9p21 and 13q14 dosages in ependymomas. A clinicopathologic study of 101 cases

Veena Rajaram, Eric C. Leuthardt, Pratima K. Singh, Jeffrey G. Ojemann, Daniel J. Brat, Richard A. Prayson, Arie Perry*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Ependymomas are glial neoplasms whose clinical behavior is difficult to predict based on histology alone. Recently, a comparative genomic hybridization study identified frequent chromosome 9p and 13q losses in anaplastic ependymomas, suggesting that p16 and RB alterations may be involved in tumor progression. In order to test this hypothesis further, 101 myxopapillary, conventional, and anaplastic ependymomas (51 spinal and 50 intracranial tumors) were tested for RB and p16 deletions using fluorescence in situ hybridization. Clinical follow-up, ranging from 2 to 198 months (median 46 months), was obtained in 90 cases (91%). RB and p16 deletions were seen in 22 of 92 (24%) and 22 of 89 (25%) informative cases, respectively. Polysomies were more frequent in the grade I and II spinal tumors, consistent with prior reports of increased aneuploidy in such cases. No significant genetic associations were seen with tumor grade, recurrence, or death, suggesting that 9p and 13q deletions do not play a prominent role in the malignant progression of ependymomas, as has been implicated in other glioma subtypes.

Original languageEnglish (US)
Pages (from-to)9-14
Number of pages6
JournalModern Pathology
Issue number1
StatePublished - Jan 2004


  • Brain tumor
  • Ependymoma
  • FISH
  • p16/RB
  • Prognosis
  • RB pathway
  • Tumor genetics

ASJC Scopus subject areas

  • Pathology and Forensic Medicine


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