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Increased polysomy of chromosome 7 in bronchial epithelium from patients at high risk for lung cancer

Technical Report ·
DOI:https://doi.org/10.2172/381379· OSTI ID:381379
Current models of carcinogenesis suggest that tissues progress through multiple genetic and epigenetic changes which ultimately lead to development of invasive cancer. Epidemiologic studies of Peto, R.R. and J.A. Doll indicate that the accumulation of these genetic changes over time, rather than any single unique genetic change, is probably responsible for development of the malignant phenotype. The bronchial epithelium of cigarette smokers is diffusely exposed to a broad spectrum of carcinogens, toxicants, and tumor promoters contained in tobacco smoke. This exposure increases the risk of developing multiple, independent premalignant foci throughout the lower respiratory tract that may contain independent gene aberrations. This {open_quotes}field cancerization{close_quotes} theory is supported by studies that have demonstrated progressive histologic changes distributed throughout the lower respiratory tract of smokers. A series of autopsy studies demonstrated that cigarette smokers exhibit premalignant histologic changes ranging from hyperplasia and metaplasia to severe dysplasia and carcinoma in situ diffusely throughout the bronchial mucosa. The proximal bronchi appear to exhibit the greatest number of changes, particularly at bifurcations. The results described are the first to quantitate the frequency for a chromosome aberration in {open_quotes}normal{close_quotes} bronchial epithelial cells.
Research Organization:
Lovelace Biomedical and Environmental Research Inst., Albuquerque, NM (United States). Inhalation Toxicology Research Inst.
DOE Contract Number:
AC04-76EV01013
OSTI ID:
381379
Report Number(s):
ITRI--146; ON: DE96008986
Country of Publication:
United States
Language:
English