Source:http://linkedlifedata.com/resource/pubmed/id/20703256
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
|
| pubmed:dateCreated |
2010-10-13
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| pubmed:abstractText |
We sought to understand the genesis of the t(9;22) by characterizing genomic breakpoints in chronic myeloid leukemia (CML) and BCR-ABL-positive acute lymphoblastic leukemia (ALL). BCR-ABL breakpoints were identified in p190 ALL (n=25), p210 ALL (n=25) and p210 CML (n=32); reciprocal breakpoints were identified in 54 cases. No evidence for significant clustering and no association with sequence motifs was found except for a breakpoint deficit in repeat regions within BCR for p210 cases. Comparison of reciprocal breakpoints, however, showed differences in the patterns of deletion/insertions between p190 and p210. To explore the possibility that recombinase-activating gene (RAG) activity might be involved in ALL, we performed extra-chromosomal recombination assays for cases with breakpoints close to potential cryptic recombination signal sequence (cRSS) sites. Of 13 ALL cases tested, 1/10 with p190 and 1/3 with p210 precisely recapitulated the forward BCR-ABL breakpoint and 1/10 with p190 precisely recapitulated the reciprocal breakpoint. In contrast, neither of the p210 CMLs tested showed functional cRSSs. Thus, although the t(9;22) does not arise from aberrant variable (V), joining (J) and diversity (D) (V(D)J) recombination, our data suggest that in a subset of ALL cases RAG might create one of the initiating double-strand breaks.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
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| pubmed:issn |
1476-5551
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| pubmed:author |
pubmed-author:CalasanzM JMJ,
pubmed-author:CrossN C PNC,
pubmed-author:GrandF HFH,
pubmed-author:Hidalgo-CurtisCC,
pubmed-author:KüngDD,
pubmed-author:KreilSS,
pubmed-author:MeloJ VJV,
pubmed-author:NadelBB,
pubmed-author:OttmanOO,
pubmed-author:ScoreJJ,
pubmed-author:Sobrinho-SimõesM AMA,
pubmed-author:WareEE,
pubmed-author:WiemelsJJ,
pubmed-author:YehR FRF
|
| pubmed:issnType |
Electronic
|
| pubmed:volume |
24
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1742-50
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| pubmed:dateRevised |
2011-11-8
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| pubmed:meshHeading |
pubmed-meshheading:20703256-Base Sequence,
pubmed-meshheading:20703256-Chromosome Breakpoints,
pubmed-meshheading:20703256-Chromosomes, Human, Pair 22,
pubmed-meshheading:20703256-Chromosomes, Human, Pair 9,
pubmed-meshheading:20703256-Fusion Proteins, bcr-abl,
pubmed-meshheading:20703256-Genome, Human,
pubmed-meshheading:20703256-Homeodomain Proteins,
pubmed-meshheading:20703256-Humans,
pubmed-meshheading:20703256-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:20703256-Molecular Sequence Data,
pubmed-meshheading:20703256-Precursor Cell Lymphoblastic Leukemia-Lymphoma,
pubmed-meshheading:20703256-Prognosis,
pubmed-meshheading:20703256-Sequence Homology, Nucleic Acid,
pubmed-meshheading:20703256-Translocation, Genetic
|
| pubmed:year |
2010
|
| pubmed:articleTitle |
Analysis of genomic breakpoints in p190 and p210 BCR-ABL indicate distinct mechanisms of formation.
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| pubmed:affiliation |
Wessex Regional Genetics Laboratory, Salisbury and Human Genetics Division, University of Southampton School of Medicine, Southampton, UK.
|
| pubmed:publicationType |
Journal Article,
Randomized Controlled Trial,
Research Support, Non-U.S. Gov't
|