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Article: Hypermethylation of gene promoters in hematological neoplasia

TitleHypermethylation of gene promoters in hematological neoplasia
Authors
Issue Date2002
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/3182
Citation
Hematological Oncology, 2002, v. 20 n. 4, p. 167-176 How to Cite?
AbstractCancer cells are associated with global hypomethylation but with focal hypermethylation of specific gene promoters organized as CpG island. DNA methyltransferases, DNMTI and 3 (3a and 3b), have been implicated in mediating maintenance and de novo methylation. Hypermethylation of gene promoters results in the inactivation of the corresponding genes, by preclusion of the formation of the transcription complex, due to the recruitment of MBP, MeCPs and histone deacetylase. This results in the deacetylation of histone and thus a compact chromatin complex unfavourable for the initiation of transcription. This methylation-associated gene silencing has been demonstrated in various genes including tumour suppressor genes (pl5, pl6, p73, VHL). Therefore, gene promoter hypermethylation collaborates with other mechanisms of gene inactivation such as deletion and intragenic mutations to fulfil Knudson's hypothesis. Hypermethylation may serve as a molecular disease marker for the detection of minimal residual disease. Emerging evidence suggests a possible prognostic value of gene promoter hypermethylation. Moreover, gene hypermethylation may also serve as a target for therapeutic invention by hypomethylating agents. Copyright © 2002 John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/162648
ISSN
2015 Impact Factor: 3.494
2015 SCImago Journal Rankings: 0.767
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_US
dc.contributor.authorLiang, Ren_US
dc.contributor.authorKwong, YLen_US
dc.date.accessioned2012-09-05T05:22:03Z-
dc.date.available2012-09-05T05:22:03Z-
dc.date.issued2002en_US
dc.identifier.citationHematological Oncology, 2002, v. 20 n. 4, p. 167-176en_US
dc.identifier.issn0278-0232en_US
dc.identifier.urihttp://hdl.handle.net/10722/162648-
dc.description.abstractCancer cells are associated with global hypomethylation but with focal hypermethylation of specific gene promoters organized as CpG island. DNA methyltransferases, DNMTI and 3 (3a and 3b), have been implicated in mediating maintenance and de novo methylation. Hypermethylation of gene promoters results in the inactivation of the corresponding genes, by preclusion of the formation of the transcription complex, due to the recruitment of MBP, MeCPs and histone deacetylase. This results in the deacetylation of histone and thus a compact chromatin complex unfavourable for the initiation of transcription. This methylation-associated gene silencing has been demonstrated in various genes including tumour suppressor genes (pl5, pl6, p73, VHL). Therefore, gene promoter hypermethylation collaborates with other mechanisms of gene inactivation such as deletion and intragenic mutations to fulfil Knudson's hypothesis. Hypermethylation may serve as a molecular disease marker for the detection of minimal residual disease. Emerging evidence suggests a possible prognostic value of gene promoter hypermethylation. Moreover, gene hypermethylation may also serve as a target for therapeutic invention by hypomethylating agents. Copyright © 2002 John Wiley & Sons, Ltd.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/3182en_US
dc.relation.ispartofHematological Oncologyen_US
dc.rightsHematological Oncology. Copyright © John Wiley & Sons Ltd.-
dc.subject.meshAnimalsen_US
dc.subject.meshCpg Islandsen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshGenes, Tumor Suppressoren_US
dc.subject.meshHematologic Neoplasms - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.titleHypermethylation of gene promoters in hematological neoplasiaen_US
dc.typeArticleen_US
dc.identifier.emailChim, CS:jcschim@hku.hken_US
dc.identifier.emailLiang, R:rliang@hku.hken_US
dc.identifier.emailKwong, YL:ylkwong@hku.hken_US
dc.identifier.authorityChim, CS=rp00408en_US
dc.identifier.authorityLiang, R=rp00345en_US
dc.identifier.authorityKwong, YL=rp00358en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/hon.694en_US
dc.identifier.pmid12469326-
dc.identifier.scopuseid_2-s2.0-0036941943en_US
dc.identifier.hkuros77932-
dc.identifier.hkuros108003-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036941943&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume20en_US
dc.identifier.issue4en_US
dc.identifier.spage167en_US
dc.identifier.epage176en_US
dc.identifier.isiWOS:000180180600002-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridChim, CS=7004597253en_US
dc.identifier.scopusauthoridLiang, R=26643224900en_US
dc.identifier.scopusauthoridKwong, YL=7102818954en_US

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