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A Region of Homozygous Deletion on Chromosome 9p21–22 in Primary Nasopharyngeal Carcinoma¹

Departments of Anatomical and Cellular Pathology [D. P. H., K-W. L., S-T. C., J. C. K. L.], Surgery, Divisionof Otorhinolaryngology [C. A. v. H., J. K. S. W.], and Clinical Oncology [P. H. K. C., S-F. L.], Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, and Department of Otolaryngology, Division of Head and Neck Cancer Research, Johns Hopkins University, Baltimore, Maryland 21205-2196 [P. C., D. S.]

Using 21 microsatellite polymorphic markers spanning both p and q arms, we have performed detailed deletion mapping on chromosome 9 in 18 primary nasopharyngeal carcinomas. All 18 tumors were informative at multiple loci. Eleven of the 18 cases (61%) demonstrated allelic deletion of chromosome 9. Among these 11, 6 cases are likely to be tumors with monosomy of chromosome 9. The other 5 cases demonstrated partial deletion by showing multiple areas of allelic loss. In one of the 5 cases, a homozygous deletion region was identified which includes D9S126, D9S171, and IFNA loci at 9p21–22, situated between loci D9S161 (9p21) and D9S162 (9p21–22). The presence of a homozygous deletion strongly suggests the presence of tumor suppressor gene(s) involved in the tumorigenesis of nasopharyngeal carcinoma. The same region has been reported to include some potential tumor suppressor gene loci in other cancers. This is the first reported finding of frequent genetic loss observed on chromosome 9 in nasopharyngeal carcinomas in addition to allelic loss on chromosome 3p at specific regions. Our results suggest that tumorigenesis and progression of nasopharyngeal carcinomas, like other solid tumors, involves multiple genetic changes associated with the inactivation of tumor suppressor genes.

¹ Supported by University and Polytechnic Grants Committee, Hong Kong Grant CUHK52/93M and by the Croucher Foundation.

² To whom requests for reprints should be addressed.

Received 4/28/94. Accepted 6/ 9/94.

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