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Mutations in the p53 Gene in Primary Human Breast Cancers¹

Navy Medical Oncology Branch [R. J. O., T. M., I. C., T. T., M. M. N., J. D. M.] and Oncogenetics Section [G. R. M., T. V., R. C.] National Cancer Institute, Bethesda, Maryland 20892, and Ospedale S. Giovanni Vecchio, Turin, Italy [D. S. L., A. P. M. C.]

Twenty-six primary breast tumors were examined for mutations in the p53 tumor suppressor gene by an RNase protection assay and nucleotide sequence analysis of PCR-amplified p53 complementary DNAs. Each method detected p53 mutations in the same three tumors (12%). One tumor contained two mutations in the same allele. Single strand conformation polymorphism analysis of genomic DNA and complementary DNA proved more sensitive in the detection of mutations. Combining this technique with the other two a total of 12 mutations in the p53 gene were demonstrated in 11 tumors (46%), and a polymorphism at codon 213 was detected in another tumor. Loss of heterozygosity on chromosome 17p was detected by Southern blot analysis in 30% of the tumor DNAs. Not all of the tumors containing a point mutation in p53 also had loss of heterozygosity of the remaining allele, suggesting that loss of heterozygosity may represent a later event.

¹ This work was supported in part by a grant from the Associazione Italiana Ricerca sul Cancro.

² Present address: Department of Clinical Oncology, Addenbrookes's Hospital, Cambridge, CB2 2QQ, England.

³ To whom requests for reprints should be addressed, at Simmons Cancer Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235-8590.

Received 9/ 3/91. Accepted 9/27/91.

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