Single-copy gain of chromosome 1q is a negative prognostic marker in pediatric nonependymal, nonpilocytic gliomas

Tomoru Miwa, Yuichi Hirose, Hikaru Sasaki, Taketo Ezaki, Kazunari Yoshida, Takeshi Kawase

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Abstract

BACKGROUND: Reports of genetic analyses on pediatric gliomas are few, and those tumors have been far less characterized than adult gliomas. OBJECTIVE: To characterize the genetic and biological features of pediatric gliomas. METHODS: We investigated 23 pediatric nonependymal, nonpilocytic gliomas for chromosomal copy number aberrations (CNAs) by comparative genomic hybridization (CGH), mutations of isocitrate dehydrogenase (IDH) genes by direct sequencing, and proliferative activity and expression of O6-methylguanine-DNA methyltransferase (MGMT) by immunohistochemistry. RESULTS: The most frequent CNA was single-copy gain of chromosome 1q, with 10 of 20 successfully investigated tumors showing the abnormality (50%). Other CNAs detected by CGH included gain on 7q (+7q) in 6, +9q in 5, +17q in 5, and + 7p in 4 cases. Gain of entire chromosome 7 was rare (2 cases), and codeletion of 1p and 19q was not detected. Gain of 1q was significantly predictive for shorter progression-free survival (PFS) and overall survival (OS), and even more closely associated with poor clinical outcome than histological grade (P = .0009 for PFS, P = .003 for OS by 1q status; P = .004 for PFS, P = .035 for OS by high-grade vs low-grade). Gain of 1q was also significantly correlated with proliferative activity (P = .0002), and tumors with 1q gain showed a trend toward higher MGMT expression (P = .27). Mutation of IDH1 gene was detected in only 2 of 17 tumors successfully analyzed. CONCLUSION: Single copy gain of 1q is associated with biological features of pediatric gliomas, and is a negative prognostic marker in patients with those tumors.

Original languageEnglish
Pages (from-to)206-212
Number of pages7
JournalNeurosurgery
Volume68
Issue number1
DOIs
Publication statusPublished - 01-01-2011

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Glioma
Chromosomes
Pediatrics
Disease-Free Survival
Comparative Genomic Hybridization
Neoplasms
Survival
Isocitrate Dehydrogenase
Mutation
Chromosomes, Human, Pair 7
DNA
Methyltransferases
Genes
Immunohistochemistry

All Science Journal Classification (ASJC) codes

  • Surgery
  • Clinical Neurology

Cite this

Miwa, Tomoru ; Hirose, Yuichi ; Sasaki, Hikaru ; Ezaki, Taketo ; Yoshida, Kazunari ; Kawase, Takeshi. / Single-copy gain of chromosome 1q is a negative prognostic marker in pediatric nonependymal, nonpilocytic gliomas. In: Neurosurgery. 2011 ; Vol. 68, No. 1. pp. 206-212.
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abstract = "BACKGROUND: Reports of genetic analyses on pediatric gliomas are few, and those tumors have been far less characterized than adult gliomas. OBJECTIVE: To characterize the genetic and biological features of pediatric gliomas. METHODS: We investigated 23 pediatric nonependymal, nonpilocytic gliomas for chromosomal copy number aberrations (CNAs) by comparative genomic hybridization (CGH), mutations of isocitrate dehydrogenase (IDH) genes by direct sequencing, and proliferative activity and expression of O6-methylguanine-DNA methyltransferase (MGMT) by immunohistochemistry. RESULTS: The most frequent CNA was single-copy gain of chromosome 1q, with 10 of 20 successfully investigated tumors showing the abnormality (50{\%}). Other CNAs detected by CGH included gain on 7q (+7q) in 6, +9q in 5, +17q in 5, and + 7p in 4 cases. Gain of entire chromosome 7 was rare (2 cases), and codeletion of 1p and 19q was not detected. Gain of 1q was significantly predictive for shorter progression-free survival (PFS) and overall survival (OS), and even more closely associated with poor clinical outcome than histological grade (P = .0009 for PFS, P = .003 for OS by 1q status; P = .004 for PFS, P = .035 for OS by high-grade vs low-grade). Gain of 1q was also significantly correlated with proliferative activity (P = .0002), and tumors with 1q gain showed a trend toward higher MGMT expression (P = .27). Mutation of IDH1 gene was detected in only 2 of 17 tumors successfully analyzed. CONCLUSION: Single copy gain of 1q is associated with biological features of pediatric gliomas, and is a negative prognostic marker in patients with those tumors.",
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Single-copy gain of chromosome 1q is a negative prognostic marker in pediatric nonependymal, nonpilocytic gliomas. / Miwa, Tomoru; Hirose, Yuichi; Sasaki, Hikaru; Ezaki, Taketo; Yoshida, Kazunari; Kawase, Takeshi.

