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The genetic epidemiology of glioma

From the Center for Genetic Epidemiology (Dr. Osborne), University of Melbourne, Carlton South, Australia; Genetic Epidemiology Unit (Drs. Osborne, Houben, and van Duijn) and Department of Epidemiology and Biostatistics (Dr. Coebergh), Erasmus University Medical School, Rotterdam; Department of Neurology (Dr. Tijssen), St. Elisabeth Hospital, Tilburg; and Comprehensive Cancer Centre South (Dr. Coebergh), Eindhoven, the Netherlands.

Address correspondence and reprint requests to Dr. C.M. van Duijn, Genetic Epidemiology Unit, Department of Epidemiology and Biostatistics, Erasmus University Medical School, P.O. Box 1738, 3000 DR Rotterdam, the Netherlands; e-mail: vanduijn{at}epib.fgg.eur.nl

With traditional epidemiologic research designs, few environmental risk factors for malignant brain tumors have been revealed, and although syndromes exist where brain tumors occur frequently, these explain a small proportion of the overall incidence. In a similar way, the search for genetic causes has been thwarted by the rarity of families with multiple affected relatives, inhibiting genetic linkage, sib-pair, or even population-based association studies. Molecular genetic studies generally involve searching for candidate proto-oncogenes and tumor suppressor genes by comparing DNA from tumor material with constitutional (germline) DNA. However, it remains difficult to distinguish causative genetic aberrations from chaotic neoplastic processes, and studies so far have not yielded consistent information on the location of such causative genetic lesions. The current literature covering the molecular genetics of glioma is discussed herein and alternative approaches that can be used to identify genetic causes of glioma described.

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