Williamson R C, Bauer F L, Oscarson J E, Ross J S, Malt R A
Cancer Res. 1978 Oct;38(10):3212-7.
Potential enhancement of intestinal neoplasia by compensatory mucosal hyperplasia was tested in rats subjected to 50% proximal small bowel resection (PSBR) 10 days after the last of 16 weekly injections of azoxymethane. Azoxymethane alone increased jejunal contents of RNA and DNA each by 26% at 17 to 18 weeks (p less than 0.01) before there was macroscopic evidence of neoplasia. Three months after PSBR alone, ileal hyperplasia was characterized by increased amounts of RNA (42 to 76%) and DNA (68 to 95%), taller villi, deeper crypts, and luminal dilation (p less than 0.05 to 0.001); however, the colon showed only patchy hyperplasia. When the combined effects of azoxymethane and PSBR were observed 26 to 30 weeks after the first injection, rats with PSBR had an increased number of colonic tumors per animal (2.9 versus 1.6 for controls; p less than 0.02). Despite the intense ileal hyperplasia produced by PSBR, ileal neoplasia did not occur. Enhanced colonic carcinogenesis followed sequential exposure of the mucosa to the carcinogen (azoxymethane) and to the promoting factor (PSBR).
在接受16周每周一次注射偶氮甲烷后10天进行50%近端小肠切除（PSBR）的大鼠中，测试了代偿性黏膜增生对肠道肿瘤形成的潜在增强作用。在出现肿瘤的宏观证据之前，单独使用偶氮甲烷在17至18周时使空肠中的RNA和DNA含量分别增加了26%（p<0.01）。单独进行PSBR三个月后，回肠增生的特征是RNA（42%至76%）和DNA（68%至95%）含量增加、绒毛更高、隐窝更深以及管腔扩张（p<0.05至0.001）；然而，结肠仅表现为散在性增生。在首次注射后26至30周观察偶氮甲烷和PSBR的联合作用时，接受PSBR的大鼠每只动物的结肠肿瘤数量增加（对照组为1.6个，PSBR组为2.9个；p<0.02）。尽管PSBR导致了强烈的回肠增生，但回肠并未发生肿瘤。结肠致癌作用增强是由于黏膜先后接触致癌物（偶氮甲烷）和促癌因素（PSBR）所致。
