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Journal Article

Citation

Han H, Qiu Q, Chen S, Liu Y, Mei P. Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi 2008; (24): 273-276.

Copyright

(Copyright © 2008, Lin chuang er bi yan hou tou jing wai ke za zhi bain ji bu)

DOI

unavailable

PMID

unavailable

Abstract

OBJECTIVE@#To investigate the therapeutic effect of pAdKDR-tk suicide gene system on tumor vessel endothelium cells (VEC) of human NPC in nude mice.@*METHOD@#Sixteen nude mice with transplantation tumor were randomized into AdKDR tk/GCV group and AdKDR-tk/PBS group, with 8 in each group. The tumor size changes and histomorphology were observed before and after treatment. Immunohistochemistry was used to detect the tumor microvessel density and VEGF expression.@*RESULT@#There's significant difference among the gross tumor volume of groups after experiment. The tumor volume in control group grew continuously and rapidly, while for the AdKDR-tk/GCV treatment group, tumor grew slowly at the first 6 days, and the tumor growth was inhibited after the 6th day, then the transplantation tumor volume gradually grew smaller. Tumor volume in treatment group was significantly smaller than that of control group after the 6th day, the 9th day and the 14th day (P<0.01). HE staining morphological observation that there's no significant difference in cell morphology of NPC between the two groups, but large amount of necrobiosis focus were found among tumor tissue. The MVD mean value of CD34 in control group was 6.63+/-1.41, with 3.50+/-0.93 of the treatment group. The statistics results demonstrated significant difference of vessel density around tumors between groups (P<0.05). The VEGF positive expression in control group was higher than that in treatment group, with significant difference of VEGF expression between two groups.@*CONCLUSION@#Adenovirus (ADV) mediated KDR promoter single herpes simplex virus thymidine kinase (AdKDR-tk)/GCV system could effectively inhibit vascular proliferation in tumors, thus inhibit the tumor growth in nude mice with NPC.


Language: zh

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