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Department of Medical Oncology, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111 [B. R. B., G. S., J. R. T.]; National Center for Human Genome Research, NIH, Bethesda, Maryland 20892 [S. d. M.]; Department of Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261 [J. M. S.]; and Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231 [E. G.]
Comparative genomic hybridization analysis was used to identify chromosomal imbalances in 20 non-small cell lung carcinoma (NSCLC) biopsies and cell lines. The chromosome arms most often overrepresented were 3q (85%), 5p (70%), 7p (65%), and 8q (65%), which were observed at high copy numbers in many cases. Other common overrepresented sites were 1q, 2p, and 20p. DNA sequence amplification was often observed, with the most frequent site being 3q26 (six cases). Other recurrent sites of amplification included 8q24, 3q13, 3q28-qter, 7q11.2, 8p11–12, 12p12, and 19q13.1–13.2. The most frequent underrepresented segment was 3p21 (50%); other recurrent sites of autosomal loss included 8p21-pter, 15q11.2–13, 5q11.2–15, 9p, 13q12–14, 17p, and 18q21-qter. These regions of copy number decreases are also common sites of allelic loss, further implicating these sites as locations of tumor suppressor genes. Although some of the overrepresented segments harbor known or suspected oncogenes/growth-regulatory genes, we have identified 3q and 5p as new sites that are very frequently overrepresented in NSCLC. These findings could represent entry points for the identification of novel amplified DNA sequences that may contribute to the development or progression of NSCLC.
1 Supported by NIH Grants CA-58184, CA-50674, and CA-06927; by an appropriation from the Commonwealth of Pennsylvania; and by a gift from the Ann Ricci Memorial Fund.
2 To whom correspondence should be addressed, at Department of Medical Oncology, Fox Chase Cancer Center, 7701 Burholme Avenue, Philadelphia, PA 19111. Phone: (215) 728-2610; Fax: (215) 728-2741.
Received 3/ 5/97. Accepted 4/18/97.
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