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Epidemiology and Cancer Control |
Laboratory for Molecular Epidemiology, Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco, CA 94143-0560 (P.C., J.K.W., R.M., M.W.); and the Molecular Epidemiology Laboratory, Department of Epidemiology, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599-7400 (K.C., S.N.E.)
2 Address correspondence and reprint requests to Margaret Wrensch, Department of Epidemiology and Biostatistics, University of California, 44 Page St., Suite 503, San Francisco, CA 94143-1215.
Abstract
HRAS rare alleles have been associated with the increased susceptibility to a variety of cancers. In the present study we examined the hypothesis that HRAS rare alleles are a risk factor for adult glioma in a population-based case-control study of adult glioma in six San Francisco Bay Area counties. We compared the prevalence of rare alleles in the variable number of tandem repeats region of HRAS in the germline DNA from 73 white adults who had gliomas with that of 65 controls. Overall, the prevalence of rare alleles in cases was not different from the prevalence of those in controls according to two definitions of rare alleles. We found that 25 of 73 (34%) of cases versus 25 of 65 (38%) of controls had at least one allele that was not 30, 46, 69, or 87 repeats; 4 of 73 (5%) of cases versus 6 of 65 (9%) of controls carried one or more alleles with 33, 39, 42, 53, 59, 63, 68, 105, or 114 repeats. The proportion of rare alleles was somewhat higher among subjects with anaplastic astrocytoma. Among women, cases were less likely than controls to have HRAS rare alleles, whereas among men, cases were slightly more likely to have HRAS rare alleles, but none of these results approach statistical significance. Our data do not suggest an excess of HRAS rare alleles among adult glioma cases.
References
Barbacid, M. (1987) ras genes. Ann. Rev. Biochem. 56,779 -827.[CrossRef][ISI][Medline]
Capon, D.J., Chen, E.Y., Levinson, A.D., Seeburg, P.H., and Goeddel, D.V. (1983) Complete nucleotide sequences of the T24 human bladder carcinoma oncogene and its normal homologue. Nature 302,33 -37.[CrossRef][Medline]
Conway, K., Edmiston, S.N., Hulka, B.S., Garrett, P.A., and Liu,
E.T. (1996) Internal sequence variations in the Ha-ras variable
number tandem repeat rare and common alleles identified by minisatellite
variant repeat polymerase chain reaction. Cancer Res.
56,4773
-4777.
Diedrich, U., Eckermann, O., and Schmidtke, J. (1988)
Rare Ha-ras and c-mos alleles in patients with intracranial tumors.
Neurology 38,587
-589.
Green, M., and Krontiris, T.G. (1993) Allelic variation of reporter gene activation by the HRAS1 minisatellite. Genomics 17,429 -434.[CrossRef][ISI][Medline]
Krontiris, T.G., Devlin, B., Karp, D.D., Robert, N.J., and Risch,
N. (1993) An association between the risk of cancer and mutations
in the HRAS1 minisatellite locus. N. Engl. J. Med.
329,517
-523.
Louis, D.N. (1997) A molecular genetic model of astrocytoma histopathology. Brain Pathol. 7, 755-764.[ISI][Medline]
Orian, J.M., Vasilopoulos, K., Yoshida, S., Kaye, A.H., Chow, C.W., and Gonzales, M.F. (1992) Overexpression of multiple oncogenes related to histological grade of astrocytic glioma. Br. J. Cancer 66,106 -112.[ISI][Medline]
Riccardi, A., Danova, M., Giordano, M., Gaetani, P., Butti, G., Zibera, C., and Mazzini, G. (1991) Proto-oncogene expression and proliferative activity in human malignant gliomas. Dev. Oncol. 66,81 -84.
SAS (1990) Vol.2 . Cary, N.C.: SAS Institute, Inc.
Trepicchio, W.L., and Krontiris, T.G. (1992) Members
of the rel/NF-kappa B family of transcriptional regulatory proteins bind the
HRAS1 minisatellite DNA sequence. Nucleic Acids Res.
20,2427
-2434.
von Deimling, A., Louis, D.N., and Wiestler, O.D. (1995) Molecular pathways in the formation of gliomas. Glia 15,328 -338.[CrossRef][ISI][Medline]
Watanabe, K., Tachibana, O., Sata, K., Yonekawa, Y., Kleihues, P., and Ohgaki, H. (1996) Overexpression of the EGF receptor and p53 mutations are mutually exclusive in the evolution of primary and secondary glioblastomas. Brain Pathol. 6, 217-224.[ISI][Medline]
Weston, A., Vineis, P., Caporaso, N.E., Krontiris, T.G., Lonergan, J.A., and Sugimura, H. (1991) Racial variation in the distribution of Ha-ras-1 alleles. Mol. Carcinog. 4, 265-268.[ISI][Medline]
Wrensch, M., Lee, M., Miike, R., Newman, B., Barger, G., Davis, R.,
Wiencke, J., and Neuhaus, J. (1997) Familial and personal medical
history of cancer and nervous system conditions among adults with glioma and
controls. Am. J. Epidemiol.
145,581
-593.
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