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Departments of Genetics [M. R. S., D. C. W.] and Pathology [C. H., P. C., J. C.], Yale University School of Medicine, New Haven, Connecticut 06510, and National Center for Human Genome Research, NIH, Bethesda, Maryland 20892 [S. d. M.]
To gain a better understanding of genetic changes in squamous cell carcinomas of the head and neck we used comparative genomic hybridization for the analysis of 13 primary tumors. Copy number increases were most frequently observed on chromosomes 3q (10 cases) and 5p (8 cases) and less frequently on 1q (4 cases), 2 (1 case), 7 (2 cases), 8q (2 cases), 9 (1 case), 10p (2 cases), 13q (2 cases), 14q (1 case), 16 (1 case), 17 (2 cases), 20p (2 cases), 21q (1 case) and 22q (1 case). Copy number decreases occurred most frequently at 3p (5 cases), 5q (4 cases), 19p (6 cases), and 19q (5 cases). Copy number decreases also were observed on 1p (2 cases), 2q (2 cases), 4p (2 cases), 4q (2 cases), 7q (2 cases), 8p (1 case), 10q (1 case), 11p (2 cases), 11q (3 cases), 13q (3 cases), 14q (1 case), 16p (1 case), 17p (3 cases), 17q (1 case), 18q (1 case), and 22 (2 cases). Eight sites exhibiting significant sequence amplification were mapped to 3q26
qter (3 cases), 11q13 (2 cases), 12p (2 cases), 2q33–36 (1 case), 7q21–22 (1 case), 7q33qter (1 case), 9p (1 case), and 13q32qter (1 case). Our data suggest that the regions 3q26qter and 5p may harbor oncogenes important for initiation or progression of squamous cell carcinomas of the head and neck. In addition, comparative genomic hybridization defines a subgroup of tumors with 11q13 involvement, the location of the PRAD1/(CCND1)/cyclin D1 gene.
1 Recipient of a grant from the Deutsche Forschungsgemeinschaft (SP 460/1-1). To whom requests for reprints should be addressed, at Department of Genetics, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510.
Received 1/25/95. Accepted 1/27/95.
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