经交链孢酚处理胎儿食管上皮组织中EGFr,Rb基因的扩增

目的：探讨互隔交链孢霉诱导食管癌的发生机制。方法：用交链孢酚（ＡＯＨ）体外处理不同时间胎儿食管上皮组织,提取组织的ＤＮＡ,从１０例食管癌组织及１０例癌旁组织中分别提取ＤＮＡ,设正常胎儿食管上皮ＤＮＡ为对照。ＥｃｏＲＩ酶切,Ｓｏｕｔｈｅｒｎ转移,与ＥＧＦｒ癌基因,Ｒｂ抗癌基因探针杂交。结果：正常对照组中ＥＧＦｒ、Ｒｂ无扩主丢失;ＡＯＨ诱导２４ｈ１周和３周的胎儿食管上皮未抗癌基因Ｒｂ的丢失,食管癌组织     

经交链孢酚处理胎儿食管上皮组织中EGFr、Rb基因的扩增

Aim To study the mechanism of esophageal cancer induced by alternariol (AOH). Methods DNA was extracted from the human fetal esophagus (HFE) treated with AOH for 24 hours,1 week and 3 weeks in vitro. As controls, DNA from normal HFE, and DNA from esophageal carcinoma tissues, “normal” epithelium tissue near carcinoma region were extracted respectively. DNA samples were digested with EcoRI enzyme and subjected to Southern blotting ,and hybridized with EGFr and Rb genes probed . Results There was amplification of EGFr gene in HFE induced by AOH in 24 hours, and the amplification continues to the third week．There were not any deletion of Rb gene in HFE treated with AOH for 24 hours in the first week and the third week． Among 10 esophageal cancer tissues, there were amplification of EGFr gene in 2 cases,and complete or partial deletion of Rb gene in 2 cases and in 10 “normal” epithelium tissues near carcinoma region were found amplification of EGFr gene in 4 cases,no deletion of Rb gene. Conclusion AOH could activate EGFr. The activation of EGFr gene is probably the initiated change in the canceration course of esophageal epithelium, and the inactivation of Rb anti-oncogene might be involved as late event in esophageal carcinogenesis.