MICROVESSEL PERMEABILITY AND TUMOR METASTASIS

微血管通透性和肿瘤转移

基本信息

  • 批准号:
    6157643
  • 负责人:
  • 金额:
    $ 15万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2000
  • 资助国家:
    美国
  • 起止时间:
    2000-08-16 至 2003-08-15
  • 项目状态:
    已结题

项目摘要

DESCRIPTION: (Adapted from the investigator's abstract) This is a first submission of an Academic Research Enhancement Award (AREA) grant from a new investigator aimed at examining the role of microvessel permeability in tumor cell extravasation using an in vivo rat mesentery vessels model. The overall objective of the proposal is to quantify the relationship between microvessel permeability and tumor growth and metastasis in intact microvessels and to test the hypothesis that VEGF induced hyperpermeability is associated with enhanced tumor cell adhesion and extravasation. Four hypotheses will be tested. 1. That VEGF induced hyperpermeability enhances tumor cell adhesion and extravasation, 2. That extravasation requires specific signaling molecules in breast cancer cells, 3. That agents that induce an increase in cAMP in endothelial cells decrease hyperpermeability caused by VEGF and 4. that these agents inhibit tumor cell adhesion and extravasation. The in vivo model used consists of perfused mesenteric microvessels from rat in which permeability is quantitatively determined by injection of fluorescently dyed molecules and monitored by fluorescent video microscopy. Adhesion and extravasation of tumor cells is similarly evaluated by following fluorescently labeled tumor cells. The proposal has 4 specific aims according to the 4 hypotheses proposed. In aim 1, the effect of VEGF on microvessel permeability will be evaluated. In specific aim 2, the effect of VEGF on tumor cell adhesion and extravasation will be determined. In specific aim 3, the effect of 8 bromo-cAMP and agents that increase cAMP such as forskolin or rolipram on VEGF induces hyperpermeability will be examined. In specific aim 4 the effect of these agents on tumor cell extravasation will be studied. It is anticipated that this project will provide a useful tool in the quantitative assessment of tumor microvessel transport and help define a new class of target for chemotherapeutic drug design.
描述:(改编自研究者的摘要)这是第一个 提交新的学术研究增强奖(AREA)资助 研究人员旨在检查微血管通透性在肿瘤中的作用 使用体内大鼠肠系膜血管模型进行细胞外渗。整体 该提案的目标是量化微血管之间的关系 完整微血管中的渗透性和肿瘤生长和转移并进行测试 VEGF 诱导的通透性过高与增强相关的假设 肿瘤细胞粘附和外渗。将测试四个假设。 1. 那 VEGF 诱导的通透性过高增强肿瘤细胞粘附和外渗, 2. 乳腺癌中的外渗需要特定的信号分子 细胞,3. 诱导内皮细胞中 cAMP 增加的药物 4. 降低 VEGF 引起的通透性过高,这些药物可抑制 肿瘤细胞粘附和外渗。使用的体内模型包括 大鼠肠系膜微血管灌注,其渗透性为 通过注射荧光染色分子进行定量测定 通过荧光视频显微镜监测。肿瘤的粘连和外渗 通过荧光标记的肿瘤细胞对细胞进行类似的评估。 根据提出的 4 个假设,该提案有 4 个具体目标。瞄准目标 1、评价VEGF对微血管通透性的影响。在 具体目标2、VEGF对肿瘤细胞粘附和外渗的影响 将被确定。在特定目标3中,8溴-cAMP和药剂的效果 增加 cAMP 的药物,如福司可林 (forskolin) 或咯利普兰 (rolipram),可诱导 VEGF 将检查渗透性过高。在具体目标 4 中,这些措施的效果 将研究肿瘤细胞外渗的药物。预计这 该项目将为肿瘤的定量评估提供有用的工具 微血管运输并帮助定义一类新的目标 化疗药物设计。

项目成果

期刊论文数量(5)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
A model for the modulation of microvessel permeability by junction strands.
通过连接链调节微血管通透性的模型。
Structural mechanisms in the abolishment of VEGF-induced microvascular hyperpermeability by cAMP.
cAMP 消除 VEGF 诱导的微血管通透性过高的结构机制。
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BINGMEI M. FU其他文献

BINGMEI M. FU的其他文献

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{{ truncateString('BINGMEI M. FU', 18)}}的其他基金

Tumor Cell Arrest and Adhesion in the Microcirculation
微循环中的肿瘤细胞阻滞和粘附
  • 批准号:
    8677782
  • 财政年份:
    2010
  • 资助金额:
    $ 15万
  • 项目类别:
Tumor Cell Arrest and Adhesion in the Microcirculation
微循环中的肿瘤细胞阻滞和粘附
  • 批准号:
    8269742
  • 财政年份:
    2010
  • 资助金额:
    $ 15万
  • 项目类别:
Tumor Cell Arrest and Adhesion in the Microcirculation
微循环中的肿瘤细胞阻滞和粘附
  • 批准号:
    7761578
  • 财政年份:
    2010
  • 资助金额:
    $ 15万
  • 项目类别:
Tumor Cell Arrest and Adhesion in the Microcirculation
微循环中的肿瘤细胞阻滞和粘附
  • 批准号:
    8068912
  • 财政年份:
    2010
  • 资助金额:
    $ 15万
  • 项目类别:
Tumor Cell Arrest and Adhesion in the Microcirculation
微循环中的肿瘤细胞阻滞和粘附
  • 批准号:
    8471667
  • 财政年份:
    2010
  • 资助金额:
    $ 15万
  • 项目类别:

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