bcrabl基因疫苗对小鼠SP20bcrabl移植瘤的影响.docVIP

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bcrabl基因疫苗对小鼠SP20bcrabl移植瘤的影响.doc

bcrabl基因疫苗对小鼠SP20bcrabl移植瘤的影响 目录 TOC \o 1-9 \h \z \u 目录 1 正文 1 文1:bcrabl基因疫苗对小鼠SP20bcrabl移植瘤的影响 1 文2:掺钕钇铝石榴石激光对小鼠移植瘤转移的影响 7 1材料和方法 8 参考文摘引言: 11 原创性声明(模板) 13 文章致谢(模板) 13 正文 bcrabl基因疫苗对小鼠SP20bcrabl移植瘤的影响 文1:bcrabl基因疫苗对小鼠SP20bcrabl移植瘤的影响 Influences of bcr-abl Gene Vaccine on Inoculated SP2/0/bcr-abl Tumor Cells in Mice Abstract To study the influence of vaccine of bcr-abl fusion gene fragment on inoculated SP2/0/bcr-abl tumor cells in mice,BALB/c mice were immunized with pVbcr-abl,pVbcr-abl/mIL7 plasmids,respectively,then SP2/0/bcr-abl cells expressing the fragment of bcr-abl fusion gene were inoculated subcutaneously into the groin of BALB/c mice in order to observe the effect of vaccine on growth of inoculated SP2/0/bcr-abl tumor cells. The results showed that there were distinct differences on the time of tumor growth,the time of tumor ulceration,tumor volume and survival time of mice bearing tumor between two immunized groups and two control groups (blank and vacant plasmid groups). The mice immunized with pVbcr-abl/mIL7 lived longer as compared to mice immunized with pVbcr-abl. The tissue of inoculated tumor was more compact,tumor organ was larger,tumor form was irregular in 2 control groups,while the tissue of inoculated tumor was looser,tumor volume was smaller,and with mass inflammatory infiltration in two immunized groups. Moreover, the metastatic tumor cells were found in the live of control groups,but not observed in two immunized groups. It is concluded that the protection occured in immunized mice which inhibited the growth of SP2/0/bcr-abl tumor cell in vivo. Key words chronic myeloid leukemia;bcr-abl fusion gene;gene vaccine;SP2/0/bcr-abl tumor Bcr-Abl融合蛋白存在于90%以上的CML患者体内,它与恶性转变及恶性克隆的维持密切相关。本研究小组曾采用含bcr-abl融合基因片段的重组反转录病毒感染小鼠SP2/0细胞系(H-2d),获得稳定表达bcr-abl融合基因片段的细胞株——SP2/0/bcr-abl,为我们检验bcr-abl基因疫苗激发的小鼠CTL应答研究奠定了物质基础[1]。在本研究中我们首先分别采用pVbcr-abl 、pVbcr-abl/mIL7两种质粒免疫BALB/c小鼠,用上述表达bcr-abl融合基因片段的、具有相同遗传背景的鼠传代肿瘤细胞攻击基因疫苗免疫的小鼠,观察CML基因疫苗对小鼠SP2/0

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