The Glial and Mesenchymal Elements of Gliosarcomas Share Similar Genetic Alterations

Rudolf H. Boerman, Kari Anderl, John Herath, Thomas Borell, Nicola Johnson, Janet Schaeffer-Klein, Allen Kirchhof, Anton K. Raap, Bernd W. Scheithauer, Robert Brian Jenkins

Research output: Contribution to journalArticle

114 Citations (Scopus)

Abstract

The cellular origin of the sarcomatous component of gliosarcomas is controversial. It is not clear if the sarcoma arises in transition from the glial cells that comprise the gliomatous component or independently arises from non-neoplastic mesenchymal cells of the tumor stroma. Using comparative genomic hybridization (CGH) along with cytogenetic analysis, fluorescence in situ hybridization (FISH) analysis, and polymerase chain reaction (PCR) analysis of microsatellite allelic imbalance, we have evaluated the genetic alterations in the gliomatous and sarcomatous components of five gliosarcomas. The glial element was grade 4 flbrillary astrocytoma (glioblastoma multiforme) in all five tumors. The sarcoma elements were fibroblastic without osseous, chondroid, or angiosarcomatous differentiation. Gain of chromosome 7, loss of chromosome 10, deletions of the chromosome 9 p-arm, and alterations of chromosome 3 were frequently observed, demonstrating that gliosarcomas can be genetically classified as belonging to the spectrum of glioblastomas. Furthermore, the sarcomatous and gliomatous portions of each gliosarcoma investigated were similar with respect to both the presence and absence of specific genetic alterations. This observation supports the hypothesis that the sarcomatous component of a gliosarcoma either arises from the same common precursor cell as the gliomatous portion, or it arises from the gliomatous portion itself.

Original languageEnglish (US)
Pages (from-to)973-981
Number of pages9
JournalJournal of Neuropathology and Experimental Neurology
Volume55
Issue number9
StatePublished - 1996

Fingerprint

Gliosarcoma
Neuroglia
Glioblastoma
Sarcoma
Allelic Imbalance
Chromosomes, Human, Pair 10
Chromosome Deletion
Chromosomes, Human, Pair 9
Chromosomes, Human, Pair 3
Chromosomes, Human, Pair 7
Comparative Genomic Hybridization
Cytogenetic Analysis
Astrocytoma
Fluorescence In Situ Hybridization
Microsatellite Repeats
Neoplasms
Polymerase Chain Reaction

Keywords

  • Comparative genomic hybridization (CGH)
  • Genetic alterations
  • Gliosarcoma

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neuroscience(all)

Cite this

Boerman, R. H., Anderl, K., Herath, J., Borell, T., Johnson, N., Schaeffer-Klein, J., ... Jenkins, R. B. (1996). The Glial and Mesenchymal Elements of Gliosarcomas Share Similar Genetic Alterations. Journal of Neuropathology and Experimental Neurology, 55(9), 973-981.

The Glial and Mesenchymal Elements of Gliosarcomas Share Similar Genetic Alterations. / Boerman, Rudolf H.; Anderl, Kari; Herath, John; Borell, Thomas; Johnson, Nicola; Schaeffer-Klein, Janet; Kirchhof, Allen; Raap, Anton K.; Scheithauer, Bernd W.; Jenkins, Robert Brian.

In: Journal of Neuropathology and Experimental Neurology, Vol. 55, No. 9, 1996, p. 973-981.

Research output: Contribution to journalArticle

Boerman, RH, Anderl, K, Herath, J, Borell, T, Johnson, N, Schaeffer-Klein, J, Kirchhof, A, Raap, AK, Scheithauer, BW & Jenkins, RB 1996, 'The Glial and Mesenchymal Elements of Gliosarcomas Share Similar Genetic Alterations', Journal of Neuropathology and Experimental Neurology, vol. 55, no. 9, pp. 973-981.
Boerman RH, Anderl K, Herath J, Borell T, Johnson N, Schaeffer-Klein J et al. The Glial and Mesenchymal Elements of Gliosarcomas Share Similar Genetic Alterations. Journal of Neuropathology and Experimental Neurology. 1996;55(9):973-981.
Boerman, Rudolf H. ; Anderl, Kari ; Herath, John ; Borell, Thomas ; Johnson, Nicola ; Schaeffer-Klein, Janet ; Kirchhof, Allen ; Raap, Anton K. ; Scheithauer, Bernd W. ; Jenkins, Robert Brian. / The Glial and Mesenchymal Elements of Gliosarcomas Share Similar Genetic Alterations. In: Journal of Neuropathology and Experimental Neurology. 1996 ; Vol. 55, No. 9. pp. 973-981.
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