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Absence of p53 Gene Mutations in Primary Nasopharyngeal Carcinomas¹

Kenneth Norris Jr. Comprehensive Cancer Center, University of Southern California, Los Angeles, California 90033 [C. H. S., Y. C. T., A. S. Y., W. M. R., M. G-Z., M. C. Y., P. A. J.], and the Chinese University of Hong Kong, Shatin, Hong Kong [D. P. H., P. C., K-W. L.]

Alterations in the p53 tumor suppressor gene and Epstein-Barr virus status were investigated in 15 nasopharyngeal carcinoma (NPC) biopsies, 4 xenografts, and 2 cell lines from the Cantonese region of southern China. One other established NPC cell line obtained from a northern Chinese patient was also studied. Restriction fragment length polymorphism analysis revealed a loss of heterozygosity for chromosome 17p, where the p53 gene resides, in only one of 15 NPC biopsies. Polymerase chain reaction-single-stranded conformational polymorphism analysis and direct sequencing failed to detect sequence alterations in exons 5 through 8 of the p53 gene in the 15 tumors and in the 4 NPC xenografts, all of which tested positive for Epstein-Barr virus. In contrast, the 3 NPC cell lines were all negative for Epstein-Barr virus and contained G C transversions in the p53 gene, with cell lines CNE-1 and CNE-2 harboring identical AGA (arginine) to ACA (threonine) changes at codon 280. These results suggest that p53 inactivation is not a necessary component of nasopharyngeal carcinogenesis in Cantonese but may be important in the establishment of cell lines derived from these tumors.

¹ Supported by USPHS Grants R01 CA40468 and R35 CA49758 from the National Cancer Institute, NIH, Department of Health and Human Services, and the Betty Lou Warren Research Fund.

² To whom requests for reprints should be addressed, at the Kenneth Norris Jr. Comprehensive Cancer Center, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA 90033-0800.

Received 3/30/92. Accepted 6/23/92.

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