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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 (2 4h ,1周和 3周 )胎儿食管上皮组织 ,提取该组织的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无扩增及丢失 ;AOH诱导 2 4h的胎儿食管上皮中即有EGFr癌基因的扩增 ,并一直持续到第 3周 ;而AOH诱导 2 4h ,1周和 3周的胎儿食管上皮未发现抗癌基因Rb的丢失 ;食管癌组织中有 2例EGFr扩增 (2 /10 ) ,2例Rb完全缺失和部分丢失 (2 /10 ) ,癌旁组织中有 4例EGFr扩增 (4/10 ) ,Rb无任何缺失 (0 /10 )。结论 :AOH激活了EGFr癌基因 ,EGFr癌基因的激活可能是食管上皮癌变的启动性变化 ,Rb抗癌基因的丢失在AOH诱导的食管癌发生中可能是一种较晚期的改变。
Objective: To investigate the mechanism of Alternaria alternata inducing esophageal cancer. Methods: Fetal esophageal epithelial tissue was treated with carbitol (AOH) in vitro for 24 hours, 1 week and 3 weeks. The DNA of this tissue was extracted from 10 esophageal cancer tissues and 10 adjacent tissues DNA, normal fetal esophageal epithelial DNA as a control. EcoRI digestion, Southern blot, hybridization with EGFr oncogene, Rb anti-oncogene probe. Results: There was no amplification and loss of EGFr and Rb in the normal control group. The amplification of EGFr oncogene in 24 hours after AOH induction continued until the third week. However, AOH induced 24 hours and 1 week Three weeks of fetal esophageal epithelium showed no loss of anti-oncogene Rb. Two cases of esophageal cancer showed EGFR amplification (2/10), two cases of complete deletion and partial loss of Rb (2/10) Four cases of EGFr amplification (4/10), Rb without any deletion (0/10). CONCLUSION: AOH activates the EGFr oncogene. The activation of the EGFr oncogene may be a start-up change in esophageal epithelial carcinogenesis. The loss of the Rb anti-oncogene may be a later change in AOH-induced esophageal cancer.