Comparative genomic hybridization in glioma: a meta-analysis of 509 cases.

Much data about genetic imbalances in tumors have been accumulated by comparative genomic hybridization (CGH). In order to distinguish between significantly and coincidentally involved regions in glioma by means of a meta-analysis, we summarized and analyzed the CGH results of 509 cases published in 26 reports between 1992 and 2001. The expansion of all aberrations to the 850-band level impressively visualized distinct patterns in astrocytoma, oligodendroglioma, and ependymoma as well as loci of frequent aberrations. For example, in astrocytoma the frequency of gains culminated at 7p12, 8q24.1, and 12q13-q15 (the loci of EGF-R, C-MYC and CDK4, respectively) and losses at 9p21 (the locus of p15 and p16) and 10q23.3 where PTEN resides. Most chromosomes were variably prone to copy number changes at different scales of aberrations. At the whole chromosome level the analysis showed +7, -10 in astrocytoma and +9, +18 in ependymoma, but +20q, -9p in astrocytoma and +1q, -22q in ependymoma at the p-q arm level. Furthermore, we could confirm the correlation between the average number of copy alterations per patient (average number of copy alterations [ANCA] index) and malignancy for astrocytoma in a refined graduation as well as for oligodendroglioma. As a new parameter, the average number of affected GTG-bands per patient (average number of affected GTG bands [ANAG] index) showed an even more striking correlation with the World Health Organization grade for gains and losses.

[1]  F. Waldman,et al.  Chromosomal abnormalities in glioblastoma multiforme tumors and glioma cell lines detected by comparative genomic hybridization , 1995, International journal of cancer.

[2]  S. Leenstra,et al.  Malignant astrocytoma‐derived region of common amplification in chromosomal band 17p12 is frequently amplified in high‐grade osteosarcomas , 1997, Genes, chromosomes & cancer.

[3]  D. Pinkel,et al.  Comparative Genomic Hybridization for Molecular Cytogenetic Analysis of Solid Tumors , 2022 .

[4]  P. Wesseling,et al.  Genetic reflection of glioblastoma biopsy material in xenografts: characterization of 11 glioblastoma xenograft lines by comparative genomic hybridization. , 2000, Journal of neurosurgery.

[5]  B. Scheithauer,et al.  Localization of common deletion regions on 1p and 19q in human gliomas and their association with histological subtype , 1999, Oncogene.

[6]  G. Thomas,et al.  Molecular analysis of genetic changes in ependymomas , 1995, Genes, chromosomes & cancer.

[7]  K Autio,et al.  DNA copy number losses in human neoplasms. , 1999, The American journal of pathology.

[8]  M. Prados,et al.  Genetic analysis of glioblastoma multiforme provides evidence for subgroups within the grade , 1998, Genes, chromosomes & cancer.

[9]  A. Ayala,et al.  Gains and losses of DNA sequences in childhood brain tumors analyzed by comparative genomic hybridization. , 2000, Cancer genetics and cytogenetics.

[10]  T. Hulsebos,et al.  A region of common deletion in 22q13.3 in human glioma associated with astrocytoma progression , 2000, International journal of cancer.

[11]  P. Meltzer,et al.  Twelve amplified and expressed genes localized in a single domain in glioma , 1996, Human Genetics.

[12]  C. Sommer,et al.  Clinically distinct subgroups of glioblastoma multiforme studied by comparative genomic hybridization. , 1996, Laboratory investigation; a journal of technical methods and pathology.

[13]  T. Nishizaki,et al.  Clinical evidence of distinct subgroups of astrocytic tumors defined by comparative genomic hybridization. , 2000, Human pathology.

[14]  R. Hamoudi,et al.  Molecular and cytogenetic analysis of glioblastoma multiforme. , 2000, Cancer genetics and cytogenetics.

[15]  H. Scherthan,et al.  Detection of Complex Genetic Alterations in Human Glioblastoma Multiforme Using Comparative Genomic Hybridization , 1996, Journal of neuropathology and experimental neurology.

[16]  T. Cremer,et al.  Characterization of double minute chromosomes’ DNA content in a human high grade astrocytoma cell line by using comparative genomic hybridization and fluorescence in situ hybridization , 1996, Human Genetics.

[17]  J. Rey,et al.  Abnormalities of chromosome 22 in human brain tumors determined by combined cytogenetic and molecular genetic approaches. , 1993, Cancer genetics and cytogenetics.

[18]  R. McLendon,et al.  Molecular genetic aspects of oligodendrogliomas including analysis by comparative genomic hybridization. , 1999, The American journal of pathology.

