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Article: Tumor-specific methylation of the 8p22 tumor suppressor gene DLC1 is an epigenetic biomaker for Hodgkin, nasal NK/T-cell and other types of lymphomas

TitleTumor-specific methylation of the 8p22 tumor suppressor gene DLC1 is an epigenetic biomaker for Hodgkin, nasal NK/T-cell and other types of lymphomas
Authors
Issue Date2007
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/epigenetics
Citation
Epigenetics, 2007, v. 2 n. 1, p. 15-21 How to Cite?
AbstractAberrant promoter methylation is an epigenetic mechanism for silencing tumor suppresor genes (TSG), and is also a biomarker for early cancer diagnosis and prognosis prediction. Recently, we and others identified DLC1 (ARHGAP7) as a functional TSG frequently methylated in multiple carcinomas. Here, we further uncovered DLC1 as one of the up-regulated genes in lymphoma cell lines after pharmacologic demethylation with 5-aza-2′-deoxycytidine (Aza). Transcriptional silencing and methylation of DLC1 was detected in most Hodgkin (HL) and non-Hodgkin lymphoma (NHL) cell lines, including 4/6 Hodgkin, 4/4 nasal NK/T-cell, 6/ 6 Burkitt and 5/5 diffuse large B-cell lymphoma cell lines. Aza treatment led to DLC1 promoter demethylation and transcriptional reactivation in silenced cell lines, indicating a methylation-mediated silencing. Aberrant methylation was further detected in 44% (14/37) Hodgkin, 77% (34/44) nasal NK/T-cell and 60-90% of various types of primary NHLs, but not in any normal lymph node or PBMC sample, and is thus tumor-specific. Analysis of microdissected Hodgkin/Reed-Sternberg (HRS) cells from HL cases confirmed the site of methylation as tumor cells. Moreover, DLC1 methylation was detected in 4/14 (29%) serum samples from HL patients. Our results indicate that DLC1 methylation is a frequent event in multiple lymphomagenesis and could serve as a tumor-specific biomarker for future lymphoma diagnosis. © 2007 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/148511
ISSN
2015 Impact Factor: 4.774
2015 SCImago Journal Rankings: 2.672
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYing, Jen_US
dc.contributor.authorLi, Hen_US
dc.contributor.authorMurray, Pen_US
dc.contributor.authorGao, Zen_US
dc.contributor.authorChen, YWen_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorLee, KYen_US
dc.contributor.authorChan, ATCen_US
dc.contributor.authorAmbinder, RFen_US
dc.contributor.authorSrivastava, Gen_US
dc.contributor.authorTao, Qen_US
dc.creatorsml 130626-
dc.date.accessioned2012-05-29T06:13:24Z-
dc.date.available2012-05-29T06:13:24Z-
dc.date.issued2007en_US
dc.identifier.citationEpigenetics, 2007, v. 2 n. 1, p. 15-21en_US
dc.identifier.issn1559-2294en_US
dc.identifier.urihttp://hdl.handle.net/10722/148511-
dc.description.abstractAberrant promoter methylation is an epigenetic mechanism for silencing tumor suppresor genes (TSG), and is also a biomarker for early cancer diagnosis and prognosis prediction. Recently, we and others identified DLC1 (ARHGAP7) as a functional TSG frequently methylated in multiple carcinomas. Here, we further uncovered DLC1 as one of the up-regulated genes in lymphoma cell lines after pharmacologic demethylation with 5-aza-2′-deoxycytidine (Aza). Transcriptional silencing and methylation of DLC1 was detected in most Hodgkin (HL) and non-Hodgkin lymphoma (NHL) cell lines, including 4/6 Hodgkin, 4/4 nasal NK/T-cell, 6/ 6 Burkitt and 5/5 diffuse large B-cell lymphoma cell lines. Aza treatment led to DLC1 promoter demethylation and transcriptional reactivation in silenced cell lines, indicating a methylation-mediated silencing. Aberrant methylation was further detected in 44% (14/37) Hodgkin, 77% (34/44) nasal NK/T-cell and 60-90% of various types of primary NHLs, but not in any normal lymph node or PBMC sample, and is thus tumor-specific. Analysis of microdissected Hodgkin/Reed-Sternberg (HRS) cells from HL cases confirmed the site of methylation as tumor cells. Moreover, DLC1 methylation was detected in 4/14 (29%) serum samples from HL patients. Our results indicate that DLC1 methylation is a frequent event in multiple lymphomagenesis and could serve as a tumor-specific biomarker for future lymphoma diagnosis. © 2007 Landes Bioscience.en_US
dc.languageengen_US
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/epigeneticsen_US
dc.relation.ispartofEpigeneticsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshChromosome Mappingen_US
dc.subject.meshChromosomes, Human, Pair 8en_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDna, Neoplasm - Geneticsen_US
dc.subject.meshEpigenesis, Geneticen_US
dc.subject.meshGtpase-Activating Proteinsen_US
dc.subject.meshGene Silencingen_US
dc.subject.meshGenes, Tumor Suppressoren_US
dc.subject.meshHodgkin Disease - Genetics - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshLymphoma - Classification - Genetics - Pathologyen_US
dc.subject.meshNose Neoplasms - Genetics - Pathologyen_US
dc.subject.meshTumor Suppressor Proteins - Geneticsen_US
dc.titleTumor-specific methylation of the 8p22 tumor suppressor gene DLC1 is an epigenetic biomaker for Hodgkin, nasal NK/T-cell and other types of lymphomasen_US
dc.typeArticleen_US
dc.identifier.emailChen, WYW: wywchen@pathology.hku.hken_US
dc.identifier.emailSrivastava, G: gopesh@pathology.hku.hken_US
dc.identifier.authorityWang, Y=rp00801en_US
dc.identifier.authoritySrivastava, G=rp00365en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.4161/epi.2.1.3883-
dc.identifier.pmid17965626-
dc.identifier.scopuseid_2-s2.0-34249744340en_US
dc.identifier.hkuros139058-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34249744340&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume2en_US
dc.identifier.issue1en_US
dc.identifier.spage15en_US
dc.identifier.epage21en_US
dc.identifier.isiWOS:000256223000005-
dc.publisher.placeUnited Statesen_US

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