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Helicobacter pylori and Telomerase Activity in Intestinal Metaplasia of the Stomach
BACKGROUND: Helicobacter pylori (H. pylori) has been considered a definitive carcinogen in gastric cancer. Telomerase is activated in gastric cancer and some premalignant gastric lesions, including intestinal metaplasia (IM). In this study, we evaluated the relationships of both H. pylori infection...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Korean Association of Internal Medicine
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531692/ https://www.ncbi.nlm.nih.gov/pubmed/12647636 http://dx.doi.org/10.3904/kjim.2002.17.4.227 |
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author | Chung, Kwun Hwang, Kyu Yoon Kim, In Ho Kim, Hong Soo Park, Sang Heum Lee, Moon Ho Kim, Chang Jin Kim, Sun Joo |
author_facet | Chung, Kwun Hwang, Kyu Yoon Kim, In Ho Kim, Hong Soo Park, Sang Heum Lee, Moon Ho Kim, Chang Jin Kim, Sun Joo |
author_sort | Chung, Kwun |
collection | PubMed |
description | BACKGROUND: Helicobacter pylori (H. pylori) has been considered a definitive carcinogen in gastric cancer. Telomerase is activated in gastric cancer and some premalignant gastric lesions, including intestinal metaplasia (IM). In this study, we evaluated the relationships of both H. pylori infection and telomerase activity with endoscopic and histologic features in IM. The effects of H. pylori eradication on endoscopic, histologic and biochemical changes were evaluated. METHODS: Endoscopic biopsies were obtained from 43 patients with IM for rapid urease, histologic and telomerase tests. The endoscopic and histologic features, H. pylori infection and telomerase were assessed. After H. pylori eradication, 15 patients were re-evaluated and compared after 4 months. RESULTS: Thirty-four (79.1%) patients were infected with H. pylori. The incidence of H. pylori infection was borderline correlated to the severity of IM (p=0.076). Telomerase was elevated in eight (18.6%) patients. Telomerase tends to be high in subtype III and endoscopic grade III of IM. After H. pylori eradication, endoscopic extent (p=0.039) and histologic severity (p=0.074) showed improvements, and telomerase decreased significantly (p=0.0001). CONCLUSION: Our data suggest that telomerase is associated with the severity and extent of IM and that H. pylori eradication improves the endoscopic and histologic features in IM, and decreases telomerase activity. H. pylori eradication can be considered one of the methods to prevent gastric cancer in patients with H. pylori-infected IM. Further long-term and large-scaled study will be needed. |
format | Online Article Text |
id | pubmed-4531692 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | Korean Association of Internal Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-45316922015-10-02 Helicobacter pylori and Telomerase Activity in Intestinal Metaplasia of the Stomach Chung, Kwun Hwang, Kyu Yoon Kim, In Ho Kim, Hong Soo Park, Sang Heum Lee, Moon Ho Kim, Chang Jin Kim, Sun Joo Korean J Intern Med Original Article BACKGROUND: Helicobacter pylori (H. pylori) has been considered a definitive carcinogen in gastric cancer. Telomerase is activated in gastric cancer and some premalignant gastric lesions, including intestinal metaplasia (IM). In this study, we evaluated the relationships of both H. pylori infection and telomerase activity with endoscopic and histologic features in IM. The effects of H. pylori eradication on endoscopic, histologic and biochemical changes were evaluated. METHODS: Endoscopic biopsies were obtained from 43 patients with IM for rapid urease, histologic and telomerase tests. The endoscopic and histologic features, H. pylori infection and telomerase were assessed. After H. pylori eradication, 15 patients were re-evaluated and compared after 4 months. RESULTS: Thirty-four (79.1%) patients were infected with H. pylori. The incidence of H. pylori infection was borderline correlated to the severity of IM (p=0.076). Telomerase was elevated in eight (18.6%) patients. Telomerase tends to be high in subtype III and endoscopic grade III of IM. After H. pylori eradication, endoscopic extent (p=0.039) and histologic severity (p=0.074) showed improvements, and telomerase decreased significantly (p=0.0001). CONCLUSION: Our data suggest that telomerase is associated with the severity and extent of IM and that H. pylori eradication improves the endoscopic and histologic features in IM, and decreases telomerase activity. H. pylori eradication can be considered one of the methods to prevent gastric cancer in patients with H. pylori-infected IM. Further long-term and large-scaled study will be needed. Korean Association of Internal Medicine 2002-12 /pmc/articles/PMC4531692/ /pubmed/12647636 http://dx.doi.org/10.3904/kjim.2002.17.4.227 Text en Copyright © 2002 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Chung, Kwun Hwang, Kyu Yoon Kim, In Ho Kim, Hong Soo Park, Sang Heum Lee, Moon Ho Kim, Chang Jin Kim, Sun Joo Helicobacter pylori and Telomerase Activity in Intestinal Metaplasia of the Stomach |
title | Helicobacter pylori and Telomerase Activity in Intestinal Metaplasia of the Stomach |
title_full | Helicobacter pylori and Telomerase Activity in Intestinal Metaplasia of the Stomach |
title_fullStr | Helicobacter pylori and Telomerase Activity in Intestinal Metaplasia of the Stomach |
title_full_unstemmed | Helicobacter pylori and Telomerase Activity in Intestinal Metaplasia of the Stomach |
title_short | Helicobacter pylori and Telomerase Activity in Intestinal Metaplasia of the Stomach |
title_sort | helicobacter pylori and telomerase activity in intestinal metaplasia of the stomach |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531692/ https://www.ncbi.nlm.nih.gov/pubmed/12647636 http://dx.doi.org/10.3904/kjim.2002.17.4.227 |
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