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为了建立一个较好的、用以验证现场食管癌的可疑发病因素的实验性癌模型,并对上皮癌变过程进行动态的观察,用甲基苄基亚硝胺诱发了A系、昆明种与615系三种小鼠的前胃癌(被认为是食管癌的延伸部分)。以每天0.25毫克或1毫克/公斤体重剂量的亚硝胺灌胃,在实验的第7~8个月均能诱发出85~100%的前胃鳞状上皮癌。大剂量组癌发展快,并较多地浸润邻近器官和转移到淋巴结、肝及肺。小鼠系别不同,对该亚硝胺致癌的敏感性略有不同,昆明种最甚,A系次之,615系最低。通过对小鼠作不同阶段的处死,对上皮在癌变过程中出现的各种病变类型的发展作了动态的观察,初步阐明了它们的病理形态特征和组织发生学。对于上皮癌变具有特殊意义的“脐样”病灶的形态发生与发展作了较为详细的描述。食管癌的病因与发病条件相当复杂。从国内外某些食管癌高发区的病因调查看来,目前已知食管癌的可疑发病因素不下一、二十种。但是要肯定它们与食管癌的因果关系,进行实验的验证,就需要建立一个比较理想的食管癌模型。我室于1972年用甲基苄基亚硝胺灌胃的方法建立了大鼠食管癌模型。本文报导用甲基苄基亚硝胺诱发小鼠前胃(被认为是食管的延伸部分)癌模型的建立,及癌变过程中病理学与组织发生学的动态观察,并比较了A系、昆明种和615系~*三种不同系别小鼠对亚硝胺致癌的敏感性,为进一步利用这个小鼠模型提供形态学的基础。
In order to establish a better experimental cancer model for the verification of suspected on-site esophageal cancer and dynamic observation of the epithelial carcinogenesis, A, Kunming and 615 were induced with methylbenzyl nitrosamine. It is a precancerous stomach of three mice (which is considered as an extension of esophageal cancer). Nitrosamine perfused at a dose of 0.25 mg or 1 mg/kg body weight daily could induce 85-100% of progastric squamous cell carcinoma in the first 7 to 8 months of the experiment. The high-dose group developed rapidly, and infiltrated more adjacent organs and metastasized to lymph nodes, liver and lungs. The mouse strains were different, and the susceptibility to carcinogenicity of this nitrosamine was slightly different. Kunming species was the worst, A department was the second, and 615 was the lowest. By performing the mice at different stages of execution, dynamic observations were made of the development of various types of lesions that appeared in the process of carcinogenesis of the epithelium, and their pathological features and histogenetics were initially elucidated. The morphogenesis and development of “umbilical-like” lesions with special significance in epithelial canceration were described in more detail. The etiology and conditions of esophageal cancer are quite complex. From the investigation of the cause of some high-risk areas of esophageal cancer at home and abroad, there are currently no less than twenty suspected suspicious factors for esophageal cancer. But to confirm their causal relationship with esophageal cancer, to verify the experiment, we need to establish an ideal model of esophageal cancer. In 1972, our laboratory established a model of rat esophageal cancer by intragastric administration of methylbenzylnitrosamine. This paper reports the establishment of a cancer model of mouse forefoot (an extension of the esophagus) induced by methylbenzylnitrosamine, and the dynamic observation of histopathology and histopathology in the process of carcinogenesis, and compares the A series and Kunming. The susceptibility of nitrosamines to carcinogenesis in mice of the three different strains of the strain and the 615 lineage* was used to provide further morphological basis for further use of this mouse model.