Li Jie, Zhang Zhongqiu, Dai Zunyan, Plass Christoph, Morrison Carl, Wang Yian, Wiest Jonathan S, Anderson Marshall W, You Ming
Division of Human Cancer genetics, The Ohio Stsate University Comprehensive Cancer Center, 420 West 12th Avenue, Columbus, OH 43210, USA.
Oncogene. 2003 Feb 27;22(8):1243-6. doi: 10.1038/sj.onc.1206192.
Previous observation has shown that the wild-type Kras2 allele is a suppressor of lung cancer in mice. Here we report that loss of heterozygosity (LOH) of chromosome 12p was detected in approximately 50% of human lung adenocarcinomas and large cell carcinomas, and Kras2 mutations were detected at codon 12 in approximately 40% of adenocarcinomas and large cell carcinomas. Interestingly, all of the lung adenocarcinomas and large cell carcinomas containing a Kras2 mutation exhibited allelic loss of the wild-type Kras2 allele when a correlation between LOH of the region on chromosome 12p and Kras2 mutation was made. These results from human lung cancer tissues provide a strong evidence in support of our previous observation in mouse models that the wild-type Kras2 is a tumor suppressor of lung cancer.
先前的观察表明,野生型Kras2等位基因是小鼠肺癌的抑制因子。在此我们报告,在大约50%的人类肺腺癌和大细胞癌中检测到12号染色体短臂杂合性缺失(LOH),并且在大约40%的腺癌和大细胞癌中检测到Kras2基因第12密码子的突变。有趣的是,当对12号染色体短臂区域的杂合性缺失与Kras2突变之间进行相关性分析时,所有含有Kras2突变的肺腺癌和大细胞癌均表现出野生型Kras2等位基因的等位基因缺失。来自人类肺癌组织的这些结果为我们先前在小鼠模型中的观察提供了有力证据,即野生型Kras2是肺癌的肿瘤抑制因子。