Beazer-Barclay Y, Levy D B, Moser A R, Dove W F, Hamilton S R, Vogelstein B, Kinzler K W
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Carcinogenesis. 1996 Aug;17(8):1757-60. doi: 10.1093/carcin/17.8.1757.
The Min mouse provides a genetically defined model for inherited and sporadic forms of human colorectal tumorigenesis. To test the suitability of this model for the evaluation and optimization of chemopreventive agents, we examined the effects of sulindac on tumorigenesis in Min mice as this compound can inhibit colorectal tumorigenesis in human familial adenomatous polyposis patients. Treatment of Min mice with sulindac in their drinking water (84 mg/l) or diet (167 and 334 p.p.m.) resulted in a significantly decreased average tumor load. The conservation of sulindac activity in the Min mouse provides an opportunity to explore the mechanism of sulindac suppression as well as to test other potential chemopreventive agents.
Min小鼠为人类遗传性和散发性结直肠癌发生提供了一个基因定义模型。为了测试该模型对化学预防剂评估和优化的适用性,我们研究了舒林酸对Min小鼠肿瘤发生的影响,因为该化合物可抑制人类家族性腺瘤性息肉病患者的结直肠癌发生。用饮用水中含84 mg/l舒林酸或饮食中含167和334 ppm舒林酸处理Min小鼠,导致平均肿瘤负荷显著降低。舒林酸在Min小鼠中的活性保留为探索舒林酸抑制机制以及测试其他潜在化学预防剂提供了机会。