Husgafvel-Pursiainen K, Ridanpää M, Anttila S, Vainio H
Finnish Institute of Occupational Health, Helsinki.
J Occup Environ Med. 1995 Jan;37(1):69-76. doi: 10.1097/00043764-199501000-00010.
This paper reviews mutational activation of ras oncogenes and inactivation of the p53 tumor suppressor gene in human lung cancer. We discuss the frequency, type, and location of mutations in these genes in relation to known etiological factors for lung cancer. The most studied examples of these are exposure to tobacco smoke, and to radon and asbestos fibers at work. We summarize data from our laboratory on K-ras and p53 mutations in fresh tissue samples from patients with resected primary lung carcinoma whose smoking and occupational histories were known. Most of the tumors examined were histologically non-small cell carcinoma (NSCLC), mainly of the squamous cell carcinoma and adenocarcinoma types. We compare the prevalence and nature of mutations in the two histological types of NSCLC.
本文综述了人类肺癌中ras癌基因的突变激活和p53肿瘤抑制基因的失活。我们讨论了这些基因中突变的频率、类型和位置,以及与已知肺癌病因学因素的关系。其中研究最多的例子是接触烟草烟雾,以及工作场所接触氡和石棉纤维。我们总结了来自我们实验室的关于已知吸烟和职业史的原发性肺癌切除患者新鲜组织样本中K-ras和p53突变的数据。大多数检查的肿瘤在组织学上是非小细胞肺癌(NSCLC),主要是鳞状细胞癌和腺癌类型。我们比较了两种组织学类型的NSCLC中突变的发生率和性质。