Taylor P R, Mason R C, Filipe M I
Department of Surgery, Guy's Hospital, London, U.K.
In Vivo. 1988 May-Aug;2(3-4):271-80.
The majority of experimental studies on the development of gastric adenocarcinoma have been performed in the rat. There is evidence for two pathways of carcinogenesis in the intact stomach following carcinogen administration. The first has a sequence of hyperplasia, dysplasia, carcinoma with a benign proliferating phase associated with damage and repair mechanisms. The second sequence progresses through increasing grades of dysplasia in an undisturbed mucosa leading to carcinoma formation. Early experiments concerning the effects of gastric surgery on carcinogen induced adenocarcinoma may have simply altered the effectiveness of the carcinogen. Recently it has been shown that surgery alone can induce adenocarcinomas and the number of tumours is related to the degree of duodenogastric reflux. The component of that reflux which seems to be responsible is pancreaticoduodenal secretions and not bile. Intestinal metaplasia is not an important intermediate stage in carcinogenesis in the rat.
大多数关于胃腺癌发生发展的实验研究是在大鼠身上进行的。有证据表明，给完整的胃施用致癌物后存在两种致癌途径。第一种途径有增生、发育异常、伴有与损伤和修复机制相关的良性增殖期的癌。第二种途径是在未受干扰的黏膜中，发育异常程度不断增加，最终导致癌的形成。早期关于胃手术对致癌物诱导的腺癌影响的实验可能只是改变了致癌物的效力。最近有研究表明，单纯手术就能诱发腺癌，肿瘤数量与十二指肠-胃反流程度有关。似乎起作用的反流成分是胰十二指肠分泌物而非胆汁。在大鼠致癌过程中，肠化生不是一个重要的中间阶段。
