Distinct genetic alterations in pediatric glioblastomas

Sun Ju Byeon, Jae Kyung Myung, SeHoon Kim, Seung Ki Kim, Ji Hoon Phi, Sung Hye Park

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Background: Pediatric high-grade tumors, especially glioblastomas (GBs), can be clinically devastating but are under-studied in comparison with adult GBs (aGBs). Molecular features of pediatric GBs (pGBs) are poorly understood and novel-targeted therapies have not been routinely used in pediatric patients with GBs. Methods: Twenty-four non-brainstem pGBs were studied. To compare pGBs with aGBs, immunohistochemical staining and fluorescent in situ hybridization were performed in paraffin-embedded tissues. Microarray gene expression analyses were performed in snap-frozen tissues of four primary pGBs, six primary aGBs, and one non-neoplastic brain. Results: Immunohistochemial p16 loss was more frequent in pGBs, whereas p53, epidermal growth factor receptor, and phosphatase and tensin homolog loss were similar to that of aGBs. No case was isocitrate dehydrogenase (IDH)1 immunopositive or showed the IDH1 R132/IDH2 R172 mutation, suggesting primary GB. Microarray analysis revealed two pGB subtypes (A and B). Type B pGBs and aGBs had similar gene expression profiles; however, the profiles of type A pGBs differed from those of aGBs. In type A pGBs, we identified 90 upand 63 down-regulated genes; platelet-derived growth factor receptor a polypeptide and CCND2 expression were significantly reduced, whereas they were up-regulated in aGBs. Conclusions: Our study found two distinct pGB gene expression profiles: one similar to that of aGBs and the other different. We identified significantly up- and down-regulated genes in pGBs that may provide better targets for diagnostic, prognostic, and therapeutic uses; however, more studies are required to determine the classification and optimal treatment of pediatric patients with GBs.

Original languageEnglish
Pages (from-to)1025-1032
Number of pages8
JournalChild's Nervous System
Volume28
Issue number7
DOIs
Publication statusPublished - 2012 Jul 1

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Glioblastoma
Pediatrics
Transcriptome
Isocitrate Dehydrogenase
Platelet-Derived Growth Factor Receptors
Therapeutic Uses
Microarray Analysis
Fluorescence In Situ Hybridization
Phosphoric Monoester Hydrolases
Epidermal Growth Factor Receptor
Paraffin
Genes
Staining and Labeling
Gene Expression

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Clinical Neurology

Cite this

Byeon, S. J., Myung, J. K., Kim, S., Kim, S. K., Phi, J. H., & Park, S. H. (2012). Distinct genetic alterations in pediatric glioblastomas. Child's Nervous System, 28(7), 1025-1032. https://doi.org/10.1007/s00381-012-1773-1
Byeon, Sun Ju ; Myung, Jae Kyung ; Kim, SeHoon ; Kim, Seung Ki ; Phi, Ji Hoon ; Park, Sung Hye. / Distinct genetic alterations in pediatric glioblastomas. In: Child's Nervous System. 2012 ; Vol. 28, No. 7. pp. 1025-1032.
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Byeon, SJ, Myung, JK, Kim, S, Kim, SK, Phi, JH & Park, SH 2012, 'Distinct genetic alterations in pediatric glioblastomas', Child's Nervous System, vol. 28, no. 7, pp. 1025-1032. https://doi.org/10.1007/s00381-012-1773-1

Distinct genetic alterations in pediatric glioblastomas. / Byeon, Sun Ju; Myung, Jae Kyung; Kim, SeHoon; Kim, Seung Ki; Phi, Ji Hoon; Park, Sung Hye.

In: Child's Nervous System, Vol. 28, No. 7, 01.07.2012, p. 1025-1032.

Research output: Contribution to journalArticle

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T1 - Distinct genetic alterations in pediatric glioblastomas

AU - Byeon, Sun Ju

AU - Myung, Jae Kyung

AU - Kim, SeHoon

AU - Kim, Seung Ki

AU - Phi, Ji Hoon

AU - Park, Sung Hye

PY - 2012/7/1

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N2 - Background: Pediatric high-grade tumors, especially glioblastomas (GBs), can be clinically devastating but are under-studied in comparison with adult GBs (aGBs). Molecular features of pediatric GBs (pGBs) are poorly understood and novel-targeted therapies have not been routinely used in pediatric patients with GBs. Methods: Twenty-four non-brainstem pGBs were studied. To compare pGBs with aGBs, immunohistochemical staining and fluorescent in situ hybridization were performed in paraffin-embedded tissues. Microarray gene expression analyses were performed in snap-frozen tissues of four primary pGBs, six primary aGBs, and one non-neoplastic brain. Results: Immunohistochemial p16 loss was more frequent in pGBs, whereas p53, epidermal growth factor receptor, and phosphatase and tensin homolog loss were similar to that of aGBs. No case was isocitrate dehydrogenase (IDH)1 immunopositive or showed the IDH1 R132/IDH2 R172 mutation, suggesting primary GB. Microarray analysis revealed two pGB subtypes (A and B). Type B pGBs and aGBs had similar gene expression profiles; however, the profiles of type A pGBs differed from those of aGBs. In type A pGBs, we identified 90 upand 63 down-regulated genes; platelet-derived growth factor receptor a polypeptide and CCND2 expression were significantly reduced, whereas they were up-regulated in aGBs. Conclusions: Our study found two distinct pGB gene expression profiles: one similar to that of aGBs and the other different. We identified significantly up- and down-regulated genes in pGBs that may provide better targets for diagnostic, prognostic, and therapeutic uses; however, more studies are required to determine the classification and optimal treatment of pediatric patients with GBs.

AB - Background: Pediatric high-grade tumors, especially glioblastomas (GBs), can be clinically devastating but are under-studied in comparison with adult GBs (aGBs). Molecular features of pediatric GBs (pGBs) are poorly understood and novel-targeted therapies have not been routinely used in pediatric patients with GBs. Methods: Twenty-four non-brainstem pGBs were studied. To compare pGBs with aGBs, immunohistochemical staining and fluorescent in situ hybridization were performed in paraffin-embedded tissues. Microarray gene expression analyses were performed in snap-frozen tissues of four primary pGBs, six primary aGBs, and one non-neoplastic brain. Results: Immunohistochemial p16 loss was more frequent in pGBs, whereas p53, epidermal growth factor receptor, and phosphatase and tensin homolog loss were similar to that of aGBs. No case was isocitrate dehydrogenase (IDH)1 immunopositive or showed the IDH1 R132/IDH2 R172 mutation, suggesting primary GB. Microarray analysis revealed two pGB subtypes (A and B). Type B pGBs and aGBs had similar gene expression profiles; however, the profiles of type A pGBs differed from those of aGBs. In type A pGBs, we identified 90 upand 63 down-regulated genes; platelet-derived growth factor receptor a polypeptide and CCND2 expression were significantly reduced, whereas they were up-regulated in aGBs. Conclusions: Our study found two distinct pGB gene expression profiles: one similar to that of aGBs and the other different. We identified significantly up- and down-regulated genes in pGBs that may provide better targets for diagnostic, prognostic, and therapeutic uses; however, more studies are required to determine the classification and optimal treatment of pediatric patients with GBs.

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