Tian Cheng ◽  
Jun Chi ◽  
Zi-Ying Lei ◽  
...  

Background/Aims: Considerable evidence indicates that long noncoding RNAs (lncRNAs) exert importantly regulatory functions during human cancer initiation and progression and are promising biotargets in the flight against cancer. Methods: In this study, we evaluated the role of the lncRNA LINC01133 in esophageal squamous cell carcinoma (ESCC). LINC01133 expression in ESCC was examined by quantitative real-time PCR. The correlations between LINC01133 expression and clinicopathological variables and survival were examined by the χ2 test, Kaplan–Meier method, log-rank test, and univariate Cox regression analysis. Results: LINC01133 expression levels were frequently lower in ESCC tissues and cell lines than in paired normal tissues and an immortalized esophageal epithelial cell line, respectively. The expression of LINC01133 decreased in a TNM stage- and lifestyle-independent manner. LINC01133 was an independent protective factor and had an anti-tumor effect in the early stage of ESCC development. More importantly, we discovered that drinking status in our cohort impaired the predictive accuracy of LINC01133 for patients with ESCC. Furthermore, a new risk model combining LINC01133 expression, drinking status, and TNM stage provided better survival discrimination compared with three other predictors. Conclusions: Our data indicate that a loss of LINC01133 expression is a potential poor prognostic biomarker and therapeutic target for ESCC and provide additional prognostic information to improve the outcomes of ESCC patients.


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