[19]  K. Sasaki,et al.  Intratumoral cytogenetic heterogeneity detected by comparative genomic hybridization and laser scanning cytometry in human gliomas. , 1998, Cancer research.

[20]  A. von Deimling,et al.  Identification of subgroups of high-grade oligodendroglial tumors by comparative genomic hybridization. , 1999, Journal of neuropathology and experimental neurology.

[21]  G. Mohapatra,et al.  Detection of multiple gains and losses of genetic material in ten glioma cell lines by comparative genomic hybridization , 1995, Genes, chromosomes & cancer.

[22]  J. Moringlane,et al.  Evidence of focal genetic microheterogeneity in glioblastoma multiforme by area-specific CGH on microdissected tumor cells. , 1999, Journal of neuropathology and experimental neurology.

[23]  J. Cairncross,et al.  Gliomas in families: chromosomal analysis by comparative genomic hybridization. , 1998, Cancer genetics and cytogenetics.

[24]  W. Cavenee,et al.  Gliomas in Families , 1992, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques.

[25]  M. Prados,et al.  Chromosomal abnormalities in glioblastoma multiforme by comparative genomic hybridization: correlation with radiation treatment outcome. , 1999, Clinical cancer research : an official journal of the American Association for Cancer Research.

[26]  W. Cavenee,et al.  Advances in the molecular genetics of gliomas. , 1997, Current opinion in oncology.

[27]  M. Ferguson-Smith,et al.  Analysis of pilocytic astrocytoma by comparative genomic hybridization , 2000, British Journal of Cancer.

[28]  C. Sommer,et al.  Characterization of genomic alterations associated with glioma progression by comparative genomic hybridization. , 1996, Oncogene.

[29]  M. Sindou,et al.  Chordoid Glioma of the Third Ventricle: A Report of Two New Cases, With Further Evidence Supporting an Ependymal Differentiation, and Review of the Literature , 2002, The American journal of surgical pathology.

[30]  S. Takayama Configurational changes in chromatids from helical to banded structures , 1976, Chromosoma.

[31]  M. Weller,et al.  Chromosomal imbalances associated with response to chemotherapy and cytotoxic cytokines in human malignant glioma cell lines. , 2001 .

[32]  A. T. Sumner Dye binding mechanisms in G‐banding of chromosomes , 1980, Journal of microscopy.

[33]  T. Yoshimine,et al.  Chromosomal aberrations detected by comparative genomic hybridization (CGH) in human astrocytic tumors. , 1998, Cancer letters.

[34]  S. Hanash,et al.  GAC1, a new member of the leucine-rich repeat superfamily on chromosome band 1q32.1, is amplified and overexpressed in malignant gliomas , 1998, Oncogene.

[35]  S. Leung,et al.  Chromosomal instability and p53 inactivation are required for genesis of glioblastoma but not for colorectal cancer in patients with germline mismatch repair gene mutation , 2000, Oncogene.

[36]  M. Werner,et al.  Comparative genomic hybridisation for the analysis of chromosomal imbalances in solid tumours and haematological malignancies , 1997, Histochemistry and Cell Biology.

[37]  M. J. van den Bent,et al.  Genetic aberrations in oligodendroglial tumours: an analysis using comparative genomic hybridization (CGH) , 1999, The Journal of pathology.

[38]  E. Schröck,et al.  Recurrent gain of chromosome arm 7q in low‐grade astrocytic tumors studied by comparative genomic hybridization , 1996, Genes, chromosomes & cancer.

[39]  A. Look,et al.  Chromosome arm 6q loss is the most common recurrent autosomal alteration detected in primary pediatric ependymoma , 1999, Genes, chromosomes & cancer.

[40]  J. Kononen,et al.  Chromosome imbalances in familial gliomas detected by comparative genomic hybridization , 2000, Genes, chromosomes & cancer.

[41]  J. Delattre,et al.  Oncogene amplification in human gliomas: a molecular cytogenetic analysis. , 1994, Oncogene.

[42]  E. Schröck,et al.  Genomic changes defining the genesis, progression, and malignancy potential in solid human tumors: A phenotype/genotype correlation , 1999, Genes, chromosomes & cancer.

[43]  T. Liehr,et al.  Patterns of genomic imbalances in human solid tumors (Review). , 2000, International journal of oncology.

[44]  M. Wolter,et al.  Chordoid Glioma of the Third Ventricle: Immunohistochemical and Molecular Genetic Characterization of a Novel Tumor Entity , 1999, Brain pathology.

