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Article: Epigenetic inactivation of the miR-34a in hematological malignancies
Title | Epigenetic inactivation of the miR-34a in hematological malignancies | ||||
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Authors | |||||
Issue Date | 2010 | ||||
Publisher | Oxford 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? | ||||
Abstract | miR-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 Identifier | http://hdl.handle.net/10722/124905 | ||||
ISSN | 2023 Impact Factor: 3.3 2023 SCImago Journal Rankings: 1.074 | ||||
ISI Accession Number ID |
Funding Information: Seed Funding Programme for Basic Research, The University of Hong Kong to Dr C.S.C. | ||||
References |
DC Field | Value | Language |
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dc.contributor.author | Chim, CS | en_HK |
dc.contributor.author | Wong, KY | en_HK |
dc.contributor.author | Qi, Y | en_HK |
dc.contributor.author | Loong, F | en_HK |
dc.contributor.author | Lam, WL | en_HK |
dc.contributor.author | Wong, LG | en_HK |
dc.contributor.author | Jin, DY | en_HK |
dc.contributor.author | Costello, JF | en_HK |
dc.contributor.author | Liang, R | en_HK |
dc.date.accessioned | 2010-10-31T11:00:43Z | - |
dc.date.available | 2010-10-31T11:00:43Z | - |
dc.date.issued | 2010 | en_HK |
dc.identifier.citation | Carcinogenesis, 2010, v. 31 n. 4, p. 745-750 | en_HK |
dc.identifier.issn | 0143-3334 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/124905 | - |
dc.description.abstract | miR-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.language | eng | en_HK |
dc.publisher | Oxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/ | en_HK |
dc.relation.ispartof | Carcinogenesis | en_HK |
dc.rights | This 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.subject.mesh | Cell Line, Tumor | - |
dc.subject.mesh | DNA Methylation | - |
dc.subject.mesh | Epigenesis, Genetic | - |
dc.subject.mesh | Hematologic Neoplasms - genetics | - |
dc.subject.mesh | MicroRNAs - antagonists and inhibitors - genetics | - |
dc.title | Epigenetic inactivation of the miR-34a in hematological malignancies | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+malignancies | en_HK |
dc.identifier.email | Chim, CS:jcschim@hku.hk | en_HK |
dc.identifier.email | Jin, DY:dyjin@hkucc.hku.hk | en_HK |
dc.identifier.email | Liang, R:rliang@hku.hk | en_HK |
dc.identifier.authority | Chim, CS=rp00408 | en_HK |
dc.identifier.authority | Jin, DY=rp00452 | en_HK |
dc.identifier.authority | Liang, R=rp00345 | en_HK |
dc.description.nature | postprint | - |
dc.identifier.doi | 10.1093/carcin/bgq033 | en_HK |
dc.identifier.pmid | 20118199 | - |
dc.identifier.scopus | eid_2-s2.0-77950910741 | en_HK |
dc.identifier.hkuros | 172191 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-77950910741&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 31 | en_HK |
dc.identifier.issue | 4 | en_HK |
dc.identifier.spage | 745 | en_HK |
dc.identifier.epage | 750 | en_HK |
dc.identifier.eissn | 1460-2180 | - |
dc.identifier.isi | WOS:000276285200028 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Chim, CS=7004597253 | en_HK |
dc.identifier.scopusauthorid | Wong, KY=36151671200 | en_HK |
dc.identifier.scopusauthorid | Qi, Y=35794231800 | en_HK |
dc.identifier.scopusauthorid | Loong, F=6602794154 | en_HK |
dc.identifier.scopusauthorid | Lam, WL=7203021871 | en_HK |
dc.identifier.scopusauthorid | Wong, LG=35793809000 | en_HK |
dc.identifier.scopusauthorid | Jin, DY=7201973614 | en_HK |
dc.identifier.scopusauthorid | Costello, JF=7201995909 | en_HK |
dc.identifier.scopusauthorid | Liang, R=26643224900 | en_HK |
dc.identifier.issnl | 0143-3334 | - |