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

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

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155 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 language	English (US)
Pages (from-to)	4042-4047
Number of pages	6
Journal	Cancer research
Volume	57
Issue number	18
State	Published - Sep 15 1997

ASJC Scopus subject areas

Oncology
Cancer Research

Cite this

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title = "Extensive genomic abnormalities in childhood medulloblastoma by comparative genomic hybridization",

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.",

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

year = "1997",

month = sep,

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language = "English (US)",

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T1 - Extensive genomic abnormalities in childhood medulloblastoma by comparative genomic hybridization

AU - Reardon, David A.

AU - Michalkiewicz, Edson

AU - Boyett, James M.

AU - Sublett, Jack E.

AU - Entrekin, Ruth E.

AU - Ragsdale, Susan T.

AU - Valentine, Marcus B.

AU - Behm, Frederick G.

AU - Li, Hao

AU - Heideman, Richard L.

AU - Kun, Larry E.

AU - Shapiro, David N.

AU - Look, A. Thomas

PY - 1997/9/15

Y1 - 1997/9/15

N2 - 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.

AB - 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.

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Extensive genomic abnormalities in childhood medulloblastoma by comparative genomic hybridization

Abstract

ASJC Scopus subject areas

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