Investigation about the role of WT1 and PKR for the carcinogenesis or progression of hepatocellular carcinoma

WT1和PKR在肝细胞癌发生或进展中的作用研究

• 批准号: 21590848
• 负责人: HIASA Yoichi
• 金额: $ 2.91万
• 依托单位: Ehime University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21590848/
• 关键词: WT1遺伝子; PKR; 肝細胞癌; アポトーシス; C型肝炎ウイルス; interleukin-8; Caspase; siRNA; PCRアレイ; H77; Annexin V; HCV粒子生成可能複製系; 細胞増殖; 細胞接着因子

We investigated about the role of Wilms' tumor 1(WT1) gene and Protein kinase R(PKR), which over-expressed in the tissue of hepatocellular carcinoma(HCC). The expression of WT1 in HCC was related with oncogenesis, recurrence, tumor growth and prognosis. The PKR was induced by interferon, as well as by ribavirin, both drugs are well known as anti-hepatitis C virus(HCV) drugs. The interaction of PKR and HCV would have some possibilities related with the hepatocarcinogenesis induced by HCV, and overexpressed WT1 and PKR might be therapeutic target of HCC.

本研究旨在探讨肝细胞癌（HCC）组织中过度表达的Wilms肿瘤1（WT1）基因和蛋白激酶R（PKR）在HCC发生发展中的作用。WT1的表达与肝癌的发生、复发、肿瘤生长及预后有关。干扰素和利巴韦林均可诱导PKR，这两种药物都是众所周知的抗丙型肝炎病毒（HCV）药物。PKR与HCV的相互作用可能与HCV诱导的肝癌发生有关，过表达的WT1和PKR可能是肝癌的治疗靶点。

项目成果

SEP (splenic elasticity for portal hypertension) score

SEP（门脉高压脾弹性）评分

• 发表时间: 2011

クリニカルトピックスWilms' tumor 1遺伝子と肝細胞癌

临床主题 肾母细胞瘤 1 基因与肝细胞癌

• 发表时间: 2010
• 作者: 日浅陽一;上杉和寛;恩地森一
• 通讯作者: 恩地森一

SEP(splenic elasticity for portal hypertension) score

SEP（门脉高压脾弹性）评分

• 发表时间: 2011

Factors predictive of sustained virological response following 72 weeks of combination therapy for genotype 1b hepatitis C

• DOI: 10.1007/s00535-010-0358-6
• 发表时间: 2011-04-01
• 期刊: JOURNAL OF GASTROENTEROLOGY
• 影响因子: 6.3
• 作者: Chayama, Kazuaki;Hayes, C. Nelson;Kumada, Hiromitsu
• 通讯作者: Kumada, Hiromitsu

Radiofrequency ablation therapy for hepatocellular carcinoma in elderly patients

• DOI: 10.1111/j.1440-1746.2009.06037.x
• 发表时间: 2010-02-01
• 期刊: JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
• 影响因子: 4.1
• 作者: Hiraoka, Atsushi;Michitaka, Kojiro;Onji, Morikazu
• 通讯作者: Onji, Morikazu