Slebos R J, Hruban R H, Dalesio O, Mooi W J, Offerhaus G J, Rodenhuis S
Division of Experimental Therapy, The Netherlands Cancer Institute, Amsterdam.
J Natl Cancer Inst. 1991 Jul 17;83(14):1024-7. doi: 10.1093/jnci/83.14.1024.
To investigate a possible relationship between the exposure to tobacco smoke and the presence of ras point mutations, we examined lung adenocarcinoma samples from 27 smokers and from 27 nonsmokers. Activating point mutations in K-ras (also known as KRAS2) and N-ras (also known as NRAS) were determined by using the polymerase chain reaction and oligonucleotide hybridization to detect the mutated sequences. Mutations were more often found in adenocarcinomas obtained from smokers (eight of 27) than in adenocarcinomas obtained from nonsmokers (two of 27) (P = .044, Fisher's exact test). All mutations were present in K-ras codon 12. None of the other parameters examined differed significantly between the ras-positive and ras-negative groups. We conclude that exposure to carcinogenic agents in tobacco smoke is an important factor in the induction of point mutations in K-ras in human lung adenocarcinomas, but that K-ras mutations may also infrequently occur in tumors of non-smokers.
为了研究接触烟草烟雾与ras点突变存在之间的可能关系，我们检测了27名吸烟者和27名不吸烟者的肺腺癌样本。通过使用聚合酶链反应和寡核苷酸杂交来检测突变序列，确定K-ras（也称为KRAS2）和N-ras（也称为NRAS）中的激活点突变。在吸烟者的腺癌中（27例中有8例）比在不吸烟者的腺癌中（27例中有2例）更常发现突变（P = 0.044，Fisher精确检验）。所有突变均存在于K-ras密码子12中。ras阳性和ras阴性组之间检查的其他参数均无显著差异。我们得出结论，接触烟草烟雾中的致癌物质是人类肺腺癌中K-ras点突变诱导的一个重要因素，但K-ras突变也可能在非吸烟者的肿瘤中偶尔发生。
