Source:http://linkedlifedata.com/resource/pubmed/id/15540901
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2004-11-15
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pubmed:abstractText |
CD26/dipeptidyl peptidase IV (DPPIV), a T-cell-activation antigen, is a 110-kD type II surface glycoprotein expressed on various types of normal cells. CD26/DPPIV is considered a multifunction housekeeping protein. Malignant cells often show altered CD26/DPPIV expression or no CD26/DPPIV expression, thus suggesting a useful marker for assessing some T-cell malignancies. In this study, cell surface protein and messenger RNA expression profiles for CD26/DPPIV were examined in 49 patients with adult T-cell leukemia (ATL), 10 carriers of human T-lymphotropic virus I (HTLV-I), and 4 HTLV-I-infected cell lines to assess the utility of CD26/DPPIV expression as a useful molecular marker for ATL pathology. In contrast to normal lymphocytes, ATL cells and HTLV-I-infected cell lines apparently down-regulated or completely lost the CD26/DPPIV antigen. Furthermore, the positive rate and antigen density for CD26/DPPIV in ATL cells gradually declined along with the advancement of ATL stage. Analysis of genomic DNA and the CD26/DPPIV transcript showed that CD26- ATL cells possessed faintly detected transcripts of the gene that were aberrantly methylated at the CpG islands within the promoter region in parallel with the advancement of ATL, a finding supported by a rescue experiment for transcript reexpression using 5-azacytidine as demethylation agent. Moreover, there was no relationship between loss of CD26/DPPIV and HTLV-I tax expression. These results indicate that ATL cells down-regulate CD26 antigens by means of epigenetic machinery and that this antigen abnormality is a useful molecular marker for the pathology of ATL.
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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:month |
Oct
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pubmed:issn |
0925-5710
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pubmed:author |
pubmed-author:HamaguchiYukioY,
pubmed-author:HarasawaHitomiH,
pubmed-author:HasegawaHirooH,
pubmed-author:KamihiraShimeruS,
pubmed-author:SugaharaKazuyukiK,
pubmed-author:TomonagaMasaoM,
pubmed-author:TsujiTomohiroT,
pubmed-author:TsurudaKazutoK,
pubmed-author:UemuraAkikoA,
pubmed-author:YamadaYasuakiY
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pubmed:issnType |
Print
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pubmed:volume |
80
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
254-60
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:15540901-Biological Markers,
pubmed-meshheading:15540901-Case-Control Studies,
pubmed-meshheading:15540901-CpG Islands,
pubmed-meshheading:15540901-DNA Methylation,
pubmed-meshheading:15540901-Dipeptidyl Peptidase 4,
pubmed-meshheading:15540901-Down-Regulation,
pubmed-meshheading:15540901-Epigenesis, Genetic,
pubmed-meshheading:15540901-Gene Expression Profiling,
pubmed-meshheading:15540901-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:15540901-Humans,
pubmed-meshheading:15540901-Leukemia-Lymphoma, Adult T-Cell,
pubmed-meshheading:15540901-Promoter Regions, Genetic,
pubmed-meshheading:15540901-RNA
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pubmed:year |
2004
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pubmed:articleTitle |
Clinical and oncologic implications in epigenetic down-regulation of CD26/dipeptidyl peptidase IV in adult T-cell leukemia cells.
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pubmed:affiliation |
Department of Laboratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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