Characterization of genes involved in the multistep leukemogenesis of ATL
参与 ATL 多步白血病发生的基因的表征
基本信息
- 批准号:08457273
- 负责人:
- 金额:$ 4.67万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (B)
- 财政年份:1996
- 资助国家:日本
- 起止时间:1996 至 1997
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Long latent period and absence of HTLV-1 gene expression in leukemic cells of ATL suggest a multistep leukemogenesis of HTLV-1-infected T cells. To explore molecular mechanisms the leukemogenesis, we characterized gene expresssion profiles in primary ATL cells comparing with those in activated normal T cells using fluorescence differential display (FDD) method. To date, 29 cDNA fragments with dysregulated expression were characterized. Overexpression of PKCbeta II was confirmed by Northern blot and immunoblot analyzes in fresh ATL cells and cell lines derived from ATL clone, as well as HTLV-1 unrelated leukemic cell lines, but not in in Vitro transformed HTLV-1-infected T cell lines or Tax-immortalized cell lines. Constitutive activation of PKCbeta II was demonstrated by immune complex kinase assay in these cells. Some of the signal transducers for protein tyrosine kinases involved in TCR signaling were also found to be aberrantly expressed in ATL.These results suggest that overexpression of PKCbeta II may be involved in transformation of HTLV-1-infected T cells in vivo. A novel receptor-like membrane of about 37kDa was found to be overexpressed in ATL.The gene was conserved among species and was mapped at human chromosome 12q21. Along with these, we found that the 5' regionHTLV-1 provirus integrated in the leukemic cells was defective in 70% of patinets, suggesting that expression of virus genes are dispensable in the late stage of leukemogenesis. Studying the function of CD30, a receptor of TNFR superfamily, that is induced in HTLV-1-infected T cells, we cloned and characterized the rat CD30, and discovered a variant form of CD30 that lacks extracellular and transmembrane domains, is expressed in alveolar macrophages and various leukemia cells including ATL.
ATL白血病细胞潜伏期长,HTLV-1基因表达缺失,提示HTLV-1感染T细胞的白血病发生是多步骤的。为了探讨白血病发生的分子机制,我们采用荧光差异显示(FDD)技术对原代ATL细胞和活化的正常T细胞的基因表达谱进行了比较。迄今为止,29个cDNA片段与失调的表达进行了表征。通过北方印迹和免疫印迹分析证实了新鲜ATL细胞和ATL克隆衍生的细胞系以及HTLV-1无关白血病细胞系中PKC β II的过表达,但在体外转化的HTLV-1感染的T细胞系或Tax永生化细胞系中没有。通过免疫复合物激酶测定证实这些细胞中PKC β II的组成性活化。在ATL中还发现了一些参与TCR信号转导的蛋白酪氨酸激酶的信号转导子的异常表达。这些结果表明,PKC β II的过表达可能参与了HTLV-1感染的T细胞在体内的转化。在ATL中发现了一个分子量约为37 kDa的新的受体样膜,该基因在物种间是保守的,定位于人类染色体12 q21。沿着的是,我们发现70%的白血病细胞中整合的HTLV-1前病毒5'区存在缺陷,提示病毒基因在白血病发生的晚期是不稳定的。为了研究TNFR超家族受体CD 30在HTLV-1感染的T细胞中的功能,我们克隆并鉴定了大鼠CD 30,并发现了一种缺乏胞外和跨膜结构域的CD 30变体形式,其在肺泡巨噬细胞和包括ATL在内的各种白血病细胞中表达。
项目成果
期刊论文数量(20)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Toshiki Watanabe: "HTLV-1-associated diseases" Int J Hematol. 66. 257-278 (1997)
Toshiki Watanabe:“HTLV-1 相关疾病”Int J Hematol。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
S Aizawa, et al.,: "Tumor necrosis factor receptor-associated factor(TRAF)5-----" J Biol Chem. 272. 2042-2045 (1997)
S Aizawa 等人:“肿瘤坏死因子受体相关因子 (TRAF)5-----” J Biol Chem。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Takeuchi H.et al: "Characterization of Genes that are Differentially Expressed in Fresh ATL Cells by Fluorescence Differential Display Method" J AIDS and Hum Retro. Supple. 19 (1996)
Takeuchi H.等人:“通过荧光差异显示方法表征新鲜 ATL 细胞中差异表达的基因”J AIDS 和 Hum Retro。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
M Shimada, Hirashima, et al.,: "Primary gastric T-cell lymphoma withiand without human T-lymphotropic virus type 1." Cancer. 80. 292-303 (1997)
M Shimada、Hirashima 等人:“有或没有 1 型人类 T 淋巴细胞病毒的原发性胃 T 细胞淋巴瘤。”
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
M Shimada-Hiratsuka ey al.: "Primary gastric lymphoma with and without human T-lymphotropic virus type 1" Cancer. 80. 292-303 (1997)
M Shimada-Hiratsuka 等人:“伴或不伴人类 T 淋巴细胞病毒 1 型的原发性胃淋巴瘤”癌症。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
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WATANABE Toshiki其他文献
WATANABE Toshiki的其他文献
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{{ truncateString('WATANABE Toshiki', 18)}}的其他基金
HTLV-1 hijacks T-cell differentiation/function by deregulatingHelios gene expression
HTLV-1通过解除Helios基因表达调控来劫持T细胞分化/功能
- 批准号:
23659484 - 财政年份:2011
- 资助金额:
$ 4.67万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Oncogene addiction of ATL cells and abnormal Polycomb-miRNA-signal transduction
ATL细胞的癌基因成瘾和异常的Polycomb-miRNA信号转导
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23390250 - 财政年份:2011
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$ 4.67万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Pursuit of a new system for a high throughput screening of drugs to develop a new strategy of prevention and treatment of ATL
追求高通量药物筛选新系统,制定ATL防治新策略
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20390267 - 财政年份:2008
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Grant-in-Aid for Scientific Research (B)
Abnormalities in TCR signal transduction in T cell non-Hodgkin's lymphoma as a basis for a new classification system.
T 细胞非霍奇金淋巴瘤中 TCR 信号转导异常作为新分类系统的基础。
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18390111 - 财政年份:2006
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Identification of zooxanthellate genes that are involved in symbiosis with a reef coral, and analyses of their function and expression
鉴定与珊瑚礁共生相关的虫黄藻基因,并分析其功能和表达
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16510157 - 财政年份:2004
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人工电流源海底电磁法勘探海底甲烷水合物及其储层估算
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16360449 - 财政年份:2004
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Grant-in-Aid for Scientific Research (B)
Studies on abnormalities of membrane receptor signaling in malignant lymphoma cells as a basis of diagnosis and treatment
恶性淋巴瘤细胞膜受体信号异常作为诊断和治疗依据的研究
- 批准号:
16390103 - 财政年份:2004
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Grant-in-Aid for Scientific Research (B)
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膜受体异常信号转导的分子分析作为恶性淋巴瘤诊断和治疗的基础
- 批准号:
14370067 - 财政年份:2002
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$ 4.67万 - 项目类别:
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Molecular studies on the formation of calcified hard tissues in marine crustaceans
海洋甲壳动物钙化硬组织形成的分子研究
- 批准号:
08833004 - 财政年份:1996
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Studies for developing a laboratory diagnostic system for cancers by means of PCR that is applicale to clinical samples such as urine and stool
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05557059 - 财政年份:1993
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