Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-9-6
pubmed:abstractText
Recent studies indicate that chronic gastritis induced by Helicobacter pylori infection is a predisposing condition for the development of both gastric adenocarcinoma and primary gastric B-cell mucosal associated lymphoid tissue (MALT) lymphoma. The chronic gastritis induced by H pylori may evolved in specific individuals in response to additional genetic, environmental, and bacterial-virulence factors. The transitions from chronic gastritis to gastric atrophy with small intestinal (type I) metaplasia, incomplete small intestinal (type II) metaplasia, large intestinal (type III) metaplasia, low-grade dysplasia, and finally high-grade dysplasia are associated with respectively increasing cancer risk. H pylori infection may also lead to the development of an abnormal clone of B-cells and formation of low-grade MALT lymphoma, which is thought to be a precursor for the development of metastatic high-grade MALT lymphoma. In some patients, low grade MALT lymphoma has been shown to regress after eradication of the H pylori infection. The specific genetic abnormalities associated with these premalignant stages of gastric carcinogenesis are currently being defined. Other conditions associated with an increased risk of gastric adenocarcinoma include autoimmune atrophic gastritis, adenomatous polyps, postgastrectomy remnants, and possibly Ménétrier's disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1049-5118
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
61-73
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Premalignant lesions of the stomach.
pubmed:affiliation
Department of Gastroenterology, University of Minnesota, Minneapolis, USA.
pubmed:publicationType
Journal Article, Review