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Article: Methylation of TET2, CBL and CEBPA in Ph-negative myeloproliferative neoplasms

TitleMethylation of TET2, CBL and CEBPA in Ph-negative myeloproliferative neoplasms
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. 10, p. 942-946 How to Cite?
AbstractA loss-of-function mutation of TET2, CBL and CEBPA has been implicated in the pathogenesis or leukaemic transformation of myeloproliferative neoplasm. As tumour suppressor genes may potentially be inactivated by promoter hypermethylation, the authors studied the methylation status of these genes in three cell lines and diagnostic marrow samples from 45 patients with myeloproliferative neoplasm (MPN) (essential thrombocythaemia, N=34; polycythaemia vera, N=7 and primary myelofibrosis, N=4) by methylation-specific PCR. TET2 was heterozygously methylated in MEG-01 and K562 but completely unmethylated in HEL. On the other hand, both CBL and CEBPA were completely unmethylated in all three cell lines. In the primary marrow samples, methylation of TET2 occurred in two (5.9%) patients with essential thrombocythaemia (4.4% of all patients), both without JAK2 V617 mutation, but not in polycythaemia vera or primary myelofibrosis. There was no association between TET2 methylation with the type of MPN (p=0.713). Hypermethylation of CBL or CEBPA was not detected in any patients. In summary, methylation of TET2, CBL and CEBPA is infrequent in MPN at diagnosis. The role of methylation of these genes at the time of leukaemic transformation warrants further study.
Persistent Identifierhttp://hdl.handle.net/10722/125088
ISSN
2015 Impact Factor: 2.912
2015 SCImago Journal Rankings: 1.260
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_HK
dc.contributor.authorWan, TSen_HK
dc.contributor.authorFung, TKen_HK
dc.contributor.authorWong, KFen_HK
dc.date.accessioned2010-10-31T11:10:42Z-
dc.date.available2010-10-31T11:10:42Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Clinical Pathology, 2010, v. 63 n. 10, p. 942-946en_HK
dc.identifier.issn0021-9746en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125088-
dc.description.abstractA loss-of-function mutation of TET2, CBL and CEBPA has been implicated in the pathogenesis or leukaemic transformation of myeloproliferative neoplasm. As tumour suppressor genes may potentially be inactivated by promoter hypermethylation, the authors studied the methylation status of these genes in three cell lines and diagnostic marrow samples from 45 patients with myeloproliferative neoplasm (MPN) (essential thrombocythaemia, N=34; polycythaemia vera, N=7 and primary myelofibrosis, N=4) by methylation-specific PCR. TET2 was heterozygously methylated in MEG-01 and K562 but completely unmethylated in HEL. On the other hand, both CBL and CEBPA were completely unmethylated in all three cell lines. In the primary marrow samples, methylation of TET2 occurred in two (5.9%) patients with essential thrombocythaemia (4.4% of all patients), both without JAK2 V617 mutation, but not in polycythaemia vera or primary myelofibrosis. There was no association between TET2 methylation with the type of MPN (p=0.713). Hypermethylation of CBL or CEBPA was not detected in any patients. In summary, methylation of TET2, CBL and CEBPA is infrequent in MPN at diagnosis. The role of methylation of these genes at the time of leukaemic transformation warrants further study.en_HK
dc.languageengen_HK
dc.publisherB M J Publishing Group. The Journal's web site is located at http://jcp.bmjjournals.com/en_HK
dc.relation.ispartofJournal of Clinical Pathologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsJournal of Clinical Pathology. Copyright © B M J Publishing Group.en_HK
dc.subject.meshCCAAT-Enhancer-Binding Proteins - genetics-
dc.subject.meshDNA Methylation-
dc.subject.meshDNA-Binding Proteins - genetics-
dc.subject.meshMyeloproliferative Disorders - genetics-
dc.subject.meshOncogene Protein v-cbl - genetics-
dc.titleMethylation of TET2, CBL and CEBPA in Ph-negative myeloproliferative neoplasmsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9746&volume=63&issue=10&spage=942&epage=946&date=2010&atitle=Methylation+of+TET2,+CBL+and+CEBPA+in+Ph-negative+myeloproliferative+neoplasmsen_HK
dc.identifier.emailChim, CS:jcschim@hku.hken_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1136/jcp.2010.080218en_HK
dc.identifier.pmid20671051-
dc.identifier.scopuseid_2-s2.0-77957824328en_HK
dc.identifier.hkuros172839en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77957824328&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume63en_HK
dc.identifier.issue10en_HK
dc.identifier.spage942en_HK
dc.identifier.epage946en_HK
dc.identifier.isiWOS:000282168400016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridWan, TS=25623981600en_HK
dc.identifier.scopusauthoridFung, TK=7102715924en_HK
dc.identifier.scopusauthoridWong, KF=7404759860en_HK

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