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Article: Epigenetic inactivation of the miR-34a in hematological malignancies

TitleEpigenetic inactivation of the miR-34a in hematological malignancies
Authors
Issue Date2010
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2010, v. 31 n. 4, p. 745-750 How to Cite?
AbstractmiR-34a is a transcriptional target of p53 and implicated in carcinogenesis. We studied the role of miR-34a methylation in a panel of hematological malignancies including acute leukemia [acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL)], chronic leukemia [chronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML)], multiple myeloma (MM) and non-Hodgkin's lymphoma (NHL). The methylation status of miR-34a promoter was studied in 12 cell lines and 188 diagnostic samples by methylation-specific polymerase chain reaction. miR-34a promoter was unmethylated in normal controls but methylated in 75% lymphoma and 37% myeloma cell lines. Hypomethylating treatment led to re-expression of pri-miR-34a transcript in lymphoma cells with homozygous miR-34a methylation. In primary samples at diagnosis, miR-34a methylation was detected in 4% CLL, 5.5% MM samples and 18.8% of NHL at diagnosis but none of ALL, AML and CML (P = 0.011). In MM patients with paired samples, miR-34a methylation status remained unchanged at progression. Amongst lymphoid malignancies, miR-34a was preferentially methylated in NHL (P = 0.018), in particular natural killer (NK)/T-cell lymphoma. In conclusion, amongst hematological malignancies, miR-34a methylation is preferentially hypermethylated in NHL, in particular NK/T-cell lymphoma, in a tumor-specific manner, therefore the role of miR-34a in lymphomagenesis warrants further study. © The Author 2010. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.
Persistent Identifierhttp://hdl.handle.net/10722/124905
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong
Funding Information:

Seed Funding Programme for Basic Research, The University of Hong Kong to Dr C.S.C.

References

 

DC FieldValueLanguage
dc.contributor.authorChim, CSen_HK
dc.contributor.authorWong, KYen_HK
dc.contributor.authorQi, Yen_HK
dc.contributor.authorLoong, Fen_HK
dc.contributor.authorLam, WLen_HK
dc.contributor.authorWong, LGen_HK
dc.contributor.authorJin, DYen_HK
dc.contributor.authorCostello, JFen_HK
dc.contributor.authorLiang, Ren_HK
dc.date.accessioned2010-10-31T11:00:43Z-
dc.date.available2010-10-31T11:00:43Z-
dc.date.issued2010en_HK
dc.identifier.citationCarcinogenesis, 2010, v. 31 n. 4, p. 745-750en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124905-
dc.description.abstractmiR-34a is a transcriptional target of p53 and implicated in carcinogenesis. We studied the role of miR-34a methylation in a panel of hematological malignancies including acute leukemia [acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL)], chronic leukemia [chronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML)], multiple myeloma (MM) and non-Hodgkin's lymphoma (NHL). The methylation status of miR-34a promoter was studied in 12 cell lines and 188 diagnostic samples by methylation-specific polymerase chain reaction. miR-34a promoter was unmethylated in normal controls but methylated in 75% lymphoma and 37% myeloma cell lines. Hypomethylating treatment led to re-expression of pri-miR-34a transcript in lymphoma cells with homozygous miR-34a methylation. In primary samples at diagnosis, miR-34a methylation was detected in 4% CLL, 5.5% MM samples and 18.8% of NHL at diagnosis but none of ALL, AML and CML (P = 0.011). In MM patients with paired samples, miR-34a methylation status remained unchanged at progression. Amongst lymphoid malignancies, miR-34a was preferentially methylated in NHL (P = 0.018), in particular natural killer (NK)/T-cell lymphoma. In conclusion, amongst hematological malignancies, miR-34a methylation is preferentially hypermethylated in NHL, in particular NK/T-cell lymphoma, in a tumor-specific manner, therefore the role of miR-34a in lymphomagenesis warrants further study. © The Author 2010. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsThis is a pre-copy-editing, author-produced PDF of an article accepted for publication in Carcinogenesis following peer review. The definitive publisher-authenticated version Carcinogenesis, 2010, v. 31 n. 4, p. 745-750 is available online at: http://dx.doi.org/10.1093/carcin/bgq033.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCell Line, Tumor-
dc.subject.meshDNA Methylation-
dc.subject.meshEpigenesis, Genetic-
dc.subject.meshHematologic Neoplasms - genetics-
dc.subject.meshMicroRNAs - antagonists and inhibitors - genetics-
dc.titleEpigenetic inactivation of the miR-34a in hematological malignanciesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=31&issue=4&spage=745&epage=750&date=2010&atitle=Epigenetic+inactivation+of+the+miR-34a+in+hematological+malignanciesen_HK
dc.identifier.emailChim, CS:jcschim@hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.emailLiang, R:rliang@hku.hken_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.identifier.authorityLiang, R=rp00345en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1093/carcin/bgq033en_HK
dc.identifier.pmid20118199-
dc.identifier.scopuseid_2-s2.0-77950910741en_HK
dc.identifier.hkuros172191en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77950910741&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue4en_HK
dc.identifier.spage745en_HK
dc.identifier.epage750en_HK
dc.identifier.eissn1460-2180-
dc.identifier.isiWOS:000276285200028-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridWong, KY=36151671200en_HK
dc.identifier.scopusauthoridQi, Y=35794231800en_HK
dc.identifier.scopusauthoridLoong, F=6602794154en_HK
dc.identifier.scopusauthoridLam, WL=7203021871en_HK
dc.identifier.scopusauthoridWong, LG=35793809000en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.scopusauthoridCostello, JF=7201995909en_HK
dc.identifier.scopusauthoridLiang, R=26643224900en_HK

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