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Article: Epigenetic inactivation of the MIR34B/C in multiple myeloma
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TitleEpigenetic inactivation of the MIR34B/C in multiple myeloma
 
AuthorsWong, KY1
Yim, RLH1
So, CC1
Jin, DY1
Liang, R1
Chim, CS1
 
Issue Date2011
 
PublisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
 
CitationBlood, 2011, v. 118 n. 22, p. 5901-5904 [How to Cite?]
DOI: http://dx.doi.org/10.1182/blood-2011-06-361022
 
AbstractWe postulated that MIR34B/C, a direct transcriptional target of TP53, might be inactivated by promoter hypermethylation in multiple myeloma (MM). MIR34B/C promoter methylation was studied in 8 normal marrow controls, 8 MM cell lines, 95 diagnostic, and 23 relapsed/progressed MMsamples by methylation-specific PCR. MIR34B/C was methylated in 6 (75.0%) MM cell lines but not normal controls. 5-Aza-2′-deoxycytidine led to MIR34B/C promoter demethylation and MIR34B reexpression. Moreover, restoration of MIR34B led to reduced cellular proliferation and enhanced apoptosis of myeloma cells. In primary samples, methylation of MIR34B/C occurred in 5.3% at diagnosis and 52.2% at relapse/disease progression (P < .001). In 12 MM patients with paired samples at diagnosis and relapse/progression, MIR34B/C methylation was acquired in 6 at relapse/progression. In conclusion, MIR34B/C is a tumor suppressor in myeloma. Hypermethylation of MIR34B/C is tumor-specific. Frequent MIR34B/C hypermethylation during relapse/progression but not at diagnosis implicated a role of MIR34B/C hypermethylation in myeloma relapse/progression. © 2011 by The American Society of Hematology.
 
ISSN0006-4971
2012 Impact Factor: 9.06
2012 SCImago Journal Rankings: 4.553
 
DOIhttp://dx.doi.org/10.1182/blood-2011-06-361022
 
ISI Accession Number IDWOS:000297576600030
Funding AgencyGrant Number
Hong Kong Research Grants Council763409M
Funding Information:

This work was supported by the Hong Kong Research Grants Council General Research Fund (#763409M).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWong, KY
 
dc.contributor.authorYim, RLH
 
dc.contributor.authorSo, CC
 
dc.contributor.authorJin, DY
 
dc.contributor.authorLiang, R
 
dc.contributor.authorChim, CS
 
dc.date.accessioned2012-05-29T06:14:30Z
 
dc.date.available2012-05-29T06:14:30Z
 
dc.date.issued2011
 
dc.description.abstractWe postulated that MIR34B/C, a direct transcriptional target of TP53, might be inactivated by promoter hypermethylation in multiple myeloma (MM). MIR34B/C promoter methylation was studied in 8 normal marrow controls, 8 MM cell lines, 95 diagnostic, and 23 relapsed/progressed MMsamples by methylation-specific PCR. MIR34B/C was methylated in 6 (75.0%) MM cell lines but not normal controls. 5-Aza-2′-deoxycytidine led to MIR34B/C promoter demethylation and MIR34B reexpression. Moreover, restoration of MIR34B led to reduced cellular proliferation and enhanced apoptosis of myeloma cells. In primary samples, methylation of MIR34B/C occurred in 5.3% at diagnosis and 52.2% at relapse/disease progression (P < .001). In 12 MM patients with paired samples at diagnosis and relapse/progression, MIR34B/C methylation was acquired in 6 at relapse/progression. In conclusion, MIR34B/C is a tumor suppressor in myeloma. Hypermethylation of MIR34B/C is tumor-specific. Frequent MIR34B/C hypermethylation during relapse/progression but not at diagnosis implicated a role of MIR34B/C hypermethylation in myeloma relapse/progression. © 2011 by The American Society of Hematology.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationBlood, 2011, v. 118 n. 22, p. 5901-5904 [How to Cite?]
DOI: http://dx.doi.org/10.1182/blood-2011-06-361022
 
dc.identifier.doihttp://dx.doi.org/10.1182/blood-2011-06-361022
 
dc.identifier.eissn1528-0020
 
dc.identifier.epage5904
 
dc.identifier.hkuros200868
 
dc.identifier.isiWOS:000297576600030
Funding AgencyGrant Number
Hong Kong Research Grants Council763409M
Funding Information:

This work was supported by the Hong Kong Research Grants Council General Research Fund (#763409M).

 
dc.identifier.issn0006-4971
2012 Impact Factor: 9.06
2012 SCImago Journal Rankings: 4.553
 
dc.identifier.issue22
 
dc.identifier.pmid21976676
 
dc.identifier.scopuseid_2-s2.0-82155183260
 
dc.identifier.spage5901
 
dc.identifier.urihttp://hdl.handle.net/10722/148661
 
dc.identifier.volume118
 
dc.languageeng
 
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://bloodjournal.hematologylibrary.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofBlood
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAzacitidine - Analogs & Derivatives - Pharmacology
 
dc.subject.meshBase Sequence
 
dc.subject.meshDna Methylation
 
dc.subject.meshDisease Progression
 
dc.subject.meshEpigenesis, Genetic - Drug Effects - Physiology
 
dc.subject.meshGene Expression Regulation, Neoplastic - Drug Effects
 
dc.subject.meshGene Silencing - Drug Effects - Physiology
 
dc.subject.meshHumans
 
dc.subject.meshMicrornas - Genetics
 
dc.subject.meshMolecular Sequence Data
 
dc.subject.meshMultiple Myeloma - Genetics - Pathology
 
dc.subject.meshPrimary Cell Culture
 
dc.subject.meshRecurrence
 
dc.subject.meshTumor Cells, Cultured
 
dc.titleEpigenetic inactivation of the MIR34B/C in multiple myeloma
 
dc.typeArticle
 
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<description.abstract>We postulated that MIR34B/C, a direct transcriptional target of TP53, might be inactivated by promoter hypermethylation in multiple myeloma (MM). MIR34B/C promoter methylation was studied in 8 normal marrow controls, 8 MM cell lines, 95 diagnostic, and 23 relapsed/progressed MMsamples by methylation-specific PCR. MIR34B/C was methylated in 6 (75.0%) MM cell lines but not normal controls. 5-Aza-2&#8242;-deoxycytidine led to MIR34B/C promoter demethylation and MIR34B reexpression. Moreover, restoration of MIR34B led to reduced cellular proliferation and enhanced apoptosis of myeloma cells. In primary samples, methylation of MIR34B/C occurred in 5.3% at diagnosis and 52.2% at relapse/disease progression (P &lt; .001). In 12 MM patients with paired samples at diagnosis and relapse/progression, MIR34B/C methylation was acquired in 6 at relapse/progression. In conclusion, MIR34B/C is a tumor suppressor in myeloma. Hypermethylation of MIR34B/C is tumor-specific. Frequent MIR34B/C hypermethylation during relapse/progression but not at diagnosis implicated a role of MIR34B/C hypermethylation in myeloma relapse/progression. &#169; 2011 by The American Society of Hematology.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong