Biphasic malignant meningioma: A comparative genomic hybridization study

A. B. Heimberger*, R. N. Wiltshire, P. Bronec, R. E. McLendon, T. J. Cummings

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


To ascertain if a carcinoma-like component within a fibroblastic meningioma represented a metastatic carcinoma to a meningioma or malignant progression, we employed traditional immunohistochemical methods as well as comparative genomic hybridization (CGH) which compares chromosomal alterations. Vimentin and epithelial membrane antigen were strongly immunoreactive in both the fibroblastic and carcinoma-like components. The CGH profile in both components had similar chromosomal alterations, including losses of 1p, 14, 16p13→p10 and 22. However, the CGH profiles from the fibroblastic component showed losses of 4p, 10q23→q24 and 18, along with gains of 1 q, 6q25→qter and 13q32→qter. The profile of the carcinoma-like component showed losses of chromosome 4, in addition to gains of 3p12→q13.1, 5q14.3→q23.2, 6pter→p23, and 13ql4.2→qter. CGH analysis of a biphasic malignant meningioma confirmed that the disparate histologic components were genetically related and likely derivative from a common precursor, demonstrating genetic instability and clonal expansion. Furthermore, CGH showed that the histologically appearing low-grade fibroblastic component had not solely the characteristic alterations of a benign meningioma but had already progressed to an atypical meningioma.

Original languageEnglish (US)
Pages (from-to)258-264
Number of pages7
JournalClinical Neuropathology
Issue number6
StatePublished - Nov 2002
Externally publishedYes


  • Clonal expansion
  • Comparative genomic hybridization
  • Meningioma

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neurology
  • Clinical Neurology


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