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RISS 인기검색어
- 검색키워드
- 저자 : Zhifu Sun (검색결과 3 건)
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Yang, Ju Dong,Seol, So-Young,Leem, Sun-Hee,Kim, Yong Hoon,Sun, Zhifu,Lee, Ju-Seog,Thorgeirsson, Snorri S.,Chu, In-Sun,Roberts, Lewis R.,Kang, Koo Jeong The Korean Academy of Medical Sciences 2011 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.26 No.11
<P>Gene expression is suppressed by DNA methylation. The goal of this study was to identify genes whose CpG site methylation and mRNA expression are associated with recurrence after surgical resection for hepatocellular carcinoma (HCC). Sixty-two HCCs were examined by both whole genome DNA methylation and transcriptome analysis. The Cox model was used to select genes associated with recurrence. A validation was performed in an independent cohort of 66 HCC patients. Among fifty-nine common genes, increased CpG site methylation and decreased mRNA expression were associated with recurrence for 12 genes (Group A), whereas decreased CpG site methylation and increased mRNA expression were associated with recurrence for 25 genes (Group B). The remaining 22 genes were defined as Group C. Complement factor H (<I>CFH</I>) and myosin VIIA and Rab interacting protein (<I>MYRIP</I>) in Group A; proline/serine-rich coiled-coil 1 (<I>PSRC1</I>), meiotic recombination 11 homolog A (<I>MRE11A</I>), and myosin IE (<I>MYO1E</I>) in Group B; and autophagy-related protein LC3 A (<I>MAP1LC3A</I>), and NADH dehydrogenase 1 alpha subcomplex assembly factor 1 (<I>NDUFAF1</I>) in Group C were validated. In conclusion, potential tumor suppressor (<I>CFH</I>, <I>MYRIP</I>) and oncogenes (<I>PSRC1</I>, <I>MRE11A</I>, <I>MYO1E</I>) in HCC are reported. The regulation of individual genes by methylation in hepatocarcinogenesis needs to be validated.</P>
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양주동,설소영,임선희,김용훈,Zhifu Sun,이주석,Snorri S. Thorgeirsson,추인선,Lewis R. Roberts,강구정 대한의학회 2011 Journal of Korean medical science Vol.26 No.11
Gene expression is suppressed by DNA methylation. The goal of this study was to identify genes whose CpG site methylation and mRNA expression are associated with recurrence after surgical resection for hepatocellular carcinoma (HCC). Sixty-two HCCs were examined by both whole genome DNA methylation and transcriptome analysis. The Cox model was used to select genes associated with recurrence. A validation was performed in an independent cohort of 66 HCC patients. Among fifty-nine common genes, increased CpG site methylation and decreased mRNA expression were associated with recurrence for 12genes (Group A), whereas decreased CpG site methylation and increased mRNA expression were associated with recurrence for 25 genes (Group B). The remaining 22 genes were defined as Group C. Complement factor H (CFH) and myosin VIIA and Rab interacting protein (MYRIP) in Group A; proline/serine-rich coiled-coil 1 (PSRC1), meiotic recombination 11 homolog A (MRE11A), and myosin IE (MYO1E) in Group B; and autophagy-related protein LC3 A (MAP1LC3A), and NADH dehydrogenase 1 alpha subcomplex assembly factor 1 (NDUFAF1) in Group C were validated. In conclusion,potential tumor suppressor (CFH, MYRIP) and oncogenes (PSRC1, MRE11A, MYO1E) in HCC are reported. The regulation of individual genes by methylation in hepatocarcinogenesis needs to be validated.
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Inactivation of LLC1 gene in nonsmall cell lung cancer
Hong, Kyeong-Man,Yang, Sei-Hoon,Chowdhuri, Sinchita Roy,Player, Audrey,Hames, Megan,Fukuoka, Junya,Meerzaman, Daoud,Dracheva, Tatiana,Sun, Zhifu,Yang, Ping,Jen, Jin Alan R. Liss, Inc 2007 International journal of cancer Vol.120 No.11
<P>Serial analysis of gene expression studies led us to identify a previously unknown gene, c20orf85, that is present in the normal lung epithelium but absent or downregulated in most primary nonsmall cell lung cancers and lung cancer cell lines. We named this gene LLC1 for Low in Lung Cancer 1. LLC1 is located on chromosome 20q13.3 and has a 70% GC content in the promoter region. It has 4 exons and encodes a protein containing 137 amino acids. By in situ hybridization, we observed that LLC1 message is localized in normal lung bronchial epithelial cells but absent in 13 of 14 lung adenocarcinoma and 9 out of 10 lung squamous carcinoma samples. Methylation at CpG sites of the LLC1 promoter was frequently observed in lung cancer cell lines and in a fraction of primary lung cancer tissues. Treatment with 5-aza deoxycytidine resulted in a reduced methylation of the LLC1 promoter concomitant with the increase of LLC1 expression. These results suggest that inactivation of LLC1 by means of promoter methylation is a frequent event in nonsmall cell lung cancer and may play a role in lung tumorigenesis. © 2007 Wiley-Liss, Inc.</P>
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