Source:http://linkedlifedata.com/resource/pubmed/id/17965626
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2007-11-5
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pubmed:abstractText |
Aberrant promoter methylation is an epigenetic mechanism for silencing tumor suppressor 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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1559-2308
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pubmed:author |
pubmed-author:AmbinderRichard FRF,
pubmed-author:ChanAnthony T CAT,
pubmed-author:ChenYun-WenYW,
pubmed-author:GaoZifenZ,
pubmed-author:LeeKwan YeungKY,
pubmed-author:LiHongyuH,
pubmed-author:MurrayPaulP,
pubmed-author:SrivastavaGopeshG,
pubmed-author:TaoQianQ,
pubmed-author:WangYajunY,
pubmed-author:YingJianmingJ
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pubmed:issnType |
Electronic
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pubmed:volume |
2
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
15-21
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pubmed:dateRevised |
2011-10-3
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pubmed:meshHeading |
pubmed-meshheading:17965626-Cell Line, Tumor,
pubmed-meshheading:17965626-Chromosome Mapping,
pubmed-meshheading:17965626-Chromosomes, Human, Pair 8,
pubmed-meshheading:17965626-DNA, Neoplasm,
pubmed-meshheading:17965626-DNA Methylation,
pubmed-meshheading:17965626-Epigenesis, Genetic,
pubmed-meshheading:17965626-GTPase-Activating Proteins,
pubmed-meshheading:17965626-Gene Silencing,
pubmed-meshheading:17965626-Genes, Tumor Suppressor,
pubmed-meshheading:17965626-Hodgkin Disease,
pubmed-meshheading:17965626-Humans,
pubmed-meshheading:17965626-Lymphoma,
pubmed-meshheading:17965626-Nose Neoplasms,
pubmed-meshheading:17965626-Tumor Suppressor Proteins
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pubmed:articleTitle |
Tumor-specific methylation of the 8p22 tumor suppressor gene DLC1 is an epigenetic biomarker for Hodgkin, nasal NK/T-cell and other types of lymphomas.
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pubmed:affiliation |
Cancer Epigenetics Laboratory, Sir YK Pao Center for Cancer, Department of Clinical Oncology, Hong Kong Cancer Institute, Chinese University of Hong Kong, Hong Kong, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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