Carrier cell mediated ovarian cancer specific gene therapy

载体细胞介导的卵巢癌特异性基因治疗

基本信息

  • 批准号:
    15591754
  • 负责人:
  • 金额:
    $ 2.24万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2003
  • 资助国家:
    日本
  • 起止时间:
    2003 至 2004
  • 项目状态:
    已结题

项目摘要

We constructed an oncolytic adenovirus, AdE3-IAI.3B that was introduced ovarian cancer specific IAI.3B promoter, and showed the effect of the growth inhibition in the ovarian cancer cell proliferation in vitro and in vivo (Cancer Research, 2003). The treatment by AdE3-IAI.3B is assumed the problem that all tumors relapses in 2-3 weeks further even if tumor reduction is temporarily done on about 30 days after the treatment. This is confirmed not only in the animal experiment but also in the clinical trial by using other oncolytic vectors. It is guessed that it is a cause that vector rapidly shifts to the whole body from the tumor, because the stagnation rate of vector in the tumor is few, and the stagnation time in the tumor is short. After AdE3-IAI.3B had been infected to 293 and A549 cells that had been known as an adenoviral production cell so far as a carrier cell and these carrier cells were adminstered to the nude mouse subcutaneous tumor model of ovarian cancer PA-1 and RMG-1 cel … More l that the IAI.3B promoter is high, both tumors completely disappeared and did not relapsed. On the other hand, the HEY cell tumor, whose adenoviral receptor is fewer than these cells, disappeared and the relapse was not admitted when both were used together, though the tumor did not disappear after the single cell treatment by 293 or A549 cells infected with AdE3-IAI.3B. It is well known that the second challenge of adenoviral vectors is completely blocked by the anti-adenoviral antibody production. However, the second challenge of adenovirus succeeded by using AdE3-IAI.3B infected 293 or A549 carrier cell. This restoration of the second adenoviral infection was completely blocked by 0. 4 um millicell membrane chamber and 50% blocked by 12 um millicell memebrane chamber. This was due to the infection achievement by direct carrier cell to target cell contact and carrier cell fragment to target cell contact. This infection style of oncoloytic adenovirus infected carrier cell was confirmed by the electron microscope. Less
我们构建了溶瘤腺病毒AdE3-IAI。在体外和体内实验中均显示了其对卵巢癌细胞增殖的生长抑制作用(cancer Research, 2003)。AdE3-IAI处理。3B假设即使在治疗后约30天暂时缩小肿瘤,所有肿瘤在2-3周后复发的问题。这不仅在动物实验中得到证实,而且在使用其他溶瘤载体的临床试验中也得到证实。猜测是矢量从肿瘤向全身快速移位的一个原因,因为矢量在肿瘤中停滞率很少,在肿瘤中停滞时间短。AdE3-IAI之后。将3B感染到293和A549细胞上,这些细胞作为载体细胞被称为腺病毒产生细胞,并将这些载体细胞给予卵巢癌裸鼠皮下肿瘤模型PA-1和RMG-1细胞,更重要的是,IAI.3B启动子高,两种肿瘤完全消失,没有复发。另一方面,腺病毒受体少于这些细胞的HEY细胞肿瘤,两者联合使用时,肿瘤消失,不承认复发,而293或A549细胞感染AdE3-IAI.3B单细胞治疗后,肿瘤未消失。众所周知,腺病毒载体的第二次攻击完全被抗腺病毒抗体的产生所阻断。然而,腺病毒的第二次攻击通过使用AdE3-IAI获得了成功。3B感染293或A549载体细胞。第二次腺病毒感染的恢复被0。4微米的膜室和50%被12微米的膜室阻挡。这是由于通过载体细胞与靶细胞的直接接触和载体细胞片段与靶细胞的直接接触实现了感染。电镜下证实了这种溶瘤腺病毒感染载体细胞的感染方式。少

