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The relation of alcohol consumption and cigarette smoking to the multiple occurrence of esophageal dysplasia and squamous cell carcinoma.

机译:饮酒和吸烟与食管异型增生和鳞状细胞癌多发的关系。

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BACKGROUND: The unique pathologic features of esophageal tumors in patients with esophageal cancer includes the presence of multiple occurrence within the esophagus. The aim of this study is to clarify the molecular mechanism of carcinogenesis of multiple esophageal squamous cell carcinomas in the Japanese. METHODS: We studied the relationship between the incidence of patients with multiple carcinomas and the coexistence of dysplasia lesions with p53 protein accumulation, alcohol consumption, and cigarette smoking. Among 76 cancer lesions and 60 cases of dysplasia, p53 accumulation was studied by means of immunohistochemical analysis. RESULTS: The incidence of patients with multiple carcinomas in the high-risk group was 33%, and the incidence of patients with a coexistence of dysplasia in the high-risk group was 67%. The incidence of patients with multiple carcinomas or the coexistence of dysplasia in the high-risk group was much higher than that of the middle-risk and low-risk groups (P <.0001 and P =.04, respectively). The average number of abnormal epitheliums, such as cancer and dysplasia, in the high-risk group was 3.2 +/- 2.1. The average number of abnormal epitheliums was much higher than that of the other groups (P =.02). For carcinoma lesions, the incidence of lesions with a positive p53 protein accumulation in the high-risk group was 91%. Regarding dysplasia lesions, the incidence of lesions with a positive p53 protein accumulation in the high-risk group was 80%. The incidence of both cancer and dysplasia lesions with a positive p53 protein accumulation in the high-risk group was higher than that of the other groups. CONCLUSIONS: The pattern of p53 accumulation in dysplasia in the high-risk group was closely similar to that in cancer of the high-risk group. These findings support the concept of field carcinogenesis of the esophagus.
机译:背景:食管癌患者食管肿瘤的独特病理特征包括食管内多次发生。这项研究的目的是弄清日本人多发食道鳞状细胞癌致癌的分子机制。方法:我们研究了多发性癌患者的发病率与异型增生病变并存与p53蛋白积累,饮酒和吸烟之间的关系。在76例癌症病变和60例不典型增生中,通过免疫组织化学分析了p53的积累。结果:高危组中多发癌患者的发生率为33%,高危组中不典型增生并存的患者为67%。高危组中多发癌或异型增生并存的发生率远高于中危和低危组(分别为P <.0001和P = .04)。高风险组中异常上皮的平均数量,例如癌症和不典型增生为3.2 +/- 2.1。异常上皮的平均数量远高于其他组(P = .02)。对于癌病灶,高风险组中p53蛋白积聚阳性的病灶的发生率为91%。对于不典型增生的病变,高风险组中p53蛋白积聚阳性的病变发生率为80%。在高危组中,p53蛋白积聚阳性的癌变和非典型增生病变的发生率均高于其他组。结论:高危组的异型增生中p53积累的模式与高危组的癌非常相似。这些发现支持食道野外致癌的概念。

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