CYP17 Promoter Polymorphism and Breast Cancer in Australian Women Under Age Forty Years
Background: The cytochrome P450c17α enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be associated with a T to C polymorphism in the 5′ promoter region of the CYP17 gene. Because steroid hormone exposure is known to influence b...
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| Published in | JNCI : Journal of the National Cancer Institute Vol. 92; no. 20; pp. 1674 - 1681 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Cary, NC
Oxford University Press
18.10.2000
Oxford Publishing Limited (England) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8874 1460-2105 1460-2105 |
| DOI | 10.1093/jnci/92.20.1674 |
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| Abstract | Background: The cytochrome P450c17α enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be associated with a T to C polymorphism in the 5′ promoter region of the CYP17 gene. Because steroid hormone exposure is known to influence breast cancer risk, we conducted a population-based, case–control-family study to assess the relationship between the CYP17 promoter polymorphism and early-onset breast cancer. Methods: Case subjects under 40 years of age at diagnosis of a first primary breast cancer, population-sampled control subjects, and the relatives of both case and control subjects were interviewed to record family history of breast cancer and other risk factors. CYP17 genotype was determined in 369 case subjects, 284 control subjects, and 91 relatives of case subjects. Genotype distributions were compared by logistic regression, and cumulative risk was estimated by a modified segregation analysis. All statistical tests were two-tailed. Results: Compared with the TT genotype (i.e., individuals homozygous for the T allele), the TC genotype was not associated with increased breast cancer risk (P = .7). Compared with the TT and TC genotypes combined, the CC genotype was associated with a relative risk of 1.81 (95% confidence interval [CI] = 1.15–2.86; P = .01) before adjustment for measured risk factors and 1.63 (95% CI = 1.00–2.64; P = .05) after adjustment. There was an excess of CC genotypes in case subjects who had at least one affected first- or second-degree relative, compared with control subjects unstratified by family history of breast cancer (23% versus 11%; P = .006), and these case subjects had a threefold to fourfold higher risk than women of other groups defined by genotype and family history of breast cancer. Analysis of breast cancer in first- and second-degree relatives of case subjects with the CC genotype, excluding two known carriers of a deleterious mutation in BRCA1 or BRCA2, gave a relative hazard in women with the CC genotype of 3.48 (95% CI = 1.13–10.74; P = .04), which is equivalent to a cumulative risk of 16% to age 70 years. Conclusions: The CC genotype may modify the effect of other familial risk factors for early-onset breast cancer. |
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| AbstractList | Background: The cytochrome P450c17α enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be associated with a T to C polymorphism in the 5′ promoter region of the CYP17 gene. Because steroid hormone exposure is known to influence breast cancer risk, we conducted a population-based, case–control-family study to assess the relationship between the CYP17 promoter polymorphism and early-onset breast cancer. Methods: Case subjects under 40 years of age at diagnosis of a first primary breast cancer, population-sampled control subjects, and the relatives of both case and control subjects were interviewed to record family history of breast cancer and other risk factors. CYP17 genotype was determined in 369 case subjects, 284 control subjects, and 91 relatives of case subjects. Genotype distributions were compared by logistic regression, and cumulative risk was estimated by a modified segregation analysis. All statistical tests were two-tailed. Results: Compared with the TT genotype (i.e., individuals homozygous for the T allele), the TC genotype was not associated with increased breast cancer risk (P = .7). Compared with the TT and TC genotypes combined, the CC genotype was associated with a relative risk of 1.81 (95% confidence interval [CI] = 1.15–2.86; P = .01) before adjustment for measured risk factors and 1.63 (95% CI = 1.00–2.64; P = .05) after adjustment. There was an excess of CC genotypes in case subjects who had at least one affected first- or second-degree relative, compared with control subjects