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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
Title | 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 |
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Authors | |
Keywords | Biomarker DLC1 Lymphoma Methylation Tumor suppressor gene |
Issue Date | 2007 |
Publisher | Landes 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? |
Abstract | Aberrant 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 Identifier | http://hdl.handle.net/10722/148511 |
ISSN | 2023 Impact Factor: 2.9 2023 SCImago Journal Rankings: 1.149 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ying, J | en_US |
dc.contributor.author | Li, H | en_US |
dc.contributor.author | Murray, P | en_US |
dc.contributor.author | Gao, Z | en_US |
dc.contributor.author | Chen, YW | en_US |
dc.contributor.author | Wang, Y | en_US |
dc.contributor.author | Lee, KY | en_US |
dc.contributor.author | Chan, ATC | en_US |
dc.contributor.author | Ambinder, RF | en_US |
dc.contributor.author | Srivastava, G | en_US |
dc.contributor.author | Tao, Q | en_US |
dc.creator | sml 130626 | - |
dc.date.accessioned | 2012-05-29T06:13:24Z | - |
dc.date.available | 2012-05-29T06:13:24Z | - |
dc.date.issued | 2007 | en_US |
dc.identifier.citation | Epigenetics, 2007, v. 2 n. 1, p. 15-21 | en_US |
dc.identifier.issn | 1559-2294 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/148511 | - |
dc.description.abstract | Aberrant 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.language | eng | en_US |
dc.publisher | Landes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/epigenetics | en_US |
dc.relation.ispartof | Epigenetics | en_US |
dc.subject | Biomarker | - |
dc.subject | DLC1 | - |
dc.subject | Lymphoma | - |
dc.subject | Methylation | - |
dc.subject | Tumor suppressor gene | - |
dc.subject.mesh | Cell Line, Tumor | en_US |
dc.subject.mesh | Chromosome Mapping | en_US |
dc.subject.mesh | Chromosomes, Human, Pair 8 | en_US |
dc.subject.mesh | Dna Methylation | en_US |
dc.subject.mesh | Dna, Neoplasm - Genetics | en_US |
dc.subject.mesh | Epigenesis, Genetic | en_US |
dc.subject.mesh | Gtpase-Activating Proteins | en_US |
dc.subject.mesh | Gene Silencing | en_US |
dc.subject.mesh | Genes, Tumor Suppressor | en_US |
dc.subject.mesh | Hodgkin Disease - Genetics - Pathology | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Lymphoma - Classification - Genetics - Pathology | en_US |
dc.subject.mesh | Nose Neoplasms - Genetics - Pathology | en_US |
dc.subject.mesh | Tumor Suppressor Proteins - Genetics | en_US |
dc.title | 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 | en_US |
dc.type | Article | en_US |
dc.identifier.email | Chen, WYW: wywchen@pathology.hku.hk | en_US |
dc.identifier.email | Srivastava, G: gopesh@pathology.hku.hk | en_US |
dc.identifier.authority | Wang, Y=rp00801 | en_US |
dc.identifier.authority | Srivastava, G=rp00365 | en_US |
dc.description.nature | link_to_OA_fulltext | en_US |
dc.identifier.doi | 10.4161/epi.2.1.3883 | - |
dc.identifier.pmid | 17965626 | - |
dc.identifier.scopus | eid_2-s2.0-34249744340 | en_US |
dc.identifier.hkuros | 139058 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-34249744340&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 2 | en_US |
dc.identifier.issue | 1 | en_US |
dc.identifier.spage | 15 | en_US |
dc.identifier.epage | 21 | en_US |
dc.identifier.isi | WOS:000256223000005 | - |
dc.publisher.place | United States | en_US |
dc.identifier.issnl | 1559-2294 | - |