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• W1868177795 abstract "Proc Amer Assoc Cancer Res, Volume 45, 20044140 The efficacy of radiotherapy for lung cancer is limited by normal tissue damage, including pulmonary, cardiac, esophageal, and spinal cord, that can lead to acute and late effects. Recent evidence indicates that the tumoricidal effects of radiation may be increased through the use of anti-angiogenic factors. The major goal of this study was to determine whether endostatin gene therapy has potential to augment radiation-mediated control of lung tumors. Plasmid pXLG-mEndo, constructed in our laboratories, consists of the mouse endostatin gene cloned into the pWS4 vector. Functionality of the expressed endostatin was tested using human umbilical vein endothelial cells (HUVEC) and Lewis Lung Carcinoma (LLC) cells in culture. The kinetics and dose-dependence of endostatin expression, as well as anti-tumor efficacy of combining pXLG-mEndo with 60Co irradiation were evaluated in the C57BL/6 mouse - LLC model. LLC cells were implanted subcutaneously and different doses of pXLG-mEndo were injected intratumorally 14 days later; a dose of 10 gray (Gy) radiation was applied 16 hr thereafter. Some of the groups received the treatments a second time one week later. Immunohistochemistry with anti-CD31 antibody was used to evaluate the effects of therapy on tumor vasculature. Based on 3H-thymidine incorporation into DNA, the endostatin gene alone resulted in highly significant depression in HUVEC and LLC cell growth compared to pWS4 vector and control with no plasmids (p< 0.005). In addition, radiation increased the inhibitory effects of endostatin on both HUVEC and LLC cells over a 3-day period after irradiation (p<0.05 or less). The time course study of endostatin expression within LLC tumor revealed that the expression peak was on day 7 after pXLG-mEndo injection. In the dose-dependence study we found that intratumoral injection of 100 μg pXLG-mEndo significantly increased expression of both endostatin and vascular endothelial growth factor (VEGF) locally. Tumor growth was significantly inhibited in mice receiving pXLG-mEndo plus radiation compared with no treatment (p<0.005), radiation only (p<0.05) and plasmid only (p<0.05). The number of LLC tumor vessels per high-power field was reduced following exposure to combined treatment compared with exposure to all other treatments (P<0.05). These data demonstrate that delivery of endostatin via pXLG-mEndo as an adjuvant to radiation can significantly enhance the anti-tumor efficacy of radiation therapy in the LLC mouse tumor model. Further investigation of this unique combination therapy appears warranted. [The view, opinion, and/or findings contained in this report are those of the author(s) and should not be construed as a position, policy, decision or endorsement of the federal government or the National Medical Technology Testbed, Inc. Supported in part by an award from the U.S. Army and NMTB.]" @default.
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• W1868177795 date "2004-04-01" @default.
• W1868177795 modified "2023-09-22" @default.
• W1868177795 title "Enhancement of radiation effects by pXLG-mEndo in a lung carcinoma model" @default.
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