Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2008-03-28 |
タイトル |
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タイトル |
Microarray analysis of promoter methylation in lung cancers |
言語 |
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言語 |
eng |
キーワード |
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主題Scheme |
Other |
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主題 |
DNA methylation |
キーワード |
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主題Scheme |
Other |
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主題 |
DNA chip |
キーワード |
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主題Scheme |
Other |
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主題 |
Microarray |
キーワード |
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主題Scheme |
Other |
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主題 |
CpG island |
キーワード |
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主題Scheme |
Other |
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主題 |
Hypermethylation |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
著者 |
Fukasawa, Masayuki
Kimura, Mika
Morita, Sumiyo
Matsubara, Kenichi
Yamanaka, Sumitaka
Endo, Chiaki
Sakurada, Akira
Sato, Masami
Kondo, Takashi
Horii, Akira
Sasaki, Hiroyuki
Hatada, Izuho
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抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Aberrant DNA methylation is an important event in carcinogenesis. Of the various regions of a gene that can be methylated in cancers, the promoter is the most important for the regulation of gene expression. Here, we describe a microarray analysis of DNA methylation in the promoter regions of genes using a newly developed promoter-associated methylated DNA amplification DNA chip (PMAD). For each sample, methylated Hpa II-resistant DNA fragments and Msp I-cleaved (unmethylated + methylated) DNA fragments were amplified and labeled with Cy3 and Cy5 respectively, then hybridized to a microarray containing the promoters of 288 cancer-related genes. Signals from Hpa II-resistant (methylated) DNA (Cy3) were normalized to signals from Msp I-cleaved (unmethylated + methylated) DNA fragments (Cy5). Normalized signals from lung cancer cell lines were compared to signals from normal lung cells. About 10.9% of the cancer-related genes were hypermethylated in lung cancer cell lines. Notably, HIC1, IRF7, ASC, RIPK3, RASSF1A, FABP3, PRKCDBP, and PAX3 genes were hypermethylated in most lung cancer cell lines examined. The expression profiles of these genes correlated to the methylation profiles of the genes, indicating that the microarray analysis of DNA methylation in the promoter region of the genes is convenient for epigenetic study. Further analysis of primary tumors indicated that the frequency of hypermethylation was high for ASC (82%) and PAX3 (86%) in all tumor types, and high for RIPK3 in small cell carcinoma (57%). This demonstrates that our PMAD method is effective at finding epigenetic changes during cancer. |
書誌情報 |
Journal of human genetics
巻 51,
号 4,
p. 368-374,
発行日 2006-04
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ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1434-5161 |
書誌レコードID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA11206160 |
DOI |
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関連タイプ |
isVersionOf |
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識別子タイプ |
DOI |
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関連識別子 |
info:doi/10.1007/s10038-005-0355-4 |
フォーマット |
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内容記述タイプ |
Other |
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内容記述 |
application/pdf |
著者版フラグ |
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出版タイプ |
AM |
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出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
出版者 |
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出版者 |
Springer Science + Business Media |
資源タイプ |
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内容記述タイプ |
Other |
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内容記述 |
Journal Article |
関係URI |
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関連名称 |
http://www.springerlink.com/content/101565/ |
更新日 |
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日付 |
2017-03-27 |
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日付タイプ |
Created |