Cited 33 times in
Hypermethylation of death-associated protein (DAP) kinase CpG island is frequent not only in B-cell but also in T- and natural killer (NK)/T-cell malignancies
DC Field | Value | Language |
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dc.contributor.author | 양우익 | - |
dc.date.accessioned | 2015-07-15T17:11:02Z | - |
dc.date.available | 2015-07-15T17:11:02Z | - |
dc.date.issued | 2003 | - |
dc.identifier.issn | 1347-9032 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/114396 | - |
dc.description.abstract | Death-associated protein (DAP) kinase is a pro-apoptotic serine/threonine kinase with a death domain, which is involved in apoptosis induced by interferon-gamma, tumor necrosis factor-alpha, and Fas ligand. Down-regulation of DAP kinase gene expression by hypermethylation of its promoter region might result in resistance to apoptotic cell death, and could provide a basis for tumor development. In the present study, we employed methylation-specific polymerase chain reaction to examine the methylation status of CpG islands in the DAP kinase gene in 19 cases of T-cell malignancies (including eight adult T-cell leukemia/lymphoma), 24 of natural killer (NK)/T-cell, and 34 of B-cell. Frequency of methylation was significantly higher in B-cell (27 of 34, 79.4%) than in T-cell malignancies (nine of 19, 47.4%) (P<0.05). Fifteen of 24 (62.5%) NK/T-cell lymphomas showed DNA methylation. One B-cell lymphoma cell line with DNA methylation was resistant to apoptotic stimuli, and treatment of the cells with a demethylating agent restored apoptotic cell death. These findings suggested that suppression of DAP kinase expression by DNA methylation might play a substantial role in the development of not only B-cell, but also T- and NK/T-cell lymphomas. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 87~91 | - |
dc.relation.isPartOf | CANCER SCIENCE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Antibodies, Monoclonal/pharmacology | - |
dc.subject.MESH | Apoptosis/drug effects | - |
dc.subject.MESH | Apoptosis Regulatory Proteins | - |
dc.subject.MESH | Azacitidine/analogs & derivatives* | - |
dc.subject.MESH | Azacitidine/pharmacology | - |
dc.subject.MESH | B-Lymphocytes/enzymology | - |
dc.subject.MESH | Calcium-Calmodulin-Dependent Protein Kinases/biosynthesis | - |
dc.subject.MESH | Calcium-Calmodulin-Dependent Protein Kinases/genetics* | - |
dc.subject.MESH | CpG Islands* | - |
dc.subject.MESH | DNA Methylation*/drug effects | - |
dc.subject.MESH | Death-Associated Protein Kinases | - |
dc.subject.MESH | Decitabine | - |
dc.subject.MESH | Enzyme Induction | - |
dc.subject.MESH | Gene Expression Regulation, Neoplastic* | - |
dc.subject.MESH | Hematologic Neoplasms/enzymology | - |
dc.subject.MESH | Hematologic Neoplasms/genetics* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Jurkat Cells/drug effects | - |
dc.subject.MESH | Killer Cells, Natural/enzymology | - |
dc.subject.MESH | Leukemia-Lymphoma, Adult T-Cell/enzymology | - |
dc.subject.MESH | Leukemia-Lymphoma, Adult T-Cell/genetics | - |
dc.subject.MESH | Lymphoma, B-Cell/enzymology | - |
dc.subject.MESH | Lymphoma, B-Cell/genetics | - |
dc.subject.MESH | Lymphoma, T-Cell/enzymology | - |
dc.subject.MESH | Lymphoma, T-Cell/genetics | - |
dc.subject.MESH | Neoplasm Proteins/biosynthesis | - |
dc.subject.MESH | Neoplasm Proteins/genetics* | - |
dc.subject.MESH | Neoplastic Stem Cells/enzymology | - |
dc.subject.MESH | Promoter Regions, Genetic/genetics* | - |
dc.subject.MESH | Reverse Transcriptase Polymerase Chain Reaction | - |
dc.subject.MESH | T-Lymphocytes/enzymology | - |
dc.subject.MESH | fas Receptor/immunology | - |
dc.title | Hypermethylation of death-associated protein (DAP) kinase CpG island is frequent not only in B-cell but also in T- and natural killer (NK)/T-cell malignancies | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Pathology (병리학) | - |
dc.contributor.googleauthor | Shin-ichi Nakatsuka | - |
dc.contributor.googleauthor | Tetsuya Takakuwa | - |
dc.contributor.googleauthor | Katsuyuki Aozasa | - |
dc.contributor.googleauthor | Woo-Ick Yang | - |
dc.contributor.googleauthor | Kazuhiro Nishii | - |
dc.contributor.googleauthor | Motoko Yamaguchi | - |
dc.contributor.googleauthor | Mieko Nishiu | - |
dc.contributor.googleauthor | Yoshihiko Hoshida | - |
dc.contributor.googleauthor | Yasuhiko Tomita | - |
dc.identifier.doi | 10.1111/j.1349-7006.2003.tb01357.x | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A02300 | - |
dc.relation.journalcode | J00454 | - |
dc.identifier.eissn | 1349-7006 | - |
dc.identifier.pmid | 12708480 | - |
dc.identifier.url | http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.2003.tb01357.x/abstract | - |
dc.subject.keyword | 12708480 | - |
dc.contributor.alternativeName | Yang, Woo Ick | - |
dc.contributor.affiliatedAuthor | Yang, Woo Ick | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 94 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 87 | - |
dc.citation.endPage | 91 | - |
dc.identifier.bibliographicCitation | CANCER SCIENCE, Vol.94(1) : 87-91, 2003 | - |
dc.identifier.rimsid | 47277 | - |
dc.type.rims | ART | - |
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