unstratified by family history of breast cancer (23% versus 11%; P = .006), and these case subjects had a threefold to fourfold higher risk than women of other groups defined by genotype and family history of breast cancer. Analysis of breast cancer in first- and second-degree relatives of case subjects with the CC genotype, excluding two known carriers of a deleterious mutation in BRCA1 or BRCA2, gave a relative hazard in women with the CC genotype of 3.48 (95% CI = 1.13–10.74; P = .04), which is equivalent to a cumulative risk of 16% to age 70 years. Conclusions: The CC genotype may modify the effect of other familial risk factors for early-onset breast cancer. BACKGROUND: The cytochrome P450c17alpha enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be associated with a T to C polymorphism in the 5' promoter region of the CYP17 gene. Because steroid hormone exposure is known to influence breast cancer risk, we conducted a population-based, case-control-family study to assess the relationship between the CYP17 promoter polymorphism and early-onset breast cancer. METHODS: Case subjects under 40 years of age at diagnosis of a first primary breast cancer, population-sampled control subjects, and the relatives of both case and control subjects were interviewed to record family history of breast cancer and other risk factors. CYP17 genotype was determined in 369 case subjects, 284 control subjects, and 91 relatives of case subjects. Genotype distributions were compared by logistic regression, and cumulative risk was estimated by a modified segregation analysis. All statistical tests were two-tailed. RESULTS: Compared with the TT genotype (i.e., individuals homozygous for the T allele), the TC genotype was not associated with increased breast cancer risk (P: =.7). Compared with the TT and TC genotypes combined, the CC genotype was associated with a relative risk of 1. 81 (95% confidence interval [CI] = 1.15-2.86; P: =.01) before adjustment for measured risk factors and 1.63 (95% CI = 1.00-2.64; P: =.05) after adjustment. There was an excess of CC genotypes in case subjects who had at least one affected first- or second-degree relative, compared with control subjects unstratified by family history of breast cancer (23% versus 11%; P: =.006), and these case subjects had a threefold to fourfold higher risk than women of other groups defined by genotype and family history of breast cancer. Analysis of breast cancer in first- and second-degree relatives of case subjects with the CC genotype, excluding two known carriers of a deleterious mutation in BRCA1 or BRCA2, gave a relative hazard in women with the CC genotype of 3.48 (95% CI = 1.13-10.74; P: =.04), which is equivalent to a cumulative risk of 16% to age 70 years. CONCLUSIONS: The CC genotype may modify the effect of other familial risk factors for early-onset breast cancer. The cytochrome P450c17alpha enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be associated with a T to C polymorphism in the 5' promoter region of the CYP17 gene. Because steroid hormone exposure is known to influence breast cancer risk, we conducted a population-based, case-control-family study to assess the relationship between the CYP17 promoter polymorphism and early-onset breast cancer. Case subjects under 40 years of age at diagnosis of a first primary breast cancer, population-sampled control subjects, and the relatives of both case and control subjects were interviewed to record family history of breast cancer and other risk factors. CYP17 genotype was determined in 369 case subjects, 284 control subjects, and 91 relatives of case subjects. Genotype distributions were compared by logistic regression, and cumulative risk was estimated by a modified segregation analysis. All statistical tests were two-tailed. Compared with the TT genotype (i.e., individuals homozygous for the T allele), the TC genotype was not associated with increased breast cancer risk (P: =.7). Compared with the TT and TC genotypes combined, the CC genotype was associated with a relative risk of 1. 81 (95% confidence interval [CI] = 1.15-2.86; P: =.01) before adjustment for measured risk factors and 1.63 (95% CI = 1.00-2.64; P: =.05) after adjustment. There was an excess of CC genotypes in case subjects who had at least one affected first- or second-degree relative, compared with control subjects unstratified by family history of breast cancer (23% versus 11%; P: =.006), and these case subjects had a threefold to fourfold higher risk than women of other groups defined by genotype and family history of breast cancer. Analysis of breast cancer in first- and second-degree relatives of case subjects with the CC genotype, excluding two known carriers of a deleterious mutation in BRCA1 or BRCA2, gave a relative hazard in women with the CC genotype of 3.48 (95% CI = 1.13-10.74; P: =.04), which is equivalent to a cumulative risk of 16% to age 70 years. The CC genotype may modify the effect of other familial risk factors for early-onset breast cancer. The cytochrome P450c17alpha enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be associated with a T to C polymorphism in the 5' promoter region of the CYP17 gene. Because steroid hormone exposure is known to influence breast cancer risk, we conducted a population-based, case-control-family study to assess the relationship between the CYP17 promoter polymorphism and early-onset breast cancer.BACKGROUNDThe cytochrome P450c17alpha enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be associated with a T to C polymorphism in the 5' promoter region of the CYP17 gene. Because steroid hormone exposure is known to influence breast cancer risk, we conducted a population-based, case-control-family study to assess the relationship between the CYP17 promoter polymorphism and early-onset breast cancer.Case subjects under 40 years of age at diagnosis of a first primary breast cancer, population-sampled control subjects, and the relatives of both case and control subjects were interviewed to record family history of breast cancer and other risk factors. CYP17 genotype was determined in 369 case subjects, 284 control subjects, and 91 relatives of case subjects. Genotype distributions were compared by logistic regression, and cumulative risk was estimated by a modified segregation analysis. All statistical tests were two-tailed.METHODSCase subjects under 40 years of age at diagnosis of a first primary breast cancer, population-sampled control subjects, and the relatives of both case and control subjects were interviewed to record family history of breast cancer and other risk factors. CYP17 genotype was determined in 369 case subjects, 284 control subjects, and 91 relatives of case subjects. Genotype distributions were compared by logistic regression, and cumulative risk was estimated by a modified segregation analysis. All statistical tests were two-tailed.Compared with the TT genotype (i.e., individuals homozygous for the T allele), the TC genotype was not associated with increased breast cancer risk (P: =.7). Compared with the TT and TC genotypes combined, the CC genotype was associated with a relative risk of 1. 81 (95% confidence interval [CI] = 1.15-2.86; P: =.01) before adjustment for measured risk factors and 1.63 (95% CI = 1.00-2.64; P: =.05) after adjustment. There was an excess of CC genotypes in case subjects who had at least one affected first- or second-degree relative, compared with control subjects unstratified by family history of breast cancer (23% versus 11%; P: =.006), and these case subjects had a threefold to fourfold higher risk than women of other groups defined by genotype and family history of breast cancer. Analysis of breast cancer in first- and second-degree relatives of case subjects with the CC genotype, excluding two known carriers of a deleterious mutation in BRCA1 or BRCA2, gave a relative hazard in women with the CC genotype of 3.48 (95% CI = 1.13-10.74; P: =.04), which is equivalent to a cumulative risk of 16% to age 70 years.RESULTSCompared with the TT genotype (i.e., individuals homozygous for the T allele), the TC genotype was not associated with increased breast cancer risk (P: =.7). Compared with the TT and TC genotypes combined, the CC genotype was associated with a relative risk of 1. 81 (95% confidence interval [CI] = 1.15-2.86; P: =.01) before adjustment for measured risk factors and 1.63 (95% CI = 1.00-2.64; P: =.05) after adjustment. There was an excess of CC genotypes in case subjects who had at least one affected first- or second-degree relative, compared with control subjects unstratified by family history of breast cancer (23% versus 11%; P: =.006), and these case subjects had a threefold to fourfold higher risk than women of other groups defined by genotype and family history of breast cancer. Analysis of breast cancer in first- and second-degree relatives of case subjects with the CC genotype, excluding two known carriers of a deleterious mutation in BRCA1 or BRCA2, gave a relative hazard in women with the CC genotype of 3.48 (95% CI = 1.13-10.74; P: =.04), which is equivalent to a cumulative risk of 16% to age 70 years.The CC genotype may modify the effect of other familial risk factors for early-onset breast cancer.CONCLUSIONSThe CC genotype may modify the effect of other familial risk factors for early-onset breast cancer. |
