Linked Life Data

11205287

Source:http://linkedlifedata.com/resource/pubmed/id/11205287

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6B
pubmed:dateCreated
2001-2-6
pubmed:abstractText
The molecular mechanisms of carcinogenesis in pancreatic cancer are still poorly understood, although the inactivation of tumor suppressor genes at multiple loci is suspected. We investigated the loss of heterozygosity (LOH) on chromosome 22 in pancreatic cancer by means of a PCR-based microsatellite analysis of archival paraffin-embedded histological sections in order to better define deleted region(s) and to test whether the NF-2 gene is involved. Using a panel of thirteen markers that spanned the long arm of chromosome 22, loss of heterozygosity was identified for at least one locus in 37% of investigated pancreatic adenocarcinomas. These deletions are clustered into two separate areas of the chromosome 22--one proximal to the NF-2 gene and one distal. The NF-2 gene itself is not involved. These regions are likely locations of tumor suppressor genes that may contribute to the development of pancreatic cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0250-7005
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4451-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Mapping of genetic deletions on the long arm of chromosome 22 in human pancreatic adenocarcinomas.
pubmed:affiliation
Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, FL 33136, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't