© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 20, 1553-1557,
October 17, 2001
© 2001 Oxford University Press
REPORT |
-Radiation Sensitivity and Risk of Glioma
Affiliations of authors: M. L. Bondy, L.-E. Wang, R. El-Zein, M. S. Selvan, P. Adatto, Q. Wei (Department of Epidemiology), J. M. Bruner (Department of Pathology), V. A. Levin, W. K. A. Yung (Department of Neuro-Oncology), The University of Texas M. D. Anderson Cancer Center, Houston; M. de Andrade, Department of Health Sciences Research, Mayo Clinic and Mayo Foundation, Rochester, MN.
Correspondence to: Melissa L. Bondy, Ph.D., Department of Epidemiology, Box 189, The University of Texas M. D. Anderson Cancer Center, Houston, TX (e-mail: mbondy{at}mdanderson.org).
Background: About 9% of human cancers are brain tumors, of which 90% are gliomas.
-Radiation has been identified as a risk factor for brain tumors. In a previous pilot study, we found that lymphocytes from patients with glioma were more sensitive to
-radiation than were lymphocytes from matched control subjects. In this larger casecontrol study, we compared the
-radiation sensitivity of lymphocytes from glioma patients with those from control subjects and investigated the association between mutagen sensitivity and the risk for developing glioma. Methods: We used a mutagen sensitivity assay (an indirect measure of DNA repair activity) to assess chromosomal damage. We
-irradiated (1.5 Gy) short-term lymphocyte cultures from 219 case patients with glioma and from 238 healthy control subjects frequency matched by age and sex. After irradiation, cells were cultured for 4 hours, and then Colcemid was added for 1 hour to arrest cells in mitosis. Fifty metaphases were randomly selected for each sample and scored for chromatid breaks. All statistical tests were two-sided. Results: We observed a statistically significantly higher frequency of chromatid breaks per cell from case patients with glioma (mean = 0.55; 95% confidence interval [CI] = 0.50 to 0.59) than from control subjects (mean = 0.44; 95% CI = 0.41 to 0.48) (P<.001). Using 0.40 (the median number of chromatid breaks per cell in control subjects) as the cut point for defining mutagen sensitivity and adjusting for age, sex, and smoking status, we found that mutagen sensitivity was statistically significantly associated with an increased risk for glioma (odds ratio = 2.09; 95% CI = 1.43 to 3.06). When the data were divided into tertiles, the relative risk for glioma increased from the lowest tertile to the highest tertile (trend test, P<.001). Conclusion:
-Radiation-induced mutagen sensitivity of lymphocytes may be associated with an increased risk for glioma, a result that supports our earlier preliminary findings.
This article has been cited by other articles:
![]() |
Y. Liu, M. E. Scheurer, R. El-Zein, Y. Cao, K.-A. Do, M. Gilbert, K. D. Aldape, Q. Wei, C. Etzel, and M. L. Bondy Association and Interactions between DNA Repair Gene Polymorphisms and Adult Glioma Cancer Epidemiol. Biomarkers Prev., January 1, 2009; 18(1): 204 - 214. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Leng, C. A. Stidley, A. M. Bernauer, M. A. Picchi, X. Sheng, M. A. Frasco, D. Van Den Berg, F. D. Gilliland, R. E. Crowell, and S. A. Belinsky Haplotypes of DNMT1 and DNMT3B are associated with mutagen sensitivity induced by benzo[a]pyrene diol epoxide among smokers Carcinogenesis, July 1, 2008; 29(7): 1380 - 1385. [Abstract] [Full Text] [PDF] |
||||
![]() |
L.-E Wang, P. Xiong, H. Zhao, M. R. Spitz, E. M. Sturgis, and Q. Wei Chromosome Instability and Risk of Squamous Cell Carcinomas of Head and Neck Cancer Res., June 1, 2008; 68(11): 4479 - 4485. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Liu, H. Zhang, K. Zhou, L. Chen, Z. Xu, Y. Zhong, H. Liu, R. Li, Y. Y. Shugart, Q. Wei, et al. Tagging SNPs in non-homologous end-joining pathway genes and risk of glioma Carcinogenesis, September 1, 2007; 28(9): 1906 - 1913. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Lu, L.-E Wang, P. Xiong, E. M. Sturgis, M. R. Spitz, and Q. Wei 172G>T variant in the 5' untranslated region of DNA repair gene RAD51 reduces risk of squamous cell carcinoma of the head and neck and interacts with a P53 codon 72 variant Carcinogenesis, May 1, 2007; 28(5): 988 - 994. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Erdei, S.-J. Lee, Q. Wei, L.-E. Wang, Y.-S. Song, D. Bovbjerg, and M. Berwick Reliability of mutagen sensitivity assay: an inter-laboratory comparison Mutagenesis, July 1, 2006; 21(4): 261 - 264. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. G. Natarajan, N. Ganesan, P. Carter-Nolan, C. A. Tucker, P. G. Shields, and L. L. Adams-Campbell {gamma}-Radiation-Induced Chromosomal Mutagen Sensitivity Is Associated with Breast Cancer Risk in African-American Women: Caffeine Modulates the Outcome of Mutagen Sensitivity Assay. Cancer Epidemiol. Biomarkers Prev., March 1, 2006; 15(3): 437 - 442. [Abstract] [Full Text] [PDF] |
||||
![]() |
L.-E Wang, P. Xiong, S. S. Strom, L. H. Goldberg, J. E. Lee, M. I. Ross, P. F. Mansfield, J. E. Gershenwald, V. G. Prieto, J. N. Cormier, et al. In Vitro Sensitivity to Ultraviolet B Light and Skin Cancer Risk: A Case-Control Analysis J Natl Cancer Inst, December 21, 2005; 97(24): 1822 - 1831. [Abstract] [Full Text] [PDF] |
||||
![]() |
L.-E Wang, M. L. Bondy, H. Shen, R. El-Zein, K. Aldape, Y. Cao, V. Pudavalli, V. A. Levin, W. K. A. Yung, and Q. Wei Polymorphisms of DNA Repair Genes and Risk of Glioma Cancer Res., August 15, 2004; 64(16): 5560 - 5563. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Wrensch, Y. Minn, T. Chew, M. Bondy, and M. S. Berger Epidemiology of primary brain tumors: Current concepts and review of the literature Neuro-oncol, October 1, 2002; 4(4): 278 - 299. [Abstract] [PDF] |
||||
![]() |
A. K. Nersesyan Re: {gamma}-Radiation Sensitivity and Risk of Glioma J Natl Cancer Inst, June 19, 2002; 94(12): 949 - 949. [Full Text] [PDF] |
||||
![]() |
K. J. Dornfeld and T. S. Lawrence A Predisposition Supposition for Glioma J Natl Cancer Inst, October 17, 2001; 93(20): 1512 - 1513. [Full Text] [PDF] |
||||





