Array CGH analysis reveals chromosomal aberrations in mouse lung adenocarcinomas induced by the human lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
Copyright policy )Array CGH analysis reveals chromosomal aberrations in mouse lung adenocarcinomas induced by the human lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
Exposure to genotoxic carcinogens in tobacco smoke is a major cause of lung cancer. However, the effect this has on DNA copy number and genomic stability during lung carcinogenesis is unclear. Here we used bacterial artificial chromosome array-based comparative genomic hybridization to examine the effect of NNK, a potent human lung carcinogen present in tobacco smoke, on the major genomic changes occurring during mouse lung adenocarcinogenesis. Observed were significantly more gross chromosomal changes in NNK-induced tumors compared with the spontaneous tumors. An average of 5.6 chromosomes were affected by large-scale changes in DNA copy number per NNK-induced tumor compared with only 2.0 in spontaneous lung tumors (p = 0.017). Further analysis showed that gains on chromosomes 6 and 8, and losses on chromosomes 11 and 14 were more common in NNK-induced tumors (p
- Penn State Milton S. Hershey Medical Center United States
- Pennsylvania State University United States
Chromosome Aberrations, Lung Neoplasms, Nitrosamines, Gene Dosage, Nucleic Acid Hybridization, DNA, Adenocarcinoma, Mice, Cell Line, Tumor, Karyotyping, Carcinogens, Animals, Humans, Oligonucleotide Array Sequence Analysis
Chromosome Aberrations, Lung Neoplasms, Nitrosamines, Gene Dosage, Nucleic Acid Hybridization, DNA, Adenocarcinoma, Mice, Cell Line, Tumor, Karyotyping, Carcinogens, Animals, Humans, Oligonucleotide Array Sequence Analysis
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