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| 題名: | Effects of (-)-menthol on the distribution and metabolism of 2-aminofluorene in various tissues of Sprague-Dawley rats |
| 作者: | Lin, JP;Cheng, KC;Chen, GW;Yang, MD;Chiu, TH;Chung, JG |
| 貢獻者: | 醫學院醫學系微生物學科;China Med Univ, Dept Microbiol, Taichung 400, Taiwan;China Med Univ, Sch Chinese Med, Taichung 400, Taiwan;Jen Ai Hosp, Dept Surg, Taichung 400, Taiwan;China Med Univ Hosp, Dept Surg, Taichung 400, Taiwan;China Med Univ Hosp, OBS, GYN, Taichung 400, Taiwan |
| 日期: | 2003 |
| 上傳時間: | 2010-09-24 15:01:26 (UTC+8) |
| 出版者: | INT INST ANTICANCER RESEARCH |
| 摘要: | The expression of the suppressor of cytokine signalling-1 (SOCS1) protein is induced in response to stimulation by several cytokines. The induced SOCS1 inhibits the signalling pathway through the association with a variety of tyrosine kinase proteins. In this study, the mutation analyses, CpG island methylation status, and the expression of the SOCS1 gene in 112 chronic myeloid leukaemia (CML) samples, five leukaemia cell lines, and 30 normal controls were analysed. No genetic mutations of SOCS1 gene were noted in the CML samples. The SOCS1 gene was hypermethylated in 67% and 46% of the blastic and chronic phase CML samples respectively (P < 0.0001). However, there was no methylation of the SOCS1 gene in normal controls or CML in molecular remission. The methylation status of the SOCS1 gene is consistent with the results of the real-time quantitative reverse transcription polymerase chain reaction and immunocytochemistry staining. Our results demonstrate that the SOCS1 gene silencing is caused by the methylation of CpG islands in CML and is reversed to an unmethylated status in molecular remission. As SOCS1 has universal activity to negatively regulate several cytokine signalling pathways, the loss of the negative regulation of cytokine signalling by the SOCS1 may play a role in the pathogenesis of CML progression. |
| 關聯: | IN VIVO 17(5):441-455 |
| 顯示於類別: | [醫學系] 期刊論文
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