Distribution of p53 and K-ras mutations in human lung cancer tissues.

11) was found in non-smokers. Among cell types, K- injections. Mutations in K-ras were found in 50% of the ras mutations were found in 7/13 (54%) squamous cell animals at codon 12, but no mutations were detected in the carcinoma (SC) and 5/12 (42%) adenocarcinoma (AC) p53 gene (12). In another study, 77‐94% of tumors contained patients. A → T transversions (all six transversions) were K-ras mutations, but only one tumor had a point mutation in present only in SC. In p53, 18/27 (67%) tumors contained the p53 gene, indicating a distinctive mutation pattern in the mutations in exons 7 and 8, frequently at codons 226, 270, K-ras gene (13). In molecular genetic studies, K-ras mutations, 275 and 281. The number of tumors with p53 mutations mostly G → T transversions in codon 12, have been found in in smokers (70%) and in non-smokers (65%) was similar, 30‐60% of adenocarcinoma (AC) and in 10% of squamous and the mutation frequency did not differ except for a cell carcinoma (SC) from smokers (14‐16). Mutations in the higher number of G → A (6/7) and T → C (5/6) transitions p53 gene are widely distributed throughout exons 4‐9 and the in non-smokers. Among cell types, the number of tumors most prevalent mutations are G → T transversions found in with p53 mutations was 9/13 (69%) in SC and 8/12 (67%) tobacco-associated lung cancer (11,17‐19). A mixture of highly in AC. The A → G (11/16) transitions and A → C (4/4) mutagenic polycyclic aromatic hydrocarbons (PAH) found in transversions in p53 were more frequent in SC than in AC tobacco smoke preferentially attack the guanine base. Strauss (P , 0.04 for A → G; P , 0.02 for A → C). The varying (20) suggested that the predominant G → T transversion occurs mutation patterns in both the K-ras and p53 genes between in DNA replication, either by a mispairing of the PAHsmokers and non-smokers and among cell types suggest adducted guanine with adenine or by a preferential insertion of that other than cigarette smoke, environmental and dietary adenine opposite the non-instructive modified base. Therefore, factors may also be involved in the genesis of lung cancer analysis of patterns of mutations in these two genes may among these patients. provide clues to the etiology and molecular pathogenesis of lung cancer. In this study we examined the genetic alterations using