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 Volume 71, Number 5, July 29, 2008
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NEUROLOGY 2008;71:365-373
© 2008 American Academy of Neurology
Special Articles: Invited Articles

Invited Article: The expanding impact of molecular biology on the diagnosis and treatment of gliomas

Warren P. Mason, MD, FRCPC and J. Gregory Cairncross, MD, FRCPC

From the Department of Medicine (W.P.M.), the University of Toronto and Princess Margaret Hospital, Toronto, Ontario; and the Department of Clinical Neurosciences (J.G.C.), University of Calgary and Foothills Medical Centre, Calgary, Alberta, Canada.

Address correspondence and reprint requests to Dr. Warren P. Mason, Princess Margaret Hospital, 610 University Avenue, Suite 18-717, Toronto, ON, Canada M5G 2M9 warren.mason{at}uhn.on.ca

For nearly a century, glial neoplasms have been classified by microscopic features alone with treatment prescribed based on histology using a "one-size-fits-all" formula. However, recent advances in our understanding of the molecular events underlying gliomagenesis are beginning to change the way we think about the diagnostic classification of gliomas. Indeed, several recurring molecular derangements are now being viewed as cornerstones of a new diagnostic framework because these alterations appear to be superior to traditional microscopic classification schemes as guideposts for treatment selection and prognosis. Moreover, molecular analysis of tumor tissue is identifying aberrant growth signaling pathways in glioma which can now be blocked selectively by a new generation of targeted therapies, including small molecule inhibitors and monoclonal antibodies. Time will tell whether these new agents can be successfully introduced into the clinical arena. In the meantime, the molecular characteristics of gliomas are being used to select patients for both randomized trials and phase II studies.

Abbreviations: CCNU = lomustine; EGFR = epidermal growth factor receptor; EORTC = European Organization for the Research and Treatment of Cancer; GBM = glioblastoma multiforme; MGMT = O6-methylguanine DNA methyltransferase; NCIC CTG = National Cancer Institute of Canada Clinical Trials Group; PCV = procarbazine, lomustine, vincristine chemotherapy; PDGF = platelet-derived growth factor; PDGFR = platelet-derived growth factor receptor; RTOG = Radiation Therapy Oncology Group; WHO = World Health Organization.

Disclosure: The authors report no disclosures.

Received September 4, 2007. Accepted in final form March 4, 2008.






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