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SA Cationic Liposomes Complexed to Plasmids Encoding Endostatin and p53 Inhibit Lewis Lung Cancer in Mice Model

Author: LongJianMing
Tutor: QiXieFei
School: Jiangxi Medical College
Course: Internal Medicine
Keywords: Lewis lung Endostatin gene p53 gene Antiangiogenic
CLC: R734.2
Type: Master's thesis
Year: 2005
Downloads: 54
Quote: 0
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Abstract


Objective : To observe the SA cationic liposome -mediated endostatin gene and / or p53 gene of mice with Lewis lung tumor growth and metastasis inhibition . Method to establish an animal model of lung cancer : C57BL/6j black rat subcutaneous injection of Lewis lung cell suspension . Tumor after intratumoral injection of SA cationic liposome-mediated endostatin gene and / or p53 gene , 2 times per week for 6 weeks . The observed changes in tumor size in mice nutritional status , and survival of the end of the experiment , the mice were killed calculate the lung surface metastases number . Results: 1, species then 4 to 6 days after the tumor , tumor showed progressive growth with time and the control group of mice , the mice treated with tumor in the first 3 days after the start of treatment , tumor growth rate i.e. slowed , 1 week after the volume of tumor began to shrink , on day 18 , the control group and the experimental control group, tumor size were 4685 ± 176mm ~ 3 and 6054 ± 213mm ~~ 3 , tumor size p53 group , pEnd group , and p53 pEnd group were 77 ± 10mm ~ 3,39 ± 10mm ~ 3, 48 ± 10mm ~ 3, there are very significant differences ( P lt; 0.01 ) between the two . Blank control group and the experimental control group of mice the size of the tumor without significant differences ( P gt ; 0.05) , tumor volume over the same period of the treated mice there was no significant difference ( P gt ; 0.05) . 2 , control mice with the tumor increased activity , diet , the ability to respond to external stimuli are gradually weakened late was Cachexia state . The treated mice during the observation period , activity , diet , the ability to respond to external stimuli had no significant change. 3 lung metastatic foci in the blank control group was 18.4 ± 5.1 , experimental control group was 17.1 ± 4.7 , and p53 treatment group was 3.5 ± 1.2 pEnd treatment group and p53 pEnd combined treatment group showed no metastases . Between the two have very significant ( P lt; 0.01 ) . 4 , the average survival period in the blank control group was 28.2 ± 4.1 days , experimental control group was 31.2 ± 3.7 days , while p53 treatment group , pEnd treatment group , p53 pEnd combination therapy group were 50 days to

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