Methodological establishment for vital observation of tumor microcirculation and development of cancer therapy based on the characteristics of tumor microvessl

肿瘤微循环活体观察方法学的建立及基于肿瘤微血管特点的癌症治疗研究

基本信息

批准号：
16591406
负责人：
SOHARA Yasunori
金额：
$ 2.11万
依托单位：
Jichi Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2006
项目状态：
已结题

项目摘要

Lung metastasis is one of the worst factors for postoperative prognosis in primary lung cancer. In this study, we planed to develop new cancer therapy based on characteristics of tumor micro-vessel of lung metastasis through studies of vital observation of tumor microcirculation.During 2004, we established the method for making pulmonary metastasis of SATO lung cancer in Donryu rat, the system for vital observation of tumor microcirculation on surface of the lung by fluorescent microscopy, and the system for vital observation of tumor feeding arteries for lung metastasis by soft X ray micro-angiography.During 2005, we studied the characteristics of tumor micro-vessel by fluorescent microscopy and soft X ray micro-angiography.During 2006, we studied the effect of ZD6126 to tumor micro-vessel, the effect of chemo-immunotherapy (0K432 with CDDP) to anti-tumor lymphocytes, and the effect of hypoxia to feeding arteries of lung metastasis.(RESULTS)1) We established the model of lung metastasis of SATO lung cancer.2) We elucidated the characteristics of tumor micro-vessels.3) ZD6126 injure the tumor through the destruction of tumor micro-vessels.4) OK432 with CDDP accumulate anti-tumor lymphocytes to tumor micro-vessels.5) Hypoxia evokes vasoconstriction of tumor feeding arteries.This result indicates the ability of tumor vascular targeting therapy.

肺转移是原发性肺癌术后预后最差的因素之一。在这项研究中，我们计划通过对肿瘤微循环的活体观察研究，根据肺转移的肿瘤微血管的特点开发新的癌症治疗方法。2004年，我们建立了Donryu大鼠SATO肺癌肺转移的方法，荧光显微镜肺表面肿瘤微循环活体观察系统、软X射线显微血管造影肺转移肿瘤供血动脉活体观察系统。 2005年，我们通过荧光显微镜和软X射线显微血管造影研究了肿瘤微血管的特征。2006年，我们研究了ZD6126对肿瘤微血管的作用，化疗免疫疗法（0K432与CDDP）抗肿瘤微血管的作用。 -肿瘤淋巴细胞、缺氧对肺转移瘤供血动脉的影响。(结果)1)建立了肿瘤淋巴细胞肺转移模型。 SATO肺癌。2）我们阐明了肿瘤微血管的特征。3）ZD6126通过破坏肿瘤微血管来损伤肿瘤。4）OK432与CDDP一起将抗肿瘤淋巴细胞聚集到肿瘤微血管。5）缺氧引起肿瘤供血动脉的血管收缩。这一结果表明肿瘤血管靶向治疗的能力。