Source:http://linkedlifedata.com/resource/pubmed/id/21106984
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
2011-2-18
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| pubmed:abstractText |
Deregulated expression of CRLF2 (CRLF2-d) arises via its juxtaposition to the IGH@ enhancer or P2RY8 promoter. Among 865 BCP-ALL children treated on MRC ALL97, 52 (6%) had CRLF2-d, but it was more prevalent among Down syndrome patients (54%). P2RY8-CRLF2 (n = 43) was more frequent than IGH@-CRLF2 (n = 9). CRLF2-d was not associated with age, sex, or white cell count, but IGH@-CRLF2 patients were older than P2RY8-CRLF2 patients (median 8 vs 4 years, P = .0017). Patients with CRLF2-d were more likely to present with enlarged livers and spleens (38% vs 18%, P < .001). CRLF2-d was not seen in conjunction with established chromosomal translocations but 6 (12%) cases had high hyperdiploidy, and 5 (10%) had iAMP21. Univariate analysis suggested that CRLF2-d was associated with an inferior outcome: (event-free survival [EFS] hazard ratio 2.27 [95% confidence interval 1.48-3.47], P < .001; OS 3.69 [2.34-5.84], P < .001). However, multivariate analysis indicated that its effect was mediated by other risk factors such as cytogenetics and DS status (EFS 1.45 [0.88-2.39], P = .140; OS 1.90 [1.08-3.36], P = .027). Although the outcome of IGH@-CRLF2 patients appeared inferior compared with P2RY8-CRLF2 patients, the result was not significant (EFS 2.69 [1.15-6.31], P = .023; OS 2.86 [1.15-6.79], P = .021). Therefore, we concluded that patients with CRLF2-d should be classified into the intermediate cytogenetic risk group.
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| pubmed:commentsCorrections | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
1528-0020
|
| pubmed:author |
pubmed-author:EnsorHannah MHM,
pubmed-author:HarrisonChristine JCJ,
pubmed-author:JonesLisaL,
pubmed-author:KinseySally ESE,
pubmed-author:MasicDinoD,
pubmed-author:MitchellChristopher DCD,
pubmed-author:MoormanAnthony VAV,
pubmed-author:MorrisonHeatherH,
pubmed-author:RichardsSue MSM,
pubmed-author:RussellLisa JLJ,
pubmed-author:SchwabClaireC,
pubmed-author:VoraAjay JAJ
|
| pubmed:issnType |
Electronic
|
| pubmed:day |
17
|
| pubmed:volume |
117
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
2129-36
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| pubmed:dateRevised |
2011-6-22
|
| pubmed:meshHeading |
pubmed-meshheading:21106984-Adolescent,
pubmed-meshheading:21106984-Child,
pubmed-meshheading:21106984-Child, Preschool,
pubmed-meshheading:21106984-Chromosome Aberrations,
pubmed-meshheading:21106984-Disease-Free Survival,
pubmed-meshheading:21106984-Down Syndrome,
pubmed-meshheading:21106984-Enhancer Elements, Genetic,
pubmed-meshheading:21106984-Female,
pubmed-meshheading:21106984-Gene Expression,
pubmed-meshheading:21106984-Genes, Immunoglobulin Heavy Chain,
pubmed-meshheading:21106984-Humans,
pubmed-meshheading:21106984-In Situ Hybridization, Fluorescence,
pubmed-meshheading:21106984-Infant,
pubmed-meshheading:21106984-Kaplan-Meier Estimate,
pubmed-meshheading:21106984-Male,
pubmed-meshheading:21106984-Precursor B-Cell Lymphoblastic Leukemia-Lymphoma,
pubmed-meshheading:21106984-Prognosis,
pubmed-meshheading:21106984-Promoter Regions, Genetic,
pubmed-meshheading:21106984-Receptors, Cytokine,
pubmed-meshheading:21106984-Receptors, Purinergic P2,
pubmed-meshheading:21106984-Translocation, Genetic
|
| pubmed:year |
2011
|
| pubmed:articleTitle |
Demographic, clinical, and outcome features of children with acute lymphoblastic leukemia and CRLF2 deregulation: results from the MRC ALL97 clinical trial.
|
| pubmed:affiliation |
Leukaemia Research Cytogenetics Group, Northern Institute for Cancer Research, Newcastle University, Newcastle-upon-Tyne, UK.
|
| pubmed:publicationType |
Journal Article,
Clinical Trial
|