| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
1 Division of Cancer Prevention and Control, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida; 2 Department of Community and Family Medicine and the Duke Comprehensive Cancer Center, Duke University, Durham, North Carolina; and Departments of 3 Health Sciences Research, 4 Laboratory Medicine and Pathology, 5 Medicine, 6 Medical Oncology, and 7 Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota
Requests for reprints: Thomas A. Sellers, Division of Cancer Prevention and Control, H. Lee Moffitt Cancer Center and Research Institute, 12902 Magnolia Drive, Tampa, FL 33602. Phone: 813-632-1315; Fax: 813-632-1334. E-mail: sellerta{at}moffitt.usf.edu
Recent experimental evidence has shown that catechol estrogens can be activated through metabolism to form depurinating DNA adducts and thereby initiate cancer. Limited data are available regarding this pathway in epithelial ovarian cancer. We conducted a case-control study of 503 incident epithelial ovarian cancer cases at the Mayo Clinic in Rochester, MN, and Jacksonville, FL, and a 48-county region in North Carolina. Six hundred nine cancer-free controls were frequency matched to the cases on age, race, and residence. After an interview to obtain data on risk factors, a sample of blood was collected for DNA isolation. Subjects were genotyped for seven common single nucleotide polymorphisms in four genes involved in catechol estrogen formation (CYP1A1 and CYP1B1) or conjugation (COMT and SULT1A1). Data were analyzed using logistic regression, stratified by race, and with adjustment for design factors and potential confounders. None of the individual genotypes were significantly associated with ovarian cancer risk. However, an oligogenic model that considered the joint effects of the four candidate genes provided evidence for an association between combinations of these genes and ovarian cancer status (P = 0.015). Although preliminary, this study provides some support for the hypothesis that low-penetrance susceptibility alleles may influence risk of epithelial ovarian cancer.
This article has been cited by other articles:
|
|
 |
|
  L. E. Kelemen, T. A. Sellers, J. M. Schildkraut, J. M. Cunningham, R. A. Vierkant, V. S. Pankratz, Z. S. Fredericksen, M. K. Gadre, D. N. Rider, M. Liebow, et al. Genetic Variation in the One-Carbon Transfer Pathway and Ovarian Cancer Risk Cancer Res., April 1, 2008; 68(7): 2498 - 2506. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. A. Sellers, Y. Huang, J. Cunningham, E. L. Goode, R. Sutphen, R. A. Vierkant, L. E. Kelemen, Z. S. Fredericksen, M. Liebow, V. S. Pankratz, et al. Association of Single Nucleotide Polymorphisms in Glycosylation Genes with Risk of Epithelial Ovarian Cancer Cancer Epidemiol. Biomarkers Prev., February 1, 2008; 17(2): 397 - 404. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Gayther, H. Song, S. J. Ramus, S. K. Kjaer, A. S. Whittemore, L. Quaye, J. Tyrer, D. Shadforth, E. Hogdall, C. Hogdall, et al. Tagging Single Nucleotide Polymorphisms in Cell Cycle Control Genes and Susceptibility to Invasive Epithelial Ovarian Cancer Cancer Res., April 1, 2007; 67(7): 3027 - 3035. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. K. Holt, M. A. Rossing, K. E. Malone, S. M. Schwartz, N. S. Weiss, and C. Chen Ovarian Cancer Risk and Polymorphisms Involved in Estrogen Catabolism Cancer Epidemiol. Biomarkers Prev., March 1, 2007; 16(3): 481 - 489. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. H. Tao, Q. Cai, W. H. Xu, N. Kataoka, W. Wen, W. Zheng, Y. B. Xiang, Z.-F. Zhang, and X. O. Shu Cytochrome P450 1B1 and Catechol-O-Methyltransferase Genetic Polymorphisms and Endometrial Cancer Risk in Chinese Women Cancer Epidemiol. Biomarkers Prev., December 1, 2006; 15(12): 2570 - 2573. [Full Text] [PDF]
|
|
|
|
 |
|
 N. L. Nock, M. S. Cicek, L. Li, X. Liu, B. A. Rybicki, A. Moreira, S. J. Plummer, G. Casey, and J. S. Witte Polymorphisms in estrogen bioactivation, detoxification and oxidative DNA base excision repair genes and prostate cancer risk Carcinogenesis, September 1, 2006; 27(9): 1842 - 1848. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Cell Growth & Differentiation |
