File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Apoptosis and proliferation in Helicobacter pylori-associated gastric intestinal metaplasia

TitleApoptosis and proliferation in Helicobacter pylori-associated gastric intestinal metaplasia
Authors
Issue Date2001
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APT
Citation
Alimentary Pharmacology And Therapeutics, 2001, v. 15 n. 9, p. 1467-1472 How to Cite?
AbstractBackground: Imbalance between apoptosis and proliferation may be one of the mechanisms underlying H. pylori associated gastric carcinogenesis. Aim: To examine the cell kinetics of gastric intestinal metaplasia and the effect of H. pylori eradication. Methods: Endoscopic gastric biopsies were obtained from 100 H. pylori-infected patients. Apoptosis was determined by triphosphate nick-end labelling (TUNEL) and apoptotic nuclei counting, whereas proliferation was assessed by Ki67 immunostaining. Gastric biopsies were repeated in a sub-group of intestinal metaplasia patients after H. pylori eradication. Results: Antral apoptotic index was significantly lower in intestinal metaplasia than in non-intestinal metaplasia (0.19% vs. 0.51%: P < 0.0001) whereas the level of proliferation was comparable (28% vs. 22%, P = 0.15). Serial antral biopsies taken from 14 intestinal metaplasia patients before and 1 year after H. pylori eradication showed a significant drop in proliferation in both intestinal metaplasia (50% vs. 12%, P < 0.001) and non-intestinal metaplasia area (47% vs. 9%, P < 0.001). A similar fall in apoptosis was detected in non-metaplastic region (0.58% vs. 0.38%, P < 0.001) but not in intestinal metaplasia (0.24% vs. 0.27%, P = 0.56), resulting in a significant increase in the apoptosis/proliferation ratio (0.005-0.021; P = 0.03). Conclusions: Dysregulation in apoptosis control of gastric intestinal metaplasia may contribute to gastric carcinogenesis, which may be retarded by clearance of H. pylori.
Persistent Identifierhttp://hdl.handle.net/10722/162470
ISSN
2015 Impact Factor: 6.32
2015 SCImago Journal Rankings: 2.833
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.contributor.authorYu, Jen_US
dc.contributor.authorTo, KFen_US
dc.contributor.authorGo, MYYen_US
dc.contributor.authorMa, PKen_US
dc.contributor.authorChan, FKLen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:20:16Z-
dc.date.available2012-09-05T05:20:16Z-
dc.date.issued2001en_US
dc.identifier.citationAlimentary Pharmacology And Therapeutics, 2001, v. 15 n. 9, p. 1467-1472en_US
dc.identifier.issn0269-2813en_US
dc.identifier.urihttp://hdl.handle.net/10722/162470-
dc.description.abstractBackground: Imbalance between apoptosis and proliferation may be one of the mechanisms underlying H. pylori associated gastric carcinogenesis. Aim: To examine the cell kinetics of gastric intestinal metaplasia and the effect of H. pylori eradication. Methods: Endoscopic gastric biopsies were obtained from 100 H. pylori-infected patients. Apoptosis was determined by triphosphate nick-end labelling (TUNEL) and apoptotic nuclei counting, whereas proliferation was assessed by Ki67 immunostaining. Gastric biopsies were repeated in a sub-group of intestinal metaplasia patients after H. pylori eradication. Results: Antral apoptotic index was significantly lower in intestinal metaplasia than in non-intestinal metaplasia (0.19% vs. 0.51%: P < 0.0001) whereas the level of proliferation was comparable (28% vs. 22%, P = 0.15). Serial antral biopsies taken from 14 intestinal metaplasia patients before and 1 year after H. pylori eradication showed a significant drop in proliferation in both intestinal metaplasia (50% vs. 12%, P < 0.001) and non-intestinal metaplasia area (47% vs. 9%, P < 0.001). A similar fall in apoptosis was detected in non-metaplastic region (0.58% vs. 0.38%, P < 0.001) but not in intestinal metaplasia (0.24% vs. 0.27%, P = 0.56), resulting in a significant increase in the apoptosis/proliferation ratio (0.005-0.021; P = 0.03). Conclusions: Dysregulation in apoptosis control of gastric intestinal metaplasia may contribute to gastric carcinogenesis, which may be retarded by clearance of H. pylori.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APTen_US
dc.relation.ispartofAlimentary Pharmacology and Therapeuticsen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAnti-Bacterial Agents - Therapeutic Useen_US
dc.subject.meshApoptosisen_US
dc.subject.meshFemaleen_US
dc.subject.meshHelicobacter Infections - Drug Therapyen_US
dc.subject.meshHelicobacter Pylori - Pathogenicityen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Nick-End Labelingen_US
dc.subject.meshIntestines - Microbiology - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMetaplasia - Microbiologyen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPyloric Antrum - Microbiology - Pathologyen_US
dc.titleApoptosis and proliferation in Helicobacter pylori-associated gastric intestinal metaplasiaen_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1046/j.1365-2036.2001.01057.xen_US
dc.identifier.pmid11552920-
dc.identifier.scopuseid_2-s2.0-0034840687en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034840687&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume15en_US
dc.identifier.issue9en_US
dc.identifier.spage1467en_US
dc.identifier.epage1472en_US
dc.identifier.isiWOS:000171126900027-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridYu, J=35351306800en_US
dc.identifier.scopusauthoridTo, KF=7101911940en_US
dc.identifier.scopusauthoridGo, MYY=7101882939en_US
dc.identifier.scopusauthoridMa, PK=18836911500en_US
dc.identifier.scopusauthoridChan, FKL=7202586434en_US
dc.identifier.scopusauthoridSung, JJY=24473715000en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats