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Comparative Study
. 2002 Jan;12(1):36-44.
doi: 10.1111/j.1750-3639.2002.tb00420.x.

Comparative genomic hybridization detects an increased number of chromosomal alterations in large cell/anaplastic medulloblastomas

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Comparative Study

Comparative genomic hybridization detects an increased number of chromosomal alterations in large cell/anaplastic medulloblastomas

Charles G Eberhart et al. Brain Pathol. 2002 Jan.

Abstract

We correlate chromosomal changes in medulloblastomas with histologic subtype, reporting the analysis of 33 medulloblastoma specimens by comparative genomic hybridization, and a subset by fluorescence in situ hybridization. Of the 33 tumors, 5 were desmoplastic/nodular, 10 were histologically classic, and 18 were large cell/anaplastic. Chromosomal gains and losses were more common in anaplastic medulloblastomas than in non-anaplastic ones. We identified 4 medulloblastomas with c-myc amplification and 5 medulloblastomas with N-myc amplification; all 9 were of the large cell/anaplastic subtype. Additional regions with high level gains included 2q14-22, 3p23, 5p14-pter, 8q24, 9p22-23, 10p12-pter, 12q24, 12p11-12, 17p11-12, and Xp11. The majority of these high level gains occurred in anaplastic cases. We also found loss of chromosome 17p in 7 large cell/anaplastic cases but no nonanaplastic medulloblastomas. Finally, we detected a significantly increased overall number of chromosomal alterations in large cell/anaplastic medulloblastomas (6.8/case) compared to non-anaplastic ones (3.3/case). These findings support an association between myc oncogene amplification, 17p loss, and large cell/anaplastic histology.

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References

    1. Agamanolis DP, Malone JM (1995) Chromosomal abnormalities in 47 pediatric brain tumors. Cancer Genet Cytogenet 81:125–134. - PubMed
    1. Avet‐Loiseau H, Venuat AM, Terrier‐Lacombe MJ, Lellouch‐Tubiana A, Zerah M, Vassal G (1999) Comparative genomic hybridization detects many recurrent imbalances in central nervous system primitive neuroectodermal tumours in children. Br J Cancer 79:1843–1847. - PMC - PubMed
    1. Batra SK, McLendon RE, Koo JS, Castelino‐Prabhu S, Fuchs HE, Krischer JP, Friedman HS, Bigner DD, Bigner SH (1995) Prognostic implications of chromosome 17p deletions in human medulloblastomas. J Neurooncol 24:39–45. - PubMed
    1. Bayani J, Zielenska M, Marrano P, Kwan Ng Y, Taylor MD, Jay V, Rutka JT, Squire JA (2000) Molecular cytogenetic analysis of medulloblastomas and supratentorial primitive neuroectodermal tumors by using conventional banding, comparative genomic hybridization, and spectral karyotyping. J Neurosurg 93:437–448. - PubMed
    1. Biegel JA, Janss AJ, Raffel C, Sutton L, Rorke LB, Harper JM, Phillips PC (1997) Prognostic significance of chromosome 17p deletions in childhood primitive neuroectodermal tumors (medulloblastomas) of the central nervous system. Clin Cancer Res 3:473–478. - PubMed

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