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Epidemology and Cancer Control |
Department of Epidemiology and Biostatistics (M.W., T.C.) and Department of Neurological Surgery and Brain Tumor Research Center (M.S.B.), University of California at San Francisco, San Francisco, CA 94143; Department of Neurology, Stanford University, Stanford, CA 94305 (Y.M.); Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center, University of Texas, Houston, TX 77030 (M.B.)
2 Address correspondence and reprint requests to Margaret Wrensch, Department of Epidemiology and Biostatistics, Box 1215, 44 Page St. Suite 503, University of California at San Francisco, San Francisco, CA 94102.
Abstract
The purpose of this review is to provide a sufficiently detailed perspective on epidemiologic studies of primary brain tumors to encourage multidisciplinary etiologic and prognostic studies among surgeons, neuro-oncologists, epidemiologists, and molecular scientists. Molecular tumor markers that predict survival and treatment response are being identified with hope of even greater gains in this area from emerging array technologies. Regarding risk factors, studies of inherited susceptibility and constitutive polymorphisms in genes pertinent to carcinogenesis (for example, DNA repair and detoxification genes and mutagen sensitivity) have revealed provocative findings. Inverse associations of the history of allergies with glioma risk observed in 3 large studies and reports of inverse associations of glioma with common infections suggest a possible role of immune factors in glioma genesis or progression. Studies continue to suggest that brain tumors might result from workplace, dietary, and other personal and residential exposures, but studies of cell phone use and power frequency electromagnetic fields have found little to support a causal connection with brain tumors; caveats remain. The only proven causes of brain tumors (that is, rare hereditary syndromes, therapeutic radiation, and immune suppression giving rise to brain lymphomas) account for a small proportion of cases. Progress in understanding primary brain tumors might result from studies of well-defined histologic and molecular tumor types incorporating assessment of potentially relevant information on subject susceptibility and environmental and noninherited endogenous factors (viruses, radiation, and carcinogenic or protective chemical exposures through diet, workplace, oxidative metabolism, or other sources). Such studies will require the cooperation of researchers from many disciplines.
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M. Mazumdar, C.-Y. Liu, S.-F. Wang, P.-C. Pan, M.-T. Wu, D. C. Christiani, and the Kaohsiung Brain Tumor Research Group No Association between Parental or Subject Occupation and Brain Tumor Risk Cancer Epidemiol. Biomarkers Prev., July 1, 2008; 17(7): 1835 - 1837. [Full Text] [PDF] |
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A.V. Brenner, M.A. Butler, S.S. Wang, A.M. Ruder, N. Rothman, P.A. Schulte, S.J. Chanock, H.A. Fine, M.S. Linet, and P.D. Inskip Single-nucleotide polymorphisms in selected cytokine genes and risk of adult glioma Carcinogenesis, December 1, 2007; 28(12): 2543 - 2547. [Abstract] [Full Text] [PDF] |
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R. L. Sedjo, T. Byers, E. Barrera Jr., C. Cohen, E. T. H. Fontham, L. A. Newman, C. D. Runowicz, A. G. Thorson, M. J. Thun, E. Ward, et al. A Midpoint Assessment of the American Cancer Society Challenge Goal to Decrease Cancer Incidence by 25% Between 1992 and 2015 CA Cancer J Clin, November 1, 2007; 57(6): 326 - 340. [Abstract] [Full Text] [PDF] |
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K. K. Karipidis, G. Benke, M. R. Sim, T. Kauppinen, and G. Giles Occupational exposure to ionizing and non-ionizing radiation and risk of glioma Occup. Med., October 1, 2007; 57(7): 518 - 524. [Abstract] [Full Text] [PDF] |
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