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  • 1
    Online Resource
    Online Resource
    Polymorphisms in the chemokine (C-X-C motif) ligand 10 are associated with invasive aspergillosis after allogeneic stem-cell transplantation and influence CXCL10 epression in monocyte-derived dendritic cells
    American Society of Hematology ; 2008
    In:  Blood Vol. 111, No. 2 ( 2008-01-15), p. 534-536
    Details
    In: Blood, American Society of Hematology, Vol. 111, No. 2 ( 2008-01-15), p. 534-536
    Abstract: Patients after allogeneic stem-cell transplantation (alloSCT) have an increased risk for invasive aspergillosis (IA). Here, recipients of an allograft with IA (n = 81) or without IA (n = 58) were screened for 84 single nucleotide polymorphisms in 18 immune relevant genes. We found 3 markers in chemokine (C-X-C motif) ligand 10 (CXCL10, 4q21, 11 101 C 〉 T, P = .007; 1642 C 〈 G, P = .003; −1101 A 〈 G, P = .001) significantly associated with an increased risk of developing IA. Furthermore, immature dendritic cells (iDCs) exposed to Aspergillus fumigatus germlings showed markedly higher CXCL10 expression, if carrying the wild type genotype, compared with the “CGAG” high risk haplotype. In addition, serum from patients with proven/probable IA showed increased serum levels of CXCL10, compared with immunocompromised patients without IA. Thus, polymorphisms in CXCL10 determine chemokine secretion by iDCs upon exposure to A fumigatus and most likely thereby genetically determine the risk of IA after alloSCT.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2007-05-090928
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 2
    Online Resource
    Online Resource
    Genetic Polymorphisms in Chemokine Receptor 5, Interleukin 10 and Monocyte Chemoattractant Protein 1 Contribute to Cytomegalovirus Reactivation and Disease after Allogeneic Stem Cell Transplantation.
    American Society of Hematology ; 2005
    In:  Blood Vol. 106, No. 11 ( 2005-11-16), p. 3248-3248
    Details
    In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 3248-3248
    Abstract: Human Cytomegalovirus (HCMV) infection is still one of the most challenging complications after allogeneic stem cell transplantation (alloSCT). Here, we demonstrate that defined single nucleotide polymorphisms (SNPs) are associated with the susceptibility to HCMV infection after alloSCT. Genotyping of 83 patients (with HCMV reactivation) and 71 controls (no HCMV reactivation) was performed. All donors and SCT recipients were Caucasians. Patients suffered from chronic myeloproliferative disorders (n = 16) and AML /ALL /SAA /NHL /MDS (n = 117). For 21 patients, underlying disease could not be determined retrospectively. Genotyping was performed by PyroseqencingTM on the PSQTM HS96A System (Biotage AB, Uppsala Sweden) or on ABI 7900 ABI PRISM® Sequence Detection System using TaqMan® Assay-By-DesignTM and Assay-On-Demand TM (Applied Biosystems). By Armitage’s-Trend-Test, no significant association for 78 /87 markers and the occurrence of HCMV reactivation or disease (p & gt; 0.05) was found. However, 9 markers showed a significant association with HCMV reactivation and /or disease. These markers are located in CCR5, MCP 1and IL10. If comparing individuals with HCMV-DNAemia versus no reactivation regardless of disease, 5 markers showed a significant association (in MCP 1and IL10). Two markers of MCP 1were significantly associated with HCMV reactivation, but none of the markers analyzed in CCR5 and IL10. Thus, we presume that HCMV reactivation is associated with polymorphisms in MCP1, whereas disease might be related to polymorphisms in CCR5 and IL10. Analyzing the clinical parameters, we found an association between CD34 selection and HCMV reactivation (p = 0.0378) or HCMV disease (p = 0.001). Furthermore, severe acute GvHD was significantly related to HCMV disease (p = 0.0015), chronic GvHD was significantly associated to HCMV disease only if reactivation versus disease was compared (p = 0.034). Treatment with corticosteroids led to HCMV reactivation (p = 0.036). In conclusion, screening of alloSCT patients for the presence of defined polymorphisms may help to predict the individual risk of HCMV reactivation and disease, and thus justifying additional antiviral prophylaxis.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V106.11.3248.3248
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2005
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Polymorphisms in Genes of Folate Metabolism and Response to High-Dose Methotrexate in Patients with Primary Central Nervous System Lymphoma.
    American Society of Hematology ; 2005
    In:  Blood Vol. 106, No. 11 ( 2005-11-16), p. 4439-4439
    Details
    In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 4439-4439
    Abstract: The antifolate methotrexate (MTX) was shown to be the single most-effective agent in first-line treatment of patients with primary central nervous system lymphoma (PCNSL) when given intravenously in high doses. MTX inhibits 5,10-methylentetrahydrofolate reductase (MTHFR) as well as thymidylate synthase (TS) in target cells what eventually results in decreased DNA synthesis. Intracellular uptake of both folate and MTX is mediated by the reduced folate carrier (RFC). Genetic polymorphisms for all three proteins were described: a C to T base transition at nucleotide 667 (C677T) and an A to C transition at 1298 (A1298C) of MTHFR; a 28-base pair (bp) tandemly repeated sequence polymorphic in the numbers of the repeat (2R/2R; 3R/3R; and 2R/3R) in the 5′-UTR of TS; a 6bp insertion-(+6bp)/deletion(−6bp)-polymorphism in the 3′-UTR of TS; and a polymorphism at nucleotide 80 (G80A) of RFC. We hypothesized that these polymorphisms may be directly linked to response, survival and toxicity in patients with PCNSL who are treated with single high-dose MTX. We prospectively collected blood from 152 subjects who were enrolled into a German multicenter PCNSL trial. They were scheduled to receive HD-MTX 4 g/m2 every 2 weeks. Genomic DNA was extracted from mononuclear cells using QIAGEN DNA Blood Mini Kit®. Genotyping of the two MTHFR (C677T; A1298C) and the RFC (G80A) single nucleotide polymorphisms (SNPs) was performed by melting point analysis with Master Hybridization Probes® using the Light Cycler® technology. Genotyping of the TS 28bp tandem/triplet repeats in the 5′-UTR was performed by conventional PCR followed by high resolution agarose gel electrophoresis. The TS +6bp/−6bp polymorphism in the 3′-UTR was analyzed with PCR, followed by restriction enzyme digest with draI and agarose gel electrophoresis. The fragment sizes were 70 bp and 88 bp for the 6 bp insertion allele and 152 bp for the 6 bp deletion allele. Allele frequencies for heterozygosity and for homozygous mutations of the two MTHFR and the RFC SNPs as well as of the two TS polymorphisms were as expected for a Caucasian population. For the currently 120 evaluable patients logistic regression analysis, Armitage Trend test and Kaplan-Meier survival curves were performed to analyze the role of the polymorphisms as potential predictors for MTX response. Up to now, we only found a trend for an association between response to treatment and survival for the 2 MTHFR mutations. We will analyze haematological and non-haematological toxicities which will be presented at the meeting with updated results for survival and response in the patients who will have completed treatment until then.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V106.11.4439.4439
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2005
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
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