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Departments of Hematology-Oncology [D. A. R., R. L. H., A. T. L.], Experimental Oncology [J. E. S., R. E. E., S. T. R., M. B. V., D. N. S., A. T. L.], Pathology [F. G. B.], Biostatistics [H. L., J. M. B.], Surgery [E. M.], and Radiation Oncology [L. E. K.], St. Jude Children's Research Hospital, Memphis, Tennessee 38105
We analyzed 27 samples of primary medulloblastoma, using comparative genomic hybridization and a novel statistical approach to evaluate chromosomal regions for significant gain or loss of genomic DNA. An array of nonrandom changes was found in most samples. Two discrete regions of high-level DNA amplification of chromosome bands 5p15.3 and 11q22.3 were observed in 3 of 27 tumors. Nonrandom genomic losses were most frequent in regions on chromosomes 10q (41% of samples), 11 (41%), 16q (37%), 17p (37%), and 8p (33%). Regions of DNA gain most often involved chromosomes 17q (48%) and 7 (44%). These findings suggest a greater degree of genomic imbalance in medulloblastoma than has been recognized previously and highlight chromosomal loci likely to contain oncogenes or tumor suppressor genes that may contribute to the molecular pathogenesis of this tumor.
1 Supported in part by the National Cancer Institute, NIH Grants CA 71907 and CA 23099, Cancer Center CORE Grant CA 21765, and by the American Lebanese Associated Charities (ALSAC), St. Jude Children's Research Hospital.
2 To whom requests for reprints should be addressed, at the Department of Hematology-Oncology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105. Phone: (901) 495-3695; Fax: (901) 521-9005.
Received 9/ 5/96. Accepted 7/17/97.
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