Source:http://linkedlifedata.com/resource/pubmed/id/16320248
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
2006-2-8
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| pubmed:abstractText |
Gene amplification is one of the mechanisms to activate oncogenes in many cancers, including esophageal adenocarcinoma (EA). In the present study, we used two-dimensional restriction landmark genome scanning to clone a NotI/DpnII fragment that showed increased genomic dosage in 1 of 44 EAs analyzed. This fragment maps to 3q26.3-q27, and subsequent experiments identified two intrachromosomal amplicons within a 10-Mb DNA segment in 7 of 75 (9%) EAs. The distal amplified-core region maps centromeric to the PIK3CA locus, and a microsatellite (D3S1754) within this region exhibited significant instability (MSI), in stark contrast to the genomewide microsatellite stability found in EA. D3S1754-MSI arises in premalignant Barrett's dysplastic cells and preceded amplification of the nascent MSI allele in the corresponding EA. Seven ESTs within the amplified-core were overexpressed in amplicon-containing EAs. One of these, EST AW513672, represents a chimeric transcript that initiated from an antisense promoter sequence in the 5'UTR of a full-length LINE-1 element (L1-5'ASP). Similar chimeric transcripts encoding portions of the MET oncogene and the BCAS3 gene also were overexpressed in EAs, suggesting that L1-5'ASP activation may occur at a broad level in primary EAs. Thus, the fine dissection of a 2-Mb amplified DNA segment in 3q26.3-q27 in EA revealed multiple genetic alterations that had occurred sequentially and/or concurrently during EA development.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
1045-2257
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| pubmed:author |
pubmed-author:BeerDavid GDG,
pubmed-author:ChangAndrew CAC,
pubmed-author:GiordanoThomas JTJ,
pubmed-author:GloverThomas WTW,
pubmed-author:GruberStephen BSB,
pubmed-author:MoranJohn VJV,
pubmed-author:OrringerMark BMB,
pubmed-author:PrescottMichael SMS,
pubmed-author:ThomasDafydd GDG,
pubmed-author:WangZhuwenZ,
pubmed-author:XXX,
pubmed-author:van DekkenHermanH
|
| pubmed:issnType |
Print
|
| pubmed:volume |
45
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
319-31
|
| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:16320248-5' Untranslated Regions,
pubmed-meshheading:16320248-Adenocarcinoma,
pubmed-meshheading:16320248-Base Sequence,
pubmed-meshheading:16320248-Cell Line, Tumor,
pubmed-meshheading:16320248-Chromosomes, Human, Pair 3,
pubmed-meshheading:16320248-Esophageal Neoplasms,
pubmed-meshheading:16320248-Expressed Sequence Tags,
pubmed-meshheading:16320248-Gene Amplification,
pubmed-meshheading:16320248-Genomic Instability,
pubmed-meshheading:16320248-Humans,
pubmed-meshheading:16320248-Microsatellite Repeats,
pubmed-meshheading:16320248-Molecular Sequence Data,
pubmed-meshheading:16320248-Transcription, Genetic
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3-q27 are associated with development of esophageal adenocarcinoma.
|
| pubmed:affiliation |
Department of Surgery Thoracic Section, University of Michigan Medical School, B560 MSRB2, Box 0686, Ann Arbor, MI 48109, USA. linlin@umich.edu
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|