File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Helicobacter pylori and gastric neoplasia.

TitleHelicobacter pylori and gastric neoplasia.
Authors
Issue Date2006
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/COMII
Citation
Contributions To Microbiology., 2006, v. 13, p. 66-80 How to Cite?
AbstractHelicobacter pylori is present in the stomach of more than half of the world population. Based on compelling epidemiological evidences, it was classified by the World Health Organization as a type I gastric carcinogen. It is generally believed that gastric cancer development is a multi-step progression from chronic gastritis to atrophy, intestinal metaplasia, dysplasia, and cancer. Individuals infected with H. pylori have at least a 2-fold increase in risk of gastric cancer development though only a small proportion of infected individuals will ultimately develop this malignancy. The exact mechanisms underlying how H. pylori triggers or causes gastric cancer remain elusive. Certain H. pylori genotypes like cagA, vacA s1 or babA1 are considered to be of higher virulent potential. Apart from the bacterial factors, the host response to chronic H. pylori infection may also attribute to the cancer risk. It was found that individuals who carry pro-inflammatory cytokine gene polymorphism have a substantial increase in risk of cancer development. The combination of bacterial and host genotypes may have a synergistic effect on cancer development. Despite the strong causal link between chronic H. pylori infection and gastric cancer, the role of H. pylori eradication in preventing gastric cancer remains controversial. More long-term data may be necessary to clarify this controversy.
Persistent Identifierhttp://hdl.handle.net/10722/162999
ISSN
2014 SCImago Journal Rankings: 0.333

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.date.accessioned2012-09-05T05:26:23Z-
dc.date.available2012-09-05T05:26:23Z-
dc.date.issued2006en_US
dc.identifier.citationContributions To Microbiology., 2006, v. 13, p. 66-80en_US
dc.identifier.issn1420-9519en_US
dc.identifier.urihttp://hdl.handle.net/10722/162999-
dc.description.abstractHelicobacter pylori is present in the stomach of more than half of the world population. Based on compelling epidemiological evidences, it was classified by the World Health Organization as a type I gastric carcinogen. It is generally believed that gastric cancer development is a multi-step progression from chronic gastritis to atrophy, intestinal metaplasia, dysplasia, and cancer. Individuals infected with H. pylori have at least a 2-fold increase in risk of gastric cancer development though only a small proportion of infected individuals will ultimately develop this malignancy. The exact mechanisms underlying how H. pylori triggers or causes gastric cancer remain elusive. Certain H. pylori genotypes like cagA, vacA s1 or babA1 are considered to be of higher virulent potential. Apart from the bacterial factors, the host response to chronic H. pylori infection may also attribute to the cancer risk. It was found that individuals who carry pro-inflammatory cytokine gene polymorphism have a substantial increase in risk of cancer development. The combination of bacterial and host genotypes may have a synergistic effect on cancer development. Despite the strong causal link between chronic H. pylori infection and gastric cancer, the role of H. pylori eradication in preventing gastric cancer remains controversial. More long-term data may be necessary to clarify this controversy.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/COMIIen_US
dc.relation.ispartofContributions to microbiology.en_US
dc.subject.meshAdenocarcinoma - Microbiologyen_US
dc.subject.meshHelicobacter Infections - Complicationsen_US
dc.subject.meshHelicobacter Pylorien_US
dc.subject.meshHumansen_US
dc.subject.meshStomach Neoplasms - Microbiologyen_US
dc.titleHelicobacter pylori and gastric neoplasia.en_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.pmid16627959-
dc.identifier.scopuseid_2-s2.0-33746102980en_US
dc.identifier.volume13en_US
dc.identifier.spage66en_US
dc.identifier.epage80en_US
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats