Extensive genomic abnormalities in childhood medulloblastoma by comparative genomic hybridization

David A. Reardon, Edson Michalkiewicz, James M. Boyett, Jack E. Sublett, Ruth E. Entrekin, Susan T. Ragsdale, Marcus B. Valentine, Frederick G. Behm, Hao Li, Richard L. Heideman, Larry E. Kun, David N. Shapiro, A. Thomas Look

Research output: Contribution to journalArticle

153 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)4042-4047
Number of pages6
JournalCancer research
Volume57
Issue number18
StatePublished - Sep 15 1997

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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    Reardon, D. A., Michalkiewicz, E., Boyett, J. M., Sublett, J. E., Entrekin, R. E., Ragsdale, S. T., Valentine, M. B., Behm, F. G., Li, H., Heideman, R. L., Kun, L. E., Shapiro, D. N., & Look, A. T. (1997). Extensive genomic abnormalities in childhood medulloblastoma by comparative genomic hybridization. Cancer research, 57(18), 4042-4047.