中国肺癌杂志
中國肺癌雜誌
중국폐암잡지
CHINESE JOURNAL OF LUNG CANCER
2014年
12期
834-838
,共5页
蔡明辉%杨新颖%姜宝红%滕福康%潘雁%毛锋%申屠阳
蔡明輝%楊新穎%薑寶紅%滕福康%潘雁%毛鋒%申屠暘
채명휘%양신영%강보홍%등복강%반안%모봉%신도양
肺肿瘤%EGFR突变%EGFR-TKI%新生淋巴管
肺腫瘤%EGFR突變%EGFR-TKI%新生淋巴管
폐종류%EGFR돌변%EGFR-TKI%신생림파관
Lung neoplasms%EGFR mutation%EGFR-TKI%Lymphangiogenesis
背景与目的探索表皮生长因子受体酪氨酸激酶抑制剂(epidermal growth factor receptor-tyrosine kinase inhibitor, EGFR-TKI)对EGFR突变肺癌新生淋巴管的影响,探讨靶点治疗对新生淋巴管的抑制作用及其在肺癌治疗中所发挥的作用。方法采用EGFR双位点突变的NCI-H1975肺癌细胞株构建小鼠移植瘤模型。设立溶剂对照组和EGFR-TKI给药组,每组5只小鼠,观察EGFR-TKI对小鼠移植瘤的生长抑制作用;运用淋巴管内皮特异性抗体D2-40,采用免疫组织化学的方法,观察新生淋巴管的密度、面积、最大径,探讨EGFR-TKI对于肺癌组织淋巴管新生的影响。结果 EGFR-TKI给药组小鼠肿瘤重量、肿瘤相对体积小于溶剂对照组。EGFR-TKI给药组小鼠平均新生淋巴管密度为6.44个/例,溶剂对照组小鼠平均新生淋巴管密度为10.70个/例,EGFR-TKI给药组小鼠平均新生淋巴管密度较低(P=0.023)。EGFR-TKI给药组小鼠新生淋巴管面积、最长径小于溶剂对照组。而EGFR-TKI对新生淋巴管的肿瘤细胞侵犯没有明显影响(P=0.519)。结论 EGFR-TKI可以抑制EGFR突变肺癌组织淋巴管的新生,抑制新生淋巴管管径及面积的扩大。
揹景與目的探索錶皮生長因子受體酪氨痠激酶抑製劑(epidermal growth factor receptor-tyrosine kinase inhibitor, EGFR-TKI)對EGFR突變肺癌新生淋巴管的影響,探討靶點治療對新生淋巴管的抑製作用及其在肺癌治療中所髮揮的作用。方法採用EGFR雙位點突變的NCI-H1975肺癌細胞株構建小鼠移植瘤模型。設立溶劑對照組和EGFR-TKI給藥組,每組5隻小鼠,觀察EGFR-TKI對小鼠移植瘤的生長抑製作用;運用淋巴管內皮特異性抗體D2-40,採用免疫組織化學的方法,觀察新生淋巴管的密度、麵積、最大徑,探討EGFR-TKI對于肺癌組織淋巴管新生的影響。結果 EGFR-TKI給藥組小鼠腫瘤重量、腫瘤相對體積小于溶劑對照組。EGFR-TKI給藥組小鼠平均新生淋巴管密度為6.44箇/例,溶劑對照組小鼠平均新生淋巴管密度為10.70箇/例,EGFR-TKI給藥組小鼠平均新生淋巴管密度較低(P=0.023)。EGFR-TKI給藥組小鼠新生淋巴管麵積、最長徑小于溶劑對照組。而EGFR-TKI對新生淋巴管的腫瘤細胞侵犯沒有明顯影響(P=0.519)。結論 EGFR-TKI可以抑製EGFR突變肺癌組織淋巴管的新生,抑製新生淋巴管管徑及麵積的擴大。
배경여목적탐색표피생장인자수체락안산격매억제제(epidermal growth factor receptor-tyrosine kinase inhibitor, EGFR-TKI)대EGFR돌변폐암신생림파관적영향,탐토파점치료대신생림파관적억제작용급기재폐암치료중소발휘적작용。방법채용EGFR쌍위점돌변적NCI-H1975폐암세포주구건소서이식류모형。설립용제대조조화EGFR-TKI급약조,매조5지소서,관찰EGFR-TKI대소서이식류적생장억제작용;운용림파관내피특이성항체D2-40,채용면역조직화학적방법,관찰신생림파관적밀도、면적、최대경,탐토EGFR-TKI대우폐암조직림파관신생적영향。결과 EGFR-TKI급약조소서종류중량、종류상대체적소우용제대조조。EGFR-TKI급약조소서평균신생림파관밀도위6.44개/례,용제대조조소서평균신생림파관밀도위10.70개/례,EGFR-TKI급약조소서평균신생림파관밀도교저(P=0.023)。EGFR-TKI급약조소서신생림파관면적、최장경소우용제대조조。이EGFR-TKI대신생림파관적종류세포침범몰유명현영향(P=0.519)。결론 EGFR-TKI가이억제EGFR돌변폐암조직림파관적신생,억제신생림파관관경급면적적확대。
Background and objective hTis study aims to explore the effect of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKIs) on the lymphangiogenesis of lung cancer withEGFR mutation, as well as to determine the function of EGFR targeted therapy in relation to the inhibition of lymphangiogenesis during lung cancer treatment.Methods hTeEGFR double mutant lung cancer cell line NCI-H1975 is used to construct lung cancer xenogratf models. hTe models are divided into two groups:the solvent control group and the EGFR-TKI treatment group. Each group includes ifve mice. hTe inhibitory effect of EGFR-TKI on the growth of transplanted tumors was observed. Immunohistochemical method and lymphatic endothelium speciifc antibody D2-40 were used in the experiment to observe the inlfuence of EGFR-TKI on lymphangiogenesis in lung cancer.Results hTe weight and relative volume of tumors in the EGFR-TKI treated group were less than those in the solvent control group. hTe average lymphatic ves-sel density of EGFR-TKI-treated mice was 6.44 per case. hTis value was 10.70 per case in the solvent control group. Lower density of lymphangiogenesis was found in the EGFR-TKI treated group (P=0.023). hTe area and longest diameter of neonatal lymphatic vessel of the EGFR-TKI treated group were less than those of the solvent control group. Moreover, EGFR-TKI exhibited no signiifcant effect on the invasion of tumor cells into the lymphatic vessel (P=0.519).Conclusion EGFR-TKI can inhibit lymphangiogenesis inEGFR mutant lung cancer while suppressing vessel diameter and expansion area.