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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-11-8
pubmed:abstractText
Single nucleotide polymorphisms (SNPs) in genes of the immune system predict for aGVHD and mortality after allo-SCT. We investigated the effect of SNPs in the NOD2, BPI, and IL-23R genes on posttransplantation outcome in a cohort of 304 patients. NOD2 patient and donor genotype and BPI recipient genotype were not associated with the occurrence of aGVHD. However, IL-23R-SNP in the donor was correlated with less aGVHD. This association could be confirmed in multivariate analysis (odds ratio [OR], 0.39; P = .039), which identified in vivo T cell depletion (OR, 0.32; P < .001) and multiagent GVHD prophylaxis (OR, 0.51; P = .031) as other independent factors predicting for less-severe aGVHD. This multivariate model also revealed a trend toward less aGVHD in patients receiving a BPI G allele transplant (OR, 0.60; P = .067) and in those receiving a transplant from an HLA-matched donor (OR, 0.57; P = .058). In contrast, relapse was more frequent in patients with NOD2-SNPs (46.2% for SNP vs 33.2% for wild-type; P = .020). This association was found to be of borderline significance in multivariate analysis. Neither BPI nor IL-23R genotype predicted for relapse, and none of the investigated SNPs was correlated with 5-year overall survival. In our analysis, NOD2 SNPs did not predict aGVHD, but IL-23R(1142A>G) and BPI(A645G) SNPs appeared to be promising markers in this regard. The importance of these markers in prediction models for GVHD and relapse remain to be defined in large prospective clinical trials.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1523-6536
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1718-27
pubmed:meshHeading
pubmed-meshheading:20541026-Acute Disease, pubmed-meshheading:20541026-Adolescent, pubmed-meshheading:20541026-Adult, pubmed-meshheading:20541026-Aged, pubmed-meshheading:20541026-Child, pubmed-meshheading:20541026-Cohort Studies, pubmed-meshheading:20541026-Disease-Free Survival, pubmed-meshheading:20541026-Female, pubmed-meshheading:20541026-Gene Frequency, pubmed-meshheading:20541026-Genotype, pubmed-meshheading:20541026-Graft vs Host Disease, pubmed-meshheading:20541026-Hematopoietic Stem Cell Transplantation, pubmed-meshheading:20541026-Humans, pubmed-meshheading:20541026-Immunity, Innate, pubmed-meshheading:20541026-Male, pubmed-meshheading:20541026-Middle Aged, pubmed-meshheading:20541026-Nod2 Signaling Adaptor Protein, pubmed-meshheading:20541026-Polymorphism, Single Nucleotide, pubmed-meshheading:20541026-Receptors, Interleukin, pubmed-meshheading:20541026-Transplantation, Homologous, pubmed-meshheading:20541026-Young Adult
pubmed:year
2010
pubmed:articleTitle
Genetic variations of interleukin-23R (1143A>G) and BPI (A645G), but not of NOD2, are associated with acute graft-versus-host disease after allogeneic transplantation.
pubmed:affiliation
Department of Medicine I, University Hospital Carl-Gustav-Carus, Fetscherstraße 74, Dresden, Germany. martin.wermke@uniklinikum-dresden.de
pubmed:publicationType
Journal Article