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Article: Absence of NPM1 promoter hypermethylation in human myelodysplastic syndrome

TitleAbsence of NPM1 promoter hypermethylation in human myelodysplastic syndrome
Authors
Issue Date2010
PublisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/
Citation
Journal Of Clinical Pathology, 2010, v. 63 n. 11, p. 1008-1011 How to Cite?
AbstractNpm1 +/- heterozygous mice develop a haematological disorder with features resembling human myelodysplastic syndrome (MDS). Promoter hypermethylation of the NPM1 gene may lead to suppressed gene transcription and hence functional haploinsufficiency, which contributes to the development of MDS. Thirty-one patients with MDS and eight normal individuals were studied for promoter methylation and mRNA expression of NPM1. Methylation-specific PCR (MSP), COBRA and bisulfite sequencing were used to examine the NPM1 methylation status. Quantitative PCR was used to assess the expression of NPM1. NPM1 DNA methylation was rare, occurring in one of 31 cases as determined by MSP. There was no significant difference in NPM1 mRNA expression between MDS and normal blood samples. In conclusion, the finding suggests that NPM1 methylation is rare in MDS and does not play a major role in its pathogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/163343
ISSN
2014 Impact Factor: 2.915
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, YYen_US
dc.contributor.authorChau, Den_US
dc.contributor.authorChan, Ten_US
dc.contributor.authorGill, Hen_US
dc.contributor.authorLiang, Ren_US
dc.contributor.authorKwong, YLen_US
dc.contributor.authorTse, Een_US
dc.date.accessioned2012-09-05T05:30:19Z-
dc.date.available2012-09-05T05:30:19Z-
dc.date.issued2010en_US
dc.identifier.citationJournal Of Clinical Pathology, 2010, v. 63 n. 11, p. 1008-1011en_US
dc.identifier.issn0021-9746en_US
dc.identifier.urihttp://hdl.handle.net/10722/163343-
dc.description.abstractNpm1 +/- heterozygous mice develop a haematological disorder with features resembling human myelodysplastic syndrome (MDS). Promoter hypermethylation of the NPM1 gene may lead to suppressed gene transcription and hence functional haploinsufficiency, which contributes to the development of MDS. Thirty-one patients with MDS and eight normal individuals were studied for promoter methylation and mRNA expression of NPM1. Methylation-specific PCR (MSP), COBRA and bisulfite sequencing were used to examine the NPM1 methylation status. Quantitative PCR was used to assess the expression of NPM1. NPM1 DNA methylation was rare, occurring in one of 31 cases as determined by MSP. There was no significant difference in NPM1 mRNA expression between MDS and normal blood samples. In conclusion, the finding suggests that NPM1 methylation is rare in MDS and does not play a major role in its pathogenesis.en_US
dc.languageengen_US
dc.publisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/en_US
dc.relation.ispartofJournal of Clinical Pathologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAged, 80 And Overen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGenetic Predisposition To Diseaseen_US
dc.subject.meshHaploinsufficiencyen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMyelodysplastic Syndromes - Genetics - Metabolismen_US
dc.subject.meshNuclear Proteins - Biosynthesis - Geneticsen_US
dc.subject.meshPromoter Regions, Genetic - Geneticsen_US
dc.subject.meshRna, Messenger - Geneticsen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction - Methodsen_US
dc.subject.meshYoung Adulten_US
dc.titleAbsence of NPM1 promoter hypermethylation in human myelodysplastic syndromeen_US
dc.typeArticleen_US
dc.identifier.emailLiang, R:rliang@hku.hken_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.emailTse, E:ewctse@hku.hken_US
dc.identifier.authorityLiang, R=rp00345en_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.identifier.authorityTse, E=rp00471en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1136/jcp.2010.080465en_US
dc.identifier.pmid20924036en_US
dc.identifier.scopuseid_2-s2.0-78149359076en_US
dc.identifier.hkuros207911-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78149359076&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume63en_US
dc.identifier.issue11en_US
dc.identifier.spage1008en_US
dc.identifier.epage1011en_US
dc.identifier.eissn1472-4146-
dc.identifier.isiWOS:000283349800011-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridCheng, YY=7404914973en_US
dc.identifier.scopusauthoridChau, D=55254901600en_US
dc.identifier.scopusauthoridChan, T=37076590700en_US
dc.identifier.scopusauthoridGill, H=36113286500en_US
dc.identifier.scopusauthoridLiang, R=26643224900en_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US
dc.identifier.scopusauthoridTse, E=7005019454en_US

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