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作 者:阎晓初[1] 柳凤轩[1] 贺光友[1] 于冬梅[1] 王宗前[1]
出 处:《第三军医大学学报》1993年第4期299-303,共5页Journal of Third Military Medical University
摘 要:作者对DMH诱发大鼠大肠癌过程进行了动态研究,结果显示40只大鼠在DMH作用下,大肠粘膜显示不同程度的病变。实验第8周,大肠粘膜呈现早期增生性改变;第10~15周主要表现为粘膜轻、中度不典型增生;第18~32周除粘膜不典型增生外,大肠腺瘤和癌逐渐形成,其中检出腺瘤14个,原位癌10个,浸润性癌35个。20只对照大鼠大肠粘膜无明显病变。提示大肠癌的组织发生系经过粘膜增生→不典型增生或腺瘤→原位癌→浸润性癌的发展过程,证实不典型增生是大肠癌重要的癌前病变。The changes of mucous secretion in the 1,2-dimethylhydrazine (1,2-DMH) induced colorectal carcinogenesis were studied with mucohistochemistry in rats. It was found that the colorectal mucosa of the 40 rats under study showed various lesions and changes of mucous secretion. The mucosa of the hyperplastic region, similar to the normal mucosa of the control group, secreted predominantly sulphomucin. The dysplastic flat mucosa and adenomas secreted predominantly sialomucin and the amount of mucous secretion decreased along with intensification of the deformity of the atypical proliferative rnucosa and adenomas. Most of the induced colorectal carcinomas secreted no mucin or mixed mucin (sulphomucin and sialomucin). These findings support the concept that the increase of sialolmucin secretion or the decrease of mucous secretion in the dysplastic flat mucosa or adenomas indicates the tendency of malignancy and also confirms that the histogenesis of colorectal carcinoma undergoes through the malignant change of an adenoma or from the atypical proliferation of the flat mucosa directly.
分 类 号:R735.340.2[医药卫生—肿瘤]
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