In: Neurosurgery, Vol. 68, No. 1, 01.01.2011, p. 206-212.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Single-copy gain of chromosome 1q is a negative prognostic marker in pediatric nonependymal, nonpilocytic gliomas

AU - Miwa, Tomoru

AU - Hirose, Yuichi

AU - Sasaki, Hikaru

AU - Ezaki, Taketo

AU - Yoshida, Kazunari

AU - Kawase, Takeshi

PY - 2011/1/1

Y1 - 2011/1/1

N2 - BACKGROUND: Reports of genetic analyses on pediatric gliomas are few, and those tumors have been far less characterized than adult gliomas. OBJECTIVE: To characterize the genetic and biological features of pediatric gliomas. METHODS: We investigated 23 pediatric nonependymal, nonpilocytic gliomas for chromosomal copy number aberrations (CNAs) by comparative genomic hybridization (CGH), mutations of isocitrate dehydrogenase (IDH) genes by direct sequencing, and proliferative activity and expression of O6-methylguanine-DNA methyltransferase (MGMT) by immunohistochemistry. RESULTS: The most frequent CNA was single-copy gain of chromosome 1q, with 10 of 20 successfully investigated tumors showing the abnormality (50%). Other CNAs detected by CGH included gain on 7q (+7q) in 6, +9q in 5, +17q in 5, and + 7p in 4 cases. Gain of entire chromosome 7 was rare (2 cases), and codeletion of 1p and 19q was not detected. Gain of 1q was significantly predictive for shorter progression-free survival (PFS) and overall survival (OS), and even more closely associated with poor clinical outcome than histological grade (P = .0009 for PFS, P = .003 for OS by 1q status; P = .004 for PFS, P = .035 for OS by high-grade vs low-grade). Gain of 1q was also significantly correlated with proliferative activity (P = .0002), and tumors with 1q gain showed a trend toward higher MGMT expression (P = .27). Mutation of IDH1 gene was detected in only 2 of 17 tumors successfully analyzed. CONCLUSION: Single copy gain of 1q is associated with biological features of pediatric gliomas, and is a negative prognostic marker in patients with those tumors.

AB - BACKGROUND: Reports of genetic analyses on pediatric gliomas are few, and those tumors have been far less characterized than adult gliomas. OBJECTIVE: To characterize the genetic and biological features of pediatric gliomas. METHODS: We investigated 23 pediatric nonependymal, nonpilocytic gliomas for chromosomal copy number aberrations (CNAs) by comparative genomic hybridization (CGH), mutations of isocitrate dehydrogenase (IDH) genes by direct sequencing, and proliferative activity and expression of O6-methylguanine-DNA methyltransferase (MGMT) by immunohistochemistry. RESULTS: The most frequent CNA was single-copy gain of chromosome 1q, with 10 of 20 successfully investigated tumors showing the abnormality (50%). Other CNAs detected by CGH included gain on 7q (+7q) in 6, +9q in 5, +17q in 5, and + 7p in 4 cases. Gain of entire chromosome 7 was rare (2 cases), and codeletion of 1p and 19q was not detected. Gain of 1q was significantly predictive for shorter progression-free survival (PFS) and overall survival (OS), and even more closely associated with poor clinical outcome than histological grade (P = .0009 for PFS, P = .003 for OS by 1q status; P = .004 for PFS, P = .035 for OS by high-grade vs low-grade). Gain of 1q was also significantly correlated with proliferative activity (P = .0002), and tumors with 1q gain showed a trend toward higher MGMT expression (P = .27). Mutation of IDH1 gene was detected in only 2 of 17 tumors successfully analyzed. CONCLUSION: Single copy gain of 1q is associated with biological features of pediatric gliomas, and is a negative prognostic marker in patients with those tumors.

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