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Chromosomal aberrations of primary lung adenocarcinomas in nonsmokers
Maria P Wong1, Lai-Fan Fung, Elaine Wang
1Department of Pathology, The University of Hong Kong, Hong Kong, China.
Background:
Lung carcinoma is a common malignancy, and tobacco carcinogenesis is the major cause. Studies on individual genes or loci have suggested, that in tumors from nonsmokers, different genetic alterations are present compared with tumors from smokers. It is possible that distinct genetic pathways may be involved. However, the targets remain largely unknown; and, to the authors' knowledge, molecular cytogenetics studies on lung carcinomas from nonsmokers have not been reported.
Methods:
Comparative genomic hybridization (CGH) analysis was performed on primary lung adenocarcinoma samples from 32 patients who never smoked to identify loci of frequent aberrations.
Results:
Different extents of aberration were found in 31 of the 32 samples studied. The most frequently altered locus was gain of 16p (59% of samples) followed by gain of 20q (44% of samples), with the minimal overlapping regions at 16p13.1-p13.2 and 20q13.2, respectively. Other over-represented loci with > 30% frequency were observed at 5p (34% of samples), 7p (41% of samples), 8q (31% of samples), 17q (34% of samples), and 19q (34% of samples); and high-level DNA amplifications were detected at 1q, 7p, 12q, 19q, and 20q. DNA under-representation was observed less commonly and included 8p (28% of samples), 9p (22% of samples), 13q (28% of samples), and 18q (38% of samples).
Conclusions:
The current study identified targets of frequent genetic aberration in primary adenocarcinomas from nonsmokers. Compared with reported CGH findings in the literature, the current findings suggest that DNA gain at 16p is the distinct aberration involved in these tumors. Other frequently altered loci involve commonly reported oncogenic and tumor suppressor loci, suggesting an overlap with the genetic pathways of tobacco-induced lung carcinogenesis.
Insights
Genetic alterations in lung adenocarcinoma from nonsmokers were identified. DNA gain at 16p appears distinct in these tumors, suggesting unique pathways in lung cancer development for those who do not smoke.
Area of Science:
- Genetics
- Oncology
- Molecular Biology
Background:
- Lung carcinoma is a major malignancy, often linked to tobacco use.
- Tumors from smokers and nonsmokers may exhibit distinct genetic alterations.
- Genetic pathways in lung cancer among nonsmokers are not well understood.
Purpose of the Study:
- To identify frequently altered genetic loci in primary lung adenocarcinomas from individuals who have never smoked.
- To investigate potential distinct genetic pathways in lung cancer among nonsmokers.
Main Methods:
- Comparative genomic hybridization (CGH) analysis was performed on 32 primary lung adenocarcinoma samples from nonsmokers.
- The study aimed to identify loci with frequent genomic aberrations (gains and losses).
Main Results:
- Aberrations were found in 31 of 32 samples.
- The most frequent aberration was gain of 16p (59%), followed by gain of 20q (44%).
- Other significant alterations included gains at 5p, 7p, 8q, 17q, 19q, and high-level amplifications at 1q, 7p, 12q, 19q, 20q; losses were less common.
Conclusions:
- This study identified key genetic aberrations in lung adenocarcinomas from nonsmokers.
- DNA gain at 16p is a distinct aberration in these tumors.
- Findings suggest potential overlap with genetic pathways in tobacco-induced lung cancer.