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作 者:吕永杰[1] 程书钧[1] 郭素萍[1] 徐丽华[1] 董向阳[1]
机构地区:[1]中国医学科学院肿瘤研究所病因室
出 处:《中华医学杂志》1995年第4期214-215,共2页National Medical Journal of China
摘 要:基因易位是癌基因激活的一种机制,但是以往检测基因改变的方法较难检测基因易位。我们建立了荧光原位杂交(FISH)技术,井应用这项技术在人肺癌细胞系GLC-82和1例经SV40T转化了的人支气管上皮细胞中发现了癌基因c-myc易位。在GLC-82细胞系中c-myc基因易位到一条C组大小标记染色体的短臂。在SV40T转化支气管上皮细胞中c-myc易位到14q32,提示c-myc基因易位可能在肺癌起因中起重要作用。-myc gene amplification has been found in lungcancer, however, it can not explain all cases of lungcancer with c-myc gene overexpression. Gene transloca-tion is one of the ways by which oncogene is activated.But the old methods for detecting gene mutations arenot so effective for the detection of gene translocation,especially in solid tumors. Fluorescence in situ hy-bridization (FISH) can be used to detect gene transloca-tion more efficiently. Using FISH , we discovered c-mycgene translocation in a lung adenocarcinoma cell hneGLC-82 and SV40T-transformed human bronchial ep-ithelial cells. In GLC-82, c-myc gene translocated tothe short arm of a C group marker chromosome. In theSV40T-transformed epithelial cells , c-myc gene translo-cated to 14q32, which was the same as that found inBurkitt’s lymphomas. Translocation was related tooncogene activation. c-myc translocation may play animportant role in the carcinogenesis of lung cancer.
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