[45]  M Koslow,et al.  Pathways leading to glioblastoma multiforme: a molecular analysis of genetic alterations in 65 astrocytic tumors. , 1994, Journal of neurosurgery.

[46]  J. Kononen,et al.  Accumulation of genetic changes is associated with poor prognosis in grade II astrocytomas. , 1997, The American journal of pathology.

[47]  C. Ascoli,et al.  Atomic force microscope imaging of chromosome structure during G-banding treatments. , 1997, Genome.

[48]  A. Jauch,et al.  Copyright ©) American Society for Investigative Pathology Comparative Genomic Hybridization of Human Malignant Gliomas Reveals Multiple Amplification Sites and Nonrandom Chromosomal Gains and Losses , 2022 .

[49]  A. Ouweland,et al.  ©1999 Cancer Research Campaign Article no. bjoc.1999.0822 , 2022 .

[50]  M. Wolter,et al.  Mutation of the PTEN (MMAC1) tumor suppressor gene in a subset of glioblastomas but not in meningiomas with loss of chromosome arm 10q. , 1998, Cancer research.

[51]  K. Sasaki,et al.  Investigation of genetic alterations associated with the grade of astrocytic tumor by comparative genomic hybridization , 1998, Genes, chromosomes & cancer.

[52]  P. Cogen,et al.  Molecular genetic analysis of chromosome arm 17p and chromosome arm 22q DNA sequences in sporadic pediatric ependymomas , 1996, Genes, chromosomes & cancer.

[53]  D. Louis,et al.  Common regions of deletion on chromosome 22q12.3-q13.1 and 22q13.2 in human astrocytomas appear related to malignancy grade. , 1999, Journal of neuropathology and experimental neurology.

[54]  V. Jung,et al.  Comparative genomic hybridization reveals recurrent enhancements on chromosome 20 and in one case combined amplification sites on 15q24q26 and 20p11p12 in glioblastomas. , 2000, Cancer genetics and cytogenetics.

[55]  D. Warburton,et al.  Genomic changes in glioblastoma cell lines detected by comparative genomic hybridization , 2004, Journal of Neuro-Oncology.

[56]  S. Knuutila,et al.  DNA copy number amplifications in human neoplasms: review of comparative genomic hybridization studies. , 1998, The American journal of pathology.

[57]  A. Hui,et al.  Comparative genomic hybridization detects losses of chromosomes 22 and 16 as the most common recurrent genetic alterations in primary ependymomas. , 2000, Cancer genetics and cytogenetics.

[58]  P. Kleihues,et al.  Genetics of Glioma Progression and the Definition of Primary and Secondary Glioblastoma , 1997 .

[59]  J. Robben,et al.  Interphase cytogenetic analysis of cervical intraepithelial neoplasia. , 1998, The American journal of pathology.

[60]  D. Gisselsson,et al.  Multivariate analyses of genomic imbalances in solid tumors reveal distinct and converging pathways of karyotypic evolution , 2001, Genes, chromosomes & cancer.

[61]  P. Kleihues,et al.  The p53 gene and its role in human brain tumors , 1995, Glia.

[62]  V. Collins Gene amplification in human gliomas , 1995, Glia.

[63]  D. Louis,et al.  Molecular pathways in the formation of gliomas , 1995, Glia.

[64]  J. Squire,et al.  Application of a simplified comparative genomic hybridization technique to screen for gene amplification in pediatric solid tumors. , 1995, Pediatric pathology & laboratory medicine : journal of the Society for Pediatric Pathology, affiliated with the International Paediatric Pathology Association.

[65]  B. Schlegelberger,et al.  Assignment1 of human putative tumor suppressor genes ST13 (alias SNC6) and ST14 (alias SNC19) to human chromosome bands 22q13 and 11q24→q25 by in situ hybridization , 1999, Cytogenetic and Genome Research.

[66]  F. Sahin,et al.  The mechanism of G-banding detected by atomic force microscopy. , 2006, Scanning.

[67]  B. Scheithauer,et al.  The Glial and Mesenchymal Elements of Gliosarcomas Share Similar Genetic Alterations , 1996, Journal of neuropathology and experimental neurology.

[68]  S. Toksvig-Larsen,et al.  Trisomy 7 accumulates with age in solid tumors and non‐neoplastic synovia , 2001, Genes, chromosomes & cancer.

[69]  G. Mohapatra,et al.  Detection of p16 Gene Deletions in Gliomas: A Comparison of Fluorescence in Situ Hybridization (FISH) Versus Quantitative PCR , 1997, Journal of neuropathology and experimental neurology.