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目的 探讨交链孢酚诱导食管癌的发生机制。方法 采用免疫组化ＡＢＣ 法，分别对经ＡＯＨ 处理２４ ｈ 、１ 周和３ 周的人胎儿食管上皮组织及原发性食管癌组织、癌旁“正常”上皮进行ＥＧＦｒ 蛋白表达的检测。结果 ＡＯＨ 诱导２４ ｈ 人胎儿食管上皮中即有ＥＧＦｒ 蛋白过表达，并一直持续到第３ 周；原发性食管癌组织、癌旁“正常”上皮的表达率分别为５３ ．３ ％ 、３８ ．５ ％ ，两者无显著性差异（ Ｐ＞ ０ ．０５） ；淋巴结转移组的阳性率显著高于淋巴结未转移组，两者具有显著性差异（ Ｐ＜ ０ ．０５） 。结论 ＡＯＨ 可以激活ＥＧＦｒ ，ＥＧＦｒ 蛋白过表达可能是食管癌上皮癌变的启动性变化，并在食管癌发生发展中起重要作用，提示肿瘤实际病变区域应是超越目前病理学诊断的范围。
Objective To investigate the mechanism of carotenoid-induced esophageal cancer. Methods Immunohistochemical ABC method was used to detect the expression of EGFr protein in human fetal esophageal epithelium, primary esophageal cancer tissue and normal para - tumor adjacent to AOH for 24 h, 1 week and 3 weeks, respectively. Results AOH induced EGFR protein overexpression in 24 h human fetal esophageal epithelium and continued until the third week. The expression rates of primary epithelial esophageal cancer and adjacent normal epithelium were 53. 3%, 38. There was no significant difference between the two groups (P> 0.05). The positive rate of lymph node metastasis group was significantly higher than that of lymph node metastasis group (P <0.05). Conclusion AOH can activate EGFr. Overexpression of EGFr may be a start-up change in carcinogenesis of esophageal epithelial carcinoma and plays an important role in the development of esophageal cancer, suggesting that the actual tumor area should be beyond the scope of the current pathological diagnosis.