| Author | McCredie, Margaret R. E. Dite, Gillian S. Giles, Graham G. Cui, Jisheng Spurdle, Amanda B. Venter, Deon J. Southey, Melissa C. Hopper, John L. Chen, Xiaoqing Chenevix-Trench, Georgia Easton, Douglas F. |
| Author_xml | – sequence: 1 givenname: Amanda B. surname: Spurdle fullname: Spurdle, Amanda B. organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 2 givenname: John L. surname: Hopper fullname: Hopper, John L. organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 3 givenname: Gillian S. surname: Dite fullname: Dite, Gillian S. organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 4 givenname: Xiaoqing surname: Chen fullname: Chen, Xiaoqing organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 5 givenname: Jisheng surname: Cui fullname: Cui, Jisheng organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 6 givenname: Margaret R. E. surname: McCredie fullname: McCredie, Margaret R. E. organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 7 givenname: Graham G. surname: Giles fullname: Giles, Graham G. organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 8 givenname: Melissa C. surname: Southey fullname: Southey, Melissa C. organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 9 givenname: Deon J. surname: Venter fullname: Venter, Deon J. organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 10 givenname: Douglas F. surname: Easton fullname: Easton, Douglas F. organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K – sequence: 11 givenname: Georgia surname: Chenevix-Trench fullname: Chenevix-Trench, Georgia organization: A. B. Spurdle, X. Chen, G. Chenevix-Trench, Cancer Unit, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; J. L. Hopper, G. S. Dite, J. Cui, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. R. E. McCredie, The New South Wales Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, The Anti-Cancer Council of Victoria, Carlton, Australia; M. C. Southey, D. J. Venter, Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, Australia; D. F. Easton, Cancer Research Campaign Genetic Epidemiology Unit, Strangeways Research Laboratory, Cambridge, U.K |
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| Issue | 20 |
| Keywords | Human Genetic variability Premenopause Isozyme Transcription promoter Cytochrome P450 Genotype Malignant tumor Epidemiology Mammary gland diseases Gene Risk factor Genetics Mammary gland Public health Polymorphism |
| Language | English |
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| Notes | local:0921674 ark:/67375/HXZ-96R46X0L-0 Correspondence to: Amanda B. Spurdle, Ph.D., Cancer Unit, The Queensland Institute of Medical Research, P.O. Royal Brisbane Hospital, Queensland, 4029, Australia (e-mail: mandyS@qimr.edu.au). istex:4A44AA8BE0EE50A3911C142FA336C28B7E256AA3 PII:1460-2105 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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| PublicationTitle | JNCI : Journal of the National Cancer Institute |
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| References | 11287451 - J Natl Cancer Inst. 2001 Apr 4;93(7):554-5 |
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| Snippet | Background: The cytochrome P450c17α enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to... The cytochrome P450c17alpha enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported to be... BACKGROUND: The cytochrome P450c17alpha enzyme functions in the steroid biosynthesis pathway, and altered endogenous steroid hormone levels have been reported... |
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| SubjectTerms | Adult Age Factors Age of Onset Alleles Australia Biological and medical sciences Breast cancer Breast Neoplasms - enzymology Breast Neoplasms - genetics Case-Control Studies DNA Primers DNA, Neoplasm - analysis Enzymes Female Genes, BRCA1 - genetics Genes, Tumor Suppressor - genetics Genotype Gynecology. Andrology. Obstetrics Hormones Humans Logistic Models Mammary gland diseases Medical research Medical sciences Mutation Polymerase Chain Reaction Polymorphism, Genetic Promoter Regions, Genetic - genetics Risk Steroid 17-alpha-Hydroxylase - genetics Tumors Women |
| Title | CYP17 Promoter Polymorphism and Breast Cancer in Australian Women Under Age Forty Years |
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