课题基金 / 基金详情

NEW METASTASIS-SUPPRESSOR GENE

NEW METASTASIS-SUPPRESSOR GENE
新的转移抑制基因
批准号:
2742610
负责人:
Emma Shtivelman
金额:
$24.85万
依托单位国家:
美国
项目类别:
财政年份:
1998
资助国家:
美国
项目状态:
已结题
起止时间:
1998-07-15 至 2001-08-30

项目摘要

项目成果

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中文摘要
翻译
描述:(改编自调查人员的摘要) 小细胞肺癌等高侵袭性肿瘤的转移性扩散 对(SCLC)的了解很少。一种独特的SCID-Hu转移模型是 首次开发出允许研究小细胞肺癌转移的 活体实验环境。小细胞肺癌细胞系的分子分析 不同的转移潜能导致了一种 转移性缺失的人类新基因CC3 细胞。CC3导入小细胞肺癌细胞抑制其形成能力 SCID-Hu小鼠体内的转移性肿瘤。那么这个项目的目标就是 证实CC3是小细胞肺癌的转移抑制基因 分析CC3抑制肿瘤转移的机制。功能界别 CC3表达缺失与卵巢癌转移表型的相关性 小细胞肺癌将在体内转移实验中得到进一步证实。这个 CC3表达的临床意义和潜在的预后意义 将通过分析其在临床肿瘤中的表达来进行评估 标本。现就CC3抑制肿瘤转移的机制作一综述。 在旨在确定CC3表达对细胞的影响的实验中 转移细胞的表型。这些调查人员预计, 这些研究的结果将促进对心力衰竭机制的理解。 小细胞肺癌的转移。CC3蛋白缺失可能具有预后意义 在被诊断为小细胞肺癌和潜在其他肿瘤的患者中。一次彻底的 对CC3功能的了解最终可能会导致 新的抗转移疗法。
英文摘要
DESCRIPTION: (adapted from the investigator's abstract) Mechanisms of metastatic spread of high aggressive tumors such as small cell lung cancer (SCLC) are poorly understood. A unique SCID-hu metastasis model was developed that for the first time allows metastasis of SCLC to be studied in the experimental in vivo setting. Molecular analysis of SCLC cell lines with different metastatic potentials have led to the identification of a novel human gene designated CC3 whose expression is lacking in metastatic cells. Introduction of CC3 into SCLC cells suppresses their ability to form metastatic tumors in the SCID-hu mice. The goal of this project then is to prove that CC3 is a metastasis suppressor gene in small cell lung cancer and to analyze the mechanisms of metastasis suppression by CC3. The functional relevance of the lack of expression of CC3 to the metastatic phenotype of SCLC will be further confirmed in the in vivo metastasis assays. The clinical relevance and potential prognostic significance of CC3 expression will be evaluated through analysis of its expression in clinical tumor specimens. The mechanism of metastasis-suppression by CC3 will be addressed in experiments designed to define the effects of CC3 expression on the phenotype of metastatic cells. These investigators anticipate that the results of these studies will advance the understanding of the mechanisms of metastasis of SCLC. Lack of CC3 protein could have prognostic significance in patients diagnosed with SCLC and potentially other tumors. A thorough understanding of CC3 function might eventually lead to the development of new anti-metastatic therapies.
期刊论文(3)
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会议论文
Plant-Derived Estrogens and Cell Proliferation
  • 批准号:
    7805677
  • 项目类别:
  • 资助金额:
    $17.42万
  • 财政年份:
    2010
  • 负责人:
    Emma Shtivelman
  • 依托单位:
Plant-Derived Estrogens and Cell Proliferation
  • 批准号:
    8258471
  • 项目类别:
  • 资助金额:
    $19.99万
  • 财政年份:
    2010
  • 负责人:
    Emma Shtivelman
  • 依托单位:
INHIBITION OF NUCLEAR TRANSPORT BY TUMOR SUPPRESSOR CC3
  • 批准号:
    7460827
  • 项目类别:
  • 资助金额:
    $23.27万
  • 财政年份:
    2006
  • 负责人:
    Emma Shtivelman
  • 依托单位:
INHIBITION OF NUCLEAR TRANSPORT BY TUMOR SUPPRESSOR CC3
  • 批准号:
    7140747
  • 项目类别:
  • 资助金额:
    $23.96万
  • 财政年份:
    2006
  • 负责人:
    Emma Shtivelman
  • 依托单位:
国内基金
海外基金
ROBO4对视网膜血管生成(angiogenesis)的调控及其分子机制
  • 批准号:
    81200692
  • 项目类别:
    青年科学基金项目
  • 资助金额:
    23.0万元
  • 批准年份:
    2012
  • 负责人:
    陈凌
  • 依托单位: