Seminars in Neurosurgery 2003; 14(3): 187-192
DOI: 10.1055/s-2004-817735
Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Pathophysiology of Malignant Meningiomas

Marcus L. Ware1 , Alfredo Quinones-Hinojosa2 , Michael W. McDermott 1,2,3
  • 1Department of Neurological Surgery, University of California, San Francisco, San Francisco, California
  • 2Department of Radiation Oncology, University of California, San Francisco, San Francisco, California
  • 3The Brain Tumor Research Center, University of California, San Francisco, San Francisco, California
Further Information

Publication History

Publication Date:
02 June 2004 (online)

Preview

ABSTRACT

Although most meningiomas are benign and are treated with surgery alone, a few are malignant and can be difficult to treat. These more aggressive tumors were first characterized by their histology. With advances in molecular biology, we have learned a great deal about the development of these tumors. Cytogenetic studies have shown that benign meningiomas have mutations in chromosome 22. Further studies show that the NF2 gene, located on chromosome 22, is involved in meningioma formation. More aggressive tumors have been shown to have several mutations in other chromosomes, including chromosome 1p, 14q, and 18q. Here, we review these findings and the candidate genes involved in meningioma tumorigenesis.

REFERENCES