Glutathione S-transferases M1, T1, and P1 and Breast Cancer: A Pooled Analysis
The glutathione S -transferase ( GST ) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base transition polymorphism at codon 105 (Ile→Val) in GSTP1 were investigated in relation to breast cancer risk. Tobacco smoking and reproduc...
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Published in: | Cancer epidemiology, biomarkers & prevention Vol. 13; no. 9; pp. 1473 - 1479 |
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American Association for Cancer Research
01-09-2004
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Abstract | The glutathione S -transferase ( GST ) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base transition polymorphism at codon 105 (Ile→Val) in GSTP1 were investigated in relation to breast cancer risk. Tobacco smoking and reproductive factors were examined as potential
effect modifiers. Individual data from seven case-control studies were pooled within the International Collaborative Study
on Genetic Susceptibility to Environmental Carcinogens. To measure the effect of GSTs on breast cancer risk, odds ratios and
95% confidence intervals were computed adjusting for study center and age. The modifying effect was investigated by stratification
on variables of smoking habits and reproductive history. A total of 2,048 cases with breast cancer and 1,969 controls were
analyzed. The relative odds ratio (95% confidence interval) of breast cancer was 0.98 (0.86–1.12) with the GSTM1 null, 1.11 (0.87–1.41) with the GSTT1 null, 1.01 (0.79–1.28) with GSTP1 heterozygous mutants, and 0.93 (0.62–1.38) with GSTP1 homozygous mutants. Stratification by smoking or reproductive factors did not reveal a modifying effect of these variables,
nor was there any association between GSTM1 and age at diagnosis of breast cancer. This is the largest study investigating susceptibility to breast cancer due to polymorphisms
in the GST genes. The results conclusively show that single gene GST polymorphisms do not confer a substantial risk of breast cancer to its carriers. Furthermore, GSTs did not interact with
smoking or reproductive history to modify cancer risk. |
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AbstractList | The glutathione S-transferase (GST) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base transition polymorphism at codon 105 (Ileright arrowVal) in GSTP1 were investigated in relation to breast cancer risk. Tobacco smoking and reproductive factors were examined as potential effect modifiers. Individual data from seven case-control studies were pooled within the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. To measure the effect of GSTs on breast cancer risk, odds ratios and 95% confidence intervals were computed adjusting for study center and age. The modifying effect was investigated by stratification on variables of smoking habits and reproductive history. A total of 2,048 cases with breast cancer and 1,969 controls were analyzed. The relative odds ratio (95% confidence interval) of breast cancer was 0.98 (0.86-1.12) with the GSTM1 null, 1.11 (0.87-1.41) with the GSTT1 null, 1.01 (0.79-1.28) with GSTP1 heterozygous mutants, and 0.93 (0.62-1.38) with GSTP1 homozygous mutants. Stratification by smoking or reproductive factors did not reveal a modifying effect of these variables, nor was there any association between GSTM1 and age at diagnosis of breast cancer. This is the largest study investigating susceptibility to breast cancer due to polymorphisms in the GST genes. The results conclusively show that single gene GST polymorphisms do not confer a substantial risk of breast cancer to its carriers. Furthermore, GSTs did not interact with smoking or reproductive history to modify cancer risk. The glutathione S -transferase ( GST ) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base transition polymorphism at codon 105 (Ile→Val) in GSTP1 were investigated in relation to breast cancer risk. Tobacco smoking and reproductive factors were examined as potential effect modifiers. Individual data from seven case-control studies were pooled within the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. To measure the effect of GSTs on breast cancer risk, odds ratios and 95% confidence intervals were computed adjusting for study center and age. The modifying effect was investigated by stratification on variables of smoking habits and reproductive history. A total of 2,048 cases with breast cancer and 1,969 controls were analyzed. The relative odds ratio (95% confidence interval) of breast cancer was 0.98 (0.86–1.12) with the GSTM1 null, 1.11 (0.87–1.41) with the GSTT1 null, 1.01 (0.79–1.28) with GSTP1 heterozygous mutants, and 0.93 (0.62–1.38) with GSTP1 homozygous mutants. Stratification by smoking or reproductive factors did not reveal a modifying effect of these variables, nor was there any association between GSTM1 and age at diagnosis of breast cancer. This is the largest study investigating susceptibility to breast cancer due to polymorphisms in the GST genes. The results conclusively show that single gene GST polymorphisms do not confer a substantial risk of breast cancer to its carriers. Furthermore, GSTs did not interact with smoking or reproductive history to modify cancer risk. The glutathione S-transferase (GST) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base transition