Esophageal intraepithelial invasion of Helicobacter pylori correlates with atypical hyperplasia
Esophageal intraepithelial invasion of Helicobacter pylori correlates with atypical hyperplasia
复制标题
幽门螺杆菌食管上皮内侵袭与不典型增生相关
DOI：
10.1002/ijc.28588
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发表时间：
2014-06
影响因子：
6.4
通讯作者：
Su, M.
中科院分区：
文献类型：
--
作者：
Ying, S.;Ying, S.;Su, M.;Su, M.
幽门螺杆菌（H.幽门螺杆菌），一种存在于胃肠道中的常见病原体，在胃癌中得到了很好的表征，而其与食管癌的相关性仍然知之甚少。在这项研究中，我们的目的是评估食管上皮内H。幽门侵入和炎症以及食管鳞状上皮组织不典型增生。检查了来自中国南方和北方食管癌高发区的196例个体的食管鳞状细胞癌（ESCC）组织样本（125例来自北方高危区，71例来自南方高危区），同时在食管鳞状细胞癌（A-ESCC）附近采集了另外30例样本。H. pylori感染通过Giemsa染色、免疫组织化学染色和H. pylori 16S rRNA PCR。H.与非肿瘤组织相比，在肿瘤组织（包括ESCC和A-ESCC样本）中发现幽门螺杆菌感染（p < 0.05）。H. pylori 16 S rRNA在ESCC、A-ESCC和正常组中分别为62.5%、74.1%和26.7%。PCR检测结果显示，H. pylori毒力因子CagA基因在肿瘤（ESCC和A-ESCC）和正常组中的表达分别为54.9%和20%（p < 0.05）。探讨CagA+ H的可能原因。pylori感染导致癌变，发现CagA+ H. pylori滤液可诱导食管上皮细胞DNA链断裂，提示H. pylori感染可能是导致食管鳞状上皮不典型增生的根本原因，并参与了食管鳞癌的病理癌变过程。
Helicobacter pylori (H. pylori), a common pathogen residing in the gastrointestinal tract, has been well characterized in stomach cancer,while its correlation with esophageal cancer remains poorly understood. In this study, we aim to assess the relationship between esophageal intraepithelial H. pylori invasion and inflammation as well as atypical hyperplasia in esophageal squamous epithelial tissues. Esophageal squamous cell carcinoma (ESCC) tissue samples from 196 individuals from both southern and northern esophageal carcinoma high‐risk areas in China were examined (125 from northern high‐risk areas, 71 from southern high‐risk area), while additional 30 samples were collected adjacent to the esophageal squamous cell carcinoma (A‐ESCC). H. pylori infection was identified by Giemsa staining, immuno‐histochemical staining, and H. pylori 16S rRNA‐based PCR. A significant increase of H. pylori infection was found in tumor tissues (including ESCC and A‐ESCC samples) compared to that of non‐tumor tissues (p < 0.05). The positive rate of H. pylori 16S rRNA in ESCC, A‐ESCC, and normal groups were 62.5, 74.1, and 26.7%, respectively. The PCR results showed that the positive incidence of the H. pylori virulence factor CagA gene in tumor (ESCC and A‐ESCC) and normal groups was 54.9 and 20%, respectively (p < 0.05). To explore the possible causes of CagA+ H. pylori infection leading to carcinogenesis, we found that CagA+ H. pylori filtrate induced DNA strand breaks in esophageal epithelial NE3 cells, suggesting that H. pylori infection may be an original cause leading to atypical hyperplasia of esophageal squamous epithelial tissues and contributed to pathological carcinogenesis of ESCC.
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影响因子：
3.4
作者：
Marie MA;Altahir IE
通讯作者：
Altahir IE
影响因子：
11.2
作者：
M. Blaser;G. Perez-Perez-G.-Perez-Perez-82101131;H. Kleanthous;T. Cover;R. Peek;P. Chyou;G. Stemmermann;A. Nomura
通讯作者：
M. Blaser;G. Perez-Perez-G.-Perez-Perez-82101131;H. Kleanthous;T. Cover;R. Peek;P. Chyou;G. Stemmermann;A. Nomura
人乳头瘤病毒诱导食管上皮细胞多期癌变中端粒酶活性与恶性表型的比较研究
DOI：
10.3892/ijmm.8.6.633
发表时间：
2001-12
期刊：
Int J Mol Med,
影响因子：
--
作者：
Shen ZY;Xu LY;Li C;Cai WJ;Shen J;Chen JY;Zeng Y
通讯作者：
Zeng Y
影响因子：
6.3
作者：
K. Campbell
通讯作者：
K. Campbell
影响因子：
3.1
作者：
Nizet, V;Kim, KS;Rubens, CE
通讯作者：
Rubens, CE