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Maeck, Lienhard
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Maeck, Lienhard
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Maeck, Lienhard
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Maeck, L.
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2000Journal Article [["dc.bibliographiccitation.firstpage","842"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","British Journal of Haematology"],["dc.bibliographiccitation.lastpage","846"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Maeck, L."],["dc.contributor.author","Haase, Detlef"],["dc.contributor.author","Schoch, C."],["dc.contributor.author","Hiddemann, Wolfgang"],["dc.contributor.author","Alves, Frauke"],["dc.date.accessioned","2018-11-07T10:46:22Z"],["dc.date.available","2018-11-07T10:46:22Z"],["dc.date.issued","2000"],["dc.description.abstract","Using a polymerase chain reaction (PCR)-based approach, we examined the prevalence of loss of heterozygosity (LOH) and microsatellite instability (MSI) in relation to chromosomal imbalances in myelodysplastic syndrome (MDS). Two of 26 patients displayed MSI (8%), one of them at five loci. LOH was detected in six out of 26 cases (23%), predominantly involving markers IRF1 [5q31] and WT1 [11p]. Two patients displayed a corresponding chromosomal deletion by conventional cytogenetics. Supporting the mutator phenotype hypothesis, a significant coincidence of LOH, MSI and chromosome abnormalities was observed (P < 0.025). Moreover, our data suggest that LOH represents an initial rather than a secondary genetic event in MDS, promoting genetic instability in a subset of patients."],["dc.identifier.doi","10.1046/j.1365-2141.2000.02088.x"],["dc.identifier.isi","000088482900025"],["dc.identifier.pmid","10929039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47729"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.relation.issn","0007-1048"],["dc.title","Genetic instability in myelodysplastic syndrome: detection of microsatellite instability and loss of heterozygosity in bone marrow samples with karyotype alterations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2000Journal Article [["dc.bibliographiccitation.firstpage","650"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","British Journal of Haematology"],["dc.bibliographiccitation.lastpage","655"],["dc.bibliographiccitation.volume","111"],["dc.contributor.author","Maeck, L."],["dc.contributor.author","Kohaus, P."],["dc.contributor.author","Haase, Detlef"],["dc.contributor.author","Hiddemann, Wolfgang"],["dc.contributor.author","Alves, Frauke"],["dc.date.accessioned","2018-11-07T11:10:23Z"],["dc.date.available","2018-11-07T11:10:23Z"],["dc.date.issued","2000"],["dc.description.abstract","Loss of human MSH2 (hMSH2) protein might be involved in the multistep pathogenesis of haematological malignancies associated with genetic instability. Here, we examine cellular hMSH2 expression in bone marrow samples from 10 haematopoietically normal individuals in comparison with nine patients with myelodysplastic syndrome (MDS) [one refractory anaemia (RA), two RA with ringed sideroblasts (RARS), four RA with excess blasts (RAEB) and two RAEB in transformation (RAEB-T)]. HMSH2 protein was predominantly expressed in myeloblasts and promyelocytes. Blast cells from three patients with RAEB and one with RAEB-T displayed absent or very low hMSH2 expression. As no correlation between hMSH2 expression and chromosomal aberrations was observed, further genetic events seem to be required to induce karyotype instability."],["dc.identifier.doi","10.1046/j.1365-2141.2000.02369.x"],["dc.identifier.isi","000165827300042"],["dc.identifier.pmid","11122116"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53198"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.relation.issn","0007-1048"],["dc.title","Differential cellular expression of the human MSH2 protein in normal and myelodysplastic haematopoiesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS