Source:http://linkedlifedata.com/resource/pubmed/id/15062876
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2004-4-5
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pubmed:abstractText |
Most gastrointestinal stromal tumors (GISTs) contain activating mutations of the proto-oncogene c-kit. The GNNK- isoform of c-kit has a greater oncogenic potential than the GNNK+ isoform. We studied tumors from 29 patients with GIST, 19 of whom had c-kit mutations, and compared them to normal cells and HMC-1 mast cell line. c-kit transcripts were quantified by real-time PCR. The ratios of GNNK-/+ isoforms and of wild-type/mutant alleles were determined by RT-PCR and fluorometric quantification. On average, GISTs contained 1.9 times more c-kit transcripts than the HMC-1 cell line and GISTs with c-kit mutations contained 2.8 times more c-kit transcripts than those without (P=0.003). The median GNNK-/+ isoform ratios in GISTs with and without c-kit mutations were 4.4 and 4.1, respectively, and there was no difference in the GNNK-/+ ratios between the GISTs and the control samples. Both mutant and wild-type alleles of c-kit were expressed in similar amounts in 13/15 mutant GISTs. The oncogenic effects of KIT in GISTs are not related to the higher expression level of the GNNK- isoform. The high expression level of both mutated and wild-type allele transcripts of c-kit suggests that interactions between spontaneously activated and normal c-kit receptors are important in GIST tumorigenesis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0006-3002
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pubmed:author |
pubmed-author:CortezAnnieA,
pubmed-author:DebuireBrigitteB,
pubmed-author:EmileJean-FrançoisJF,
pubmed-author:JuliéCatherineC,
pubmed-author:Lavergne-SloveAnneA,
pubmed-author:Le CesneAxelA,
pubmed-author:LemoineAntoinetteA,
pubmed-author:SaffroyRaphaelR,
pubmed-author:TaboneSéverineS,
pubmed-author:ThéouNathalieN
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pubmed:issnType |
Print
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pubmed:day |
5
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pubmed:volume |
1688
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
250-6
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15062876-Adult,
pubmed-meshheading:15062876-Aged,
pubmed-meshheading:15062876-Base Sequence,
pubmed-meshheading:15062876-DNA Primers,
pubmed-meshheading:15062876-Female,
pubmed-meshheading:15062876-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:15062876-Humans,
pubmed-meshheading:15062876-Immunohistochemistry,
pubmed-meshheading:15062876-Intestinal Mucosa,
pubmed-meshheading:15062876-Male,
pubmed-meshheading:15062876-Middle Aged,
pubmed-meshheading:15062876-Mutation,
pubmed-meshheading:15062876-Proto-Oncogene Proteins c-kit,
pubmed-meshheading:15062876-RNA, Messenger,
pubmed-meshheading:15062876-Stomach Neoplasms,
pubmed-meshheading:15062876-Stromal Cells,
pubmed-meshheading:15062876-Transcription, Genetic
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pubmed:year |
2004
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pubmed:articleTitle |
High expression of both mutant and wild-type alleles of c-kit in gastrointestinal stromal tumors.
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pubmed:affiliation |
INSERM U268, Villejuif 94804, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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