polymorphism at codon 105 (Ile-->Val) in GSTP1 were investigated in relation to breast cancer risk. Tobacco smoking and reproductive factors were examined as potential effect modifiers. Individual data from seven case-control studies were pooled within the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. To measure the effect of GSTs on breast cancer risk, odds ratios and 95% confidence intervals were computed adjusting for study center and age. The modifying effect was investigated by stratification on variables of smoking habits and reproductive history. A total of 2,048 cases with breast cancer and 1,969 controls were analyzed. The relative odds ratio (95% confidence interval) of breast cancer was 0.98 (0.86-1.12) with the GSTM1 null, 1.11 (0.87-1.41) with the GSTT1 null, 1.01 (0.79-1.28) with GSTP1 heterozygous mutants, and 0.93 (0.62-1.38) with GSTP1 homozygous mutants. Stratification by smoking or reproductive factors did not reveal a modifying effect of these variables, nor was there any association between GSTM1 and age at diagnosis of breast cancer. This is the largest study investigating susceptibility to breast cancer due to polymorphisms in the GST genes. The results conclusively show that single gene GST polymorphisms do not confer a substantial risk of breast cancer to its carriers. Furthermore, GSTs did not interact with smoking or reproductive history to modify cancer risk. Abstract The glutathione S-transferase (GST) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base transition polymorphism at codon 105 (Ile→Val) in GSTP1 were investigated in relation to breast cancer risk. Tobacco smoking and reproductive factors were examined as potential effect modifiers. Individual data from seven case-control studies were pooled within the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. To measure the effect of GSTs on breast cancer risk, odds ratios and 95% confidence intervals were computed adjusting for study center and age. The modifying effect was investigated by stratification on variables of smoking habits and reproductive history. A total of 2,048 cases with breast cancer and 1,969 controls were analyzed. The relative odds ratio (95% confidence interval) of breast cancer was 0.98 (0.86–1.12) with the GSTM1 null, 1.11 (0.87–1.41) with the GSTT1 null, 1.01 (0.79–1.28) with GSTP1 heterozygous mutants, and 0.93 (0.62–1.38) with GSTP1 homozygous mutants. Stratification by smoking or reproductive factors did not reveal a modifying effect of these variables, nor was there any association between GSTM1 and age at diagnosis of breast cancer. This is the largest study investigating susceptibility to breast cancer due to polymorphisms in the GST genes. The results conclusively show that single gene GST polymorphisms do not confer a substantial risk of breast cancer to its carriers. Furthermore, GSTs did not interact with smoking or reproductive history to modify cancer risk. |
Author | Paolo Boffetta Christine Ambrosone Fritz F. Parl Emanuela Taioli Christine Maugard Luis F. Ribeiro Pinto Timothy R. Rebbeck Florian D. Vogl Wei Zheng Vessela Nedelcheva-Kristensen Paul Brennan |
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Cites_doi | 10.1093/carcin/11.1.33 10.1042/bj3000271 10.1093/jnci/90.7.512 10.1111/j.1432-1033.1994.00893.x 10.1042/bj3040843 10.1097/00008571-199810000-00009 10.1158/1055-9965.EPI-03-0294 10.1093/jn/129.2.565S 10.2307/2533446 10.3109/10409239509083492 10.1093/oxfordjournals.aje.a010124 10.1016/0003-9861(90)90277-6 10.1093/carcin/7.5.751 10.1016/0197-2456(86)90046-2 10.1016/S0304-3835(02)00058-7 10.1016/S0009-2797(97)00173-7 10.1038/sj.bjc.6600708 10.1093/aje/154.2.95 10.1093/jnci/91.22.1960 10.1093/carcin/14.9.1821 10.1159/000134117 10.1023/A:1016005100958 10.1136/bmj.315.7109.629 10.1136/bmj.316.7124.61 10.1006/geno.1996.0167 10.1078/1438-4639-00070 10.1038/sj.bjc.6600596 10.1093/aje/kwf018 10.1073/pnas.85.19.7293 10.1038/sj.bjc.6690055 10.1097/00008571-200006000-00004 |
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Keywords | Human Genetic variability Enzyme Isozyme Transferases Tobacco smoking Genotype Breast cancer Malignant tumor Epidemiology Mammary gland diseases Reproduction Cancerology Glutathione transferase Risk factor Genetics Public health |
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Snippet | The glutathione S -transferase ( GST ) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a... The glutathione S-transferase (GST) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base... Abstract The glutathione S-transferase (GST) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1... |
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SubjectTerms | Acyltransferases - genetics Base Sequence Biological and medical sciences Breast Neoplasms - epidemiology Breast Neoplasms - genetics Carcinogens, Environmental - pharmacokinetics Carcinogens, Environmental - toxicity Case-Control Studies Chromosome Deletion Codon DNA Mutational Analysis Female Genetic Carrier Screening Genetic Predisposition to Disease - genetics Genotype Glutathione Transferase - genetics Gynecology. Andrology. Obstetrics Humans Mammary gland diseases Medical sciences Meta-Analysis as Topic Polymorphism, Genetic - genetics Risk Factors Tumors |
Title | Glutathione S-transferases M1, T1, and P1 and Breast Cancer: A Pooled Analysis |
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