DETECTION OF ONCOGENE ALTERATIONS IN MICE INDUCED BY CHLOROPRENE

工作总结：检测到高达80%的K-ras突变 在氯丁二烯诱发的肺肿瘤中比在自发性肺肿瘤中 (30%)。类似地，K-和H-ras密码子61CTA的高频(100%) 在HG肿瘤中发现了突变，相比之下，突变的频率为56% 在自发性HG肿瘤中。肺脏和肺脏中的主要突变 HG肿瘤是K-ras密码子61位A到T的颠换；突变 在B6C3F小鼠自发性肺肿瘤中从未检测到这种物质， 仅在7%的自发性HG肿瘤中检出。肿瘤终点 在这项研究中与人类接触相关的是肺，在那里有大量的 然而，我们的研究也明确地发现了A到T的易位 表明了小鼠特有的器官系统，如哈德龙 腺体，提供与肺中类似的有关化学特性的数据 K-ras密码子61 CTA突变与致癌的可能机制。 这一数据是在NTP上公布的，并介绍了 致癌。这些数据是在#年的NTP同行评审中公布的 1996年12月。手稿已经准备好了。

Summary of Work: A high frequency 80% of K-ras mutations were detected in chloroprene-induced lung neoplasms than in spontaneous lung neoplasms (30%). Similarly, a high frequency (100%) of K- and H- ras codon 61 CTA mutations was identified in HG neoplasm, compared to a frequency of 56% in spontaneous HG neoplasms. The predominant mutation in both lung and HG neoplasms was an A to T transversion at K-ras codon 61; a mutation which has never been detected in spontaneous lung tumors of B6C3F, Mice, and detected in only 7% of spontaneous HG neoplasms. The tumor endpoint relevant to human exposure in this study was the lung where high numbers of A to T transversions were detected, however, our study also clearly showed that organ systems unique to the mouse such as the Harderian gland, provide data similar to that in the lung about chemical specific K-ras codon 61 CTA mutations and potential mechanisms of carcinognesis. This data was presented at the NTP and about potential mechansms of carcinogenesis. This data were presented at the NTP peer review in December 1996. The manuscript is prepared.