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Cancer Epidemiology Biomarkers & Prevention, Vol 7, Issue 11 1051-1054, Copyright © 1998 by American Association for Cancer Research
ARTICLES |
RE Neft, RE Crowell, FD Gilliland, MM Murphy, JL Lane, H Harms, T Coons, E Heaphy, SA Belinsky and JF Lechner
Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87185, USA. RNEFT@lrri.org
Lung cancer is the leading cause of cancer-related deaths. The development of sensitive screening methods to identify at-risk individuals before emergence of clinical disease would permit early intervention that could decrease this mortality. Our previous studies have shown that cells with trisomy 7 can be detected in bronchial epithelium from cancer-free smokers and former uranium miners. However, the use of more than one molecular marker could increase the chance of identifying at-risk individuals. Trisomy 20, which is found in 43-57% of non-small cell lung cancers, is a candidate marker. The purpose of the current investigation was to determine the percentage of cells with trisomy 20 in persons with a high risk for lung cancer. Bronchial epithelial cells that had been assayed for trisomy 7 were assayed for trisomy 20 by fluorescence in situ hybridization. Trisomy 20 was detected in bronchial epithelial cells from lung cancer patients and from smokers and ex-uranium miners without lung cancer. In some cases, patients who were negative for trisomy 7 exhibited trisomy 20. Consequently, more people with field cancerization were identified using both markers. However, the two markers combined did not appear to stratify the risk for lung cancer.
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