Lung cancer is the major cancer in Turkey; 45% of the deaths due to cancer in Turkish males are from lung cancer. There are 8 histopathological types of lung cancer, and most types have several genomic/genetic alterations, including amplification of oncogenes. The current study evaluated the ras oncogene in human lung cancers from Turkish patients. Thirty-six normal and pathological lung tissue specimens were obtained from patients with chest disease during surgery, frozen at -86°C, and processed within 2-3 months. Mutations in K-ras, codon 12 were analyzed using a series of DNA purification proceedures, polymerase chain reaction amplification, and dot-blotting techniques. Fifteen of the 21 cancer tissues had K-ras mutations. None of the 11 normal lung tissues nor any of the 4 other pathological tissues showed K-ras mutations. Seven of 11 epidermoid carcinomas, 3 of 3 adenocarcinomas, 2 of 3 bronchial carcinomas, 1 of 2 mesotheliomas, 1 of 1 metastatic anaplastic carcinoma, and 1 of 1 rabdomyosarcoma showed point mutations in codon 12, base pairs n 34 and/or 35. Base pair n 34 was mutated G->A in 11 samples and G->T in 4 samples, while base pair n 35 was mutated G->T in 8 samples. There were 3 triple and 3 double mutations in this group of cancers. Because G->A and G->T mutations are considered to be related to specific chemicals in cigarette smoke, and because 13 of the 15 cancer patients, who had K-ras mutations, were heavy smokers, the results from this study directly support, at the molecular level, close linkages between cigarette smoking and carcinogenic mutations in human lung tissues.

Lung cancer is the major cancer in Turkey; 45% of the deaths due to cancer in Turkish males are from lung cancer. There are 8 histopathological types of lung cancer, and most types have several genomic/genetic alterations, including amplification of oncogenes. The current study evaluated the ras oncogene in human lung cancers from Turkish patients. Thirty-six normal and pathological lung tissue specimens were obtained from patients with chest disease during surgery, frozen at -86°C, and processed within 2-3 months. Mutations in K-ras, codon 12 were analyzed using a series of DNA purification proceedures, polymerase chain reaction amplification, and dot-blotting techniques. Fifteen of the 21 cancer tissues had K-ras mutations. None of the 11 normal lung tissues nor any of the 4 other pathological tissues showed K-ras mutations. Seven of 11 epidermoid carcinomas, 3 of 3 adenocarcinomas, 2 of 3 bronchial carcinomas, 1 of 2 mesotheliomas, 1 of 1 metastatic anaplastic carcinoma, and 1 of 1 rabdomyosarcoma showed point mutations in codon 12, base pairs n 34 and/or 35. Base pair n 34 was mutated G->A in 11 samples and G->T in 4 samples, while base pair n 35 was mutated G->T in 8 samples. There were 3 triple and 3 double mutations in this group of cancers. Because G->A and G->T mutations are considered to be related to specific chemicals in cigarette smoke, and because 13 of the 15 cancer patients, who had K-ras mutations, were heavy smokers, the results from this study directly support, at the molecular level, close linkages between cigarette smoking and carcinogenic mutations in human lung tissues.