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本文研究了二甲肼（ＤＭＨ）诱发Ｗｉｓｔａｒ鼠大肠癌的组织发生，１５０只鼠每周皮下注射ＤＭＨ２０ｍｇ／ｋｇ，共２０周，５０只鼠不作任何处理为对照组。２４周时７６只动物中有６７只形成了１３０个肿瘤，另９只肉眼无肿瘤。１３０个肿瘤有７６个（５８％）起源于肠相关淋巴组织（ＧＡＬＴ），３０个（２３％）源于平坦粘膜，２２个（１７％）不能确定其来源，仅２例源于腺瘤，而且各种类型的肿瘤均可来源于ＧＡＬＴ，并且随着肿瘤浸润深度的增加所见残留淋巴滤泡的机率就越小，肉眼无病损的结肠标本组织学上可见滤泡旁或滤泡中不典型增生的腺体。我们推测ＤＭＨ诱导大肠癌发生的第一步可能是ＧＡＬＴ旁腺体不典型增生，随后该腺体移向滤泡中或滤泡增生包绕腺体，然后腺体向深层浸润并破坏滤泡，最终形成肉眼可见的肿瘤。
In this paper, the occurrence of dimethylhydrazine (DMH) induced colorectal cancer in Wistar mice was studied. 150 mice were subcutaneously injected with DMH 20mg/kg every week for 20 weeks. 50 mice were treated without any treatment as control group. At the 24th week, 67 out of 76 animals formed 130 tumors, and the other 9 had no tumors on the naked eye. Of the 130 tumors, 76 (58%) originated from gut-associated lymphoid tissue (GALT), 30 (23%) originated from the flat mucosa, 22 (17%) could not determine their origin, and only 2 cases originated from adenomas. Moreover, various types of tumors can be derived from GALT, and the probability of residual lymphoid follicles is smaller as the depth of tumor infiltration increases. Histologically, colonic specimens without lesions are histologically visible near the follicular or follicles. Atypical hyperplasia glands. We speculate that the first step in the development of colorectal cancer induced by DMH may be the atypical hyperplasia of paraglandular GALT. The gland then migrates to the follicle or the follicular hyperplasia surrounds the gland. The gland then infiltrates and destroys the follicle. A macroscopic tumor is eventually formed.