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Infrequent p53 Gene Mutations in Medulloblastomas¹

Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 63110 [R. L. S., G. M. B.]; The Johns Hopkins Oncology Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231 [D. S., B. V.]; and the Preuss Laboratory for Brain Tumor Research [D. D. B.] and the Departments of Pathology [H. S. F., S. H. B., D. D. B.] and Pediatrics [H. S. F.], Duke University Medical Center, Durham, North Carolina 27710

Cytogenetic and molecular studies of medulloblastomas have demonstrated frequent loss of sequences from the short arm of chromosome 17, possibly implicating loss or inactivation of the p53 tumor suppressor gene. We amplified exons 5 through 8 of the p53 gene by the polymerase chain reaction technique. These segments, which encompass the regions usually mutated in human tumors, were sequenced to search for p53 mutations in 12 medulloblastoma tumors, 8 xenografts, and 3 permanent cell lines. Mutation of the p53 gene was found in only 1 of 3 cell lines tested and in none of the xenografts or primary tumors studied. Our results suggest that p53 is mutated in an unusual way or that a second tumor suppressor gene on the short arm of chromosome 17 is involved in the pathogenesis of medulloblastoma.

¹ This work was supported in part by the Children's Cancer Research Fund (R. L. S.); NIH Grants CA 39771 (G. M. B.), CA 43466 (B. V.), and CA 09071 (D. S.); and the Preuss Foundation.

² To whom requests for reprints should be addressed, at Department of Pediatrics, Washington University School of Medicine, 400 South Kingshighway Blvd., St. Louis, MO 63110.

Received 6/ 3/91. Accepted 7/15/91.

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