Ton Thai-Vu, Hong Hue-Hua, Devereux Theodora R, Melnick Ronald L, Sills Robert C, Kim Yongbaek
Environmental Toxicology Program and Environmental Carcinogenesis Program, National Institute of Environmental Health Sciences, MD B3-08, 111 Alexander Drive, Research Triangle Park, NC 27709, USA.
Chem Biol Interact. 2007 Mar 20;166(1-3):112-20. doi: 10.1016/j.cbi.2006.04.015. Epub 2006 May 2.
1,3-Butadiene and chloroprene are multisite carcinogens in B6C3F1 mice with the strongest tumor response being the induction of lung neoplasms in females. Incidence of brain tumors in mice exposed to 1,3-butadiene was equivocal. This article reviews the efforts of our laboratory and others to uncover the mechanisms of butadiene and chloroprene induced lung and brain tumor responses in the B6C3F1 mouse. The formation of lung tumors by these chemicals involved mutations in the K-ras cancer gene and loss of heterozygosity in the region of K-ras on distal chromosome 6, while alterations in p53 and p16 were implicated in brain tumorigenesis.
1,3 - 丁二烯和氯丁二烯是B6C3F1小鼠中的多部位致癌物,最强的肿瘤反应是雌性小鼠肺部肿瘤的诱发。接触1,3 - 丁二烯的小鼠脑部肿瘤的发生率不明确。本文综述了我们实验室及其他机构为揭示丁二烯和氯丁二烯在B6C3F1小鼠中诱发肺部和脑部肿瘤反应的机制所做的努力。这些化学物质诱发肺部肿瘤的过程涉及K - ras癌基因的突变以及6号远端染色体上K - ras区域杂合性的缺失,而p53和p16的改变与脑部肿瘤发生有关。