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Article: Methylation profiling in multiple myeloma

TitleMethylation profiling in multiple myeloma
Authors
Issue Date2004
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/leukres
Citation
Leukemia Research, 2004, v. 28 n. 4, p. 379-385 How to Cite?
AbstractBackground: We analysed the methylation status of a panel of 10 genes including p15, p16, DAPK, p73, VHL, E-CAD, MGMT, RARβ, RIZ1, and ER. Methods: The gene promoter methylation status was studied by methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) DNA in the bone marrow of 13 patients with myeloma, and one patient with plasmacytoma. Result: None of the 10 genes tested were methylated in eight normal bone marrow samples. For the positive control, the sensitivity of M-MSP ranged from 1×10-2 for E-CAD and MGMT, to 1×10-4 for p73. Of the eight diagnostic myeloma marrow samples, hypermethylation of p15, p16, E-CAD, DAPK and ER occurred in six (75%), four (50%), seven (87.5%), eight (100%), and six (75%) patients. Similarly, of the five samples from patients who progressed from plateau phase, hypermethylation of p15, p16, E-CAD, DAPK, and ER occurred in five (80%), two (40%), five (100%), five (100%), and three (60%). None of the cases had hypermethylation of RIZ1, p73, VHL, RARβ, and MGMT. At diagnosis, all patients had concurrent hypermethylation of at least three genes, and five (62%) had concurrent methylation of four or more genes. One patient with plasmacytoma had methylation of E-CAD, ER, and DAPK. Conclusion: p15, p16, ER, DAPK, and E-CAD (but not RARβ, p73, VHL, RIZ1, and MGMT) were frequently methylated in MM at both diagnosis and disease progression. Future studies of larger scale are needed to identify the genes responsible for disease progression. © 2003 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78335
ISSN
2015 Impact Factor: 2.606
2015 SCImago Journal Rankings: 1.043
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_HK
dc.contributor.authorKwong, YLen_HK
dc.contributor.authorFung, TKen_HK
dc.contributor.authorLiang, Ren_HK
dc.date.accessioned2010-09-06T07:41:44Z-
dc.date.available2010-09-06T07:41:44Z-
dc.date.issued2004en_HK
dc.identifier.citationLeukemia Research, 2004, v. 28 n. 4, p. 379-385en_HK
dc.identifier.issn0145-2126en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78335-
dc.description.abstractBackground: We analysed the methylation status of a panel of 10 genes including p15, p16, DAPK, p73, VHL, E-CAD, MGMT, RARβ, RIZ1, and ER. Methods: The gene promoter methylation status was studied by methylation-specific polymerase chain reaction (MSP) with primers for methylated (M-MSP) and unmethylated (U-MSP) DNA in the bone marrow of 13 patients with myeloma, and one patient with plasmacytoma. Result: None of the 10 genes tested were methylated in eight normal bone marrow samples. For the positive control, the sensitivity of M-MSP ranged from 1×10-2 for E-CAD and MGMT, to 1×10-4 for p73. Of the eight diagnostic myeloma marrow samples, hypermethylation of p15, p16, E-CAD, DAPK and ER occurred in six (75%), four (50%), seven (87.5%), eight (100%), and six (75%) patients. Similarly, of the five samples from patients who progressed from plateau phase, hypermethylation of p15, p16, E-CAD, DAPK, and ER occurred in five (80%), two (40%), five (100%), five (100%), and three (60%). None of the cases had hypermethylation of RIZ1, p73, VHL, RARβ, and MGMT. At diagnosis, all patients had concurrent hypermethylation of at least three genes, and five (62%) had concurrent methylation of four or more genes. One patient with plasmacytoma had methylation of E-CAD, ER, and DAPK. Conclusion: p15, p16, ER, DAPK, and E-CAD (but not RARβ, p73, VHL, RIZ1, and MGMT) were frequently methylated in MM at both diagnosis and disease progression. Future studies of larger scale are needed to identify the genes responsible for disease progression. © 2003 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/leukresen_HK
dc.relation.ispartofLeukemia Researchen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDNA Primersen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshMultiple Myeloma - geneticsen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.titleMethylation profiling in multiple myelomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0145-2126&volume=28&spage=379&epage=385&date=2004&atitle=Methylation+profiling+in+multiple+myelomaen_HK
dc.identifier.emailChim, CS:jcschim@hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.leukres.2003.08.008en_HK
dc.identifier.pmid15109538-
dc.identifier.scopuseid_2-s2.0-1042289347en_HK
dc.identifier.hkuros87681en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1042289347&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume28en_HK
dc.identifier.issue4en_HK
dc.identifier.spage379en_HK
dc.identifier.epage385en_HK
dc.identifier.isiWOS:000220415300011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK
dc.identifier.scopusauthoridFung, TK=7102715924en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK

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