项目成果

期刊论文数量(38)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Identification of the human IAI.3B promoter element and its use in the construction of a replication-selective adenovirus for ovarian cancer therapy.
人 IAI.3B 启动子元件的鉴定及其在构建用于卵巢癌治疗的复制选择性腺病毒中的应用。
  • DOI:
  • 发表时间:
    2003
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Hamada;K.;Kohno;S.;Iwamoto;M.;Yokota;H.;Okada;M.;Tagawa;M.;Hirose;S.;Yamasaki;K.;Shirakata;Y.;Hashimoto;K.;Ito;M.
  • 通讯作者:
    M.
癌遺伝子治療薬
癌症基因治疗药物
  • DOI:
  • 发表时间:
    2003
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Harada et al.: "Introduction of wild-type p53 enhances throbospondin-1 expression in human"Cancer Letters. 191. 109-119 (2003)
Harada 等人:“引入野生型 p53 可增强人类凝血反应蛋白-1 的表达”Cancer Letters。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Hamada, K. et al.: "Identification of the human IAI.3B promoter element and its use in the construction of a replication selective adenovirus for ovarian cancer therapy"Cancer Research. 632. 2506-2512 (2003)
Hamada, K. 等人:“人 IAI.3B 启动子元件的鉴定及其在构建用于卵巢癌治疗的复制选择性腺病毒中的用途”癌症研究。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Introduction of wild-type p53 enhances thrombospondin-1 expression in human glioma cells
  • DOI:
    10.1016/s0304-3835(02)00592-x
  • 发表时间:
    2003-02-28
  • 期刊:
  • 影响因子:
    9.7
  • 作者:
    Harada, H;Nakagawa, K;Ohnishi, T
  • 通讯作者:
    Ohnishi, T
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HAMADA Katsuyuki其他文献

HAMADA Katsuyuki的其他文献

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{{ truncateString('HAMADA Katsuyuki', 18)}}的其他基金

Ovarian cancer specific gene therapy by polymer-coated oncolytic adenovirus
聚合物包被的溶瘤腺病毒进行卵巢癌特异性基因治疗
  • 批准号:
    23592453
  • 财政年份:
    2011
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
ovarian cancer-specific vaccine therapy by carrier cell
载体细胞的卵巢癌特异性疫苗治疗
  • 批准号:
    20591952
  • 财政年份:
    2008
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Carrier cell-mediated ovarian cancer-specific cellular and immunological gene therapy by induction of CTL
通过诱导 CTL 进行载体细胞介导的卵巢癌特异性细胞和免疫基因治疗
  • 批准号:
    17591745
  • 财政年份:
    2005
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
SCCA1 distal promoter for gene therapy of cervical intraepithelial neoplsia
SCCA1远端启动子用于宫颈上皮内瘤变的基因治疗
  • 批准号:
    13671724
  • 财政年份:
    2001
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Cloning of promoter of CA125 gene and tissue specific gene therapy for ovarian cancer
CA125基因启动子克隆及卵巢癌组织特异性基因治疗
  • 批准号:
    11671624
  • 财政年份:
    1999
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Cloning of promoter of squamous cell carcinoma antigen and tissue secific gene therapy for cervical cancer
鳞状细胞癌抗原启动子的克隆及宫颈癌组织特异性基因治疗
  • 批准号:
    09671688
  • 财政年份:
    1997
  • 资助金额:
    $ 2.24万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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推进溶瘤腺病毒治疗胰腺癌的系统递送
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先进的溶瘤腺病毒实现 PDAC 的系统治疗
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    2022
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全身递送靶向 TGFβ 的溶瘤腺病毒,以增强三阴性乳腺癌的抗 PD-1 和抗 CTLA-4 治疗
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全身递送靶向 TGFβ 的溶瘤腺病毒,以增强三阴性乳腺癌的抗 PD-1 和抗 CTLA-4 治疗
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配备 SA-4-1BBL 免疫检查点刺激器的溶瘤腺病毒用于肺癌免疫治疗
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在胰腺癌免疫治疗中,p53过表达溶瘤腺病毒介导的肿瘤特异性相对于化疗的优越性
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肿瘤特异性溶瘤腺病毒突破了骨和软组织肉瘤的免疫治疗耐药性
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