Genetic variation in sex-steroid receptors and synthesizing enzymes and colorectal cancer risk in women

Objectives Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control...

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Veröffentlicht in:Cancer causes & control Jg. 21; H. 6; S. 897 - 908
Hauptverfasser: Lin, Jennifer, Zee, Robert Y. L, Liu, Kuang-Yu, Zhang, Shumin M, Lee, I-Min, Manson, JoAnn E, Giovannucci, Edward, Buring, Julie E, Cook, Nancy R
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Dordrecht Dordrecht : Springer Netherlands 01.06.2010
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Springer Nature B.V
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ISSN:0957-5243, 1573-7225, 1573-7225
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Abstract Objectives Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control by evaluating genetic variation in estrogen receptors (ESR1 and ESR2), progesterone receptor (PGR), aromatase cytochrome 450 enzyme (CYP19A1), and 17 beta-hydroxysteroid dehydrogenase type 2 gene (HSD17B2). Methods We included 158 incident cases of colorectal cancer and 563 randomly chosen control subjects from 28,345 women in the Women's Health Study aged 45 or older who provided blood samples and had no history of cancer or cardiovascular disease at baseline in 1993. All cases and controls were Caucasians of European descent. A total of 63 tagging and putative functional SNPs in the 5 genes were included for analysis. Unconditional logistic regression was used to estimate odds ratio (ORs) and 95% confidence intervals (CIs). Results There was no association between variation in ESR1, ESR2, PGR, CYP19A1 and HSD17B2 and colorectal cancer risk after correction for multiple comparisons (p values after correction ≥0.25). There was also no association with any of the haplotypes examined (p ≥ 0.15) and no evidence of joint effects of variants in the 5 genes (p ≥ 0.51). Conclusion Our data offer insufficient support for an association between variation in ESR1, ESR2, PGR, CYP19A1, and HSD17B2 and risk for developing colorectal cancer.
AbstractList Objectives Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control by evaluating genetic variation in estrogen receptors (ESR1 and ESR2), progesterone receptor (PGR), aromatase cytochrome 450 enzyme (CYP19A1), and 17 beta-hydroxysteroid dehydrogenase type 2 gene (HSD17B2). Methods We included 158 incident cases of colorectal cancer and 563 randomly chosen control subjects from 28,345 women in the Women's Health Study aged 45 or older who provided blood samples and had no history of cancer or cardiovascular disease at baseline in 1993. All cases and controls were Caucasians of European descent. A total of 63 tagging and putative functional SNPs in the 5 genes were included for analysis. Unconditional logistic regression was used to estimate odds ratio (ORs) and 95% confidence intervals (CIs). Results There was no association between variation in ESR1, ESR2, PGR, CYP19A1 and HSD17B2 and colorectal cancer risk after correction for multiple comparisons (p values after correction ≥0.25). There was also no association with any of the haplotypes examined (p ≥ 0.15) and no evidence of joint effects of variants in the 5 genes (p ≥ 0.51). Conclusion Our data offer insufficient support for an association between variation in ESR1, ESR2, PGR, CYP19A1, and HSD17B2 and risk for developing colorectal cancer.
Objectives: Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control by evaluating genetic variation in estrogen receptors (ESR1 and ESR2), progesterone receptor (PGR), aromatase cytochrome 450 enzyme (CYP19A1), and 17 beta-hydroxysteroid dehydrogenase type 2 gene (HSD17B2). Methods: We included 158 incident cases of colorectal cancer and 563 randomly chosen control subjects from 28,345 women in the Women's Health Study aged 45 or older who provided blood samples and had no history of cancer or cardiovascular disease at baseline in 1993. All cases and controls were Caucasians of European descent. A total of 63 tagging and putative functional SNPs in the 5 genes were included for analysis. Unconditional logistic regression was used to estimate odds ratio (ORs) and 95% confidence intervals (CIs). Results: There was no association between variation in ESR1, ESR2, PGR, CYP19A1 and HSD17B2 and colorectal cancer risk after correction for multiple comparisons (p values after correction .0.25). There was also no association with any of the haplotypes examined (p.0.15) and no evidence of joint effects of variants in the 5 genes (p.0.51). Conclusion: Our data offer insufficient support for an association between variation in ESR1, ESR2, PGR, CYP19A1, and HSD17B2 and risk for developing colorectal cancer.
Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control by evaluating genetic variation in estrogen receptors (ESR1 and ESR2), progesterone receptor (PGR), aromatase cytochrome 450 enzyme (CYP19A1), and 17 beta-hydroxysteroid dehydrogenase type 2 gene (HSD17B2). We included 158 incident cases of colorectal cancer and 563 randomly chosen control subjects from 28,345 women in the Women's Health Study aged 45 or older who provided blood samples and had no history of cancer or cardiovascular disease at baseline in 1993. All cases and controls were Caucasians of European descent. A total of 63 tagging and putative functional SNPs in the 5 genes were included for analysis. Unconditional logistic regression was used to estimate odds ratio (ORs) and 95% confidence intervals (CIs). There was no association between variation in ESR1, ESR2, PGR, CYP19A1 and HSD17B2 and colorectal cancer risk after correction for multiple comparisons (p values after correction ≥0.25). There was also no association with any of the haplotypes examined (p ≥ 0.15) and no evidence of joint effects of variants in the 5 genes (p ≥ 0.51). Our data offer insufficient support for an association between variation in ESR1, ESR2, PGR, CYP19A1, and HSD17B2 and risk for developing colorectal cancer.[PUBLICATION ABSTRACT]
Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control by evaluating genetic variation in estrogen receptors (ESR1 and ESR2), progesterone receptor (PGR), aromatase cytochrome 450 enzyme (CYP19A1), and 17 beta-hydroxysteroid dehydrogenase type 2 gene (HSD17B2). We included 158 incident cases of colorectal cancer and 563 randomly chosen control subjects from 28,345 women in the Women's Health Study aged 45 or older who provided blood samples and had no history of cancer or cardiovascular disease at baseline in 1993. All cases and controls were Caucasians of European descent. A total of 63 tagging and putative functional SNPs in the 5 genes were included for analysis. Unconditional logistic regression was used to estimate odds ratio (ORs) and 95% confidence intervals (CIs). There was no association between variation in ESR1, ESR2, PGR, CYP19A1 and HSD17B2 and colorectal cancer risk after correction for multiple comparisons (p values after correction > or =0.25). There was also no association with any of the haplotypes examined (p > or = 0.15) and no evidence of joint effects of variants in the 5 genes (p > or = 0.51). Our data offer insufficient support for an association between variation in ESR1, ESR2, PGR, CYP19A1, and HSD17B2 and risk for developing colorectal cancer.
Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control by evaluating genetic variation in estrogen receptors (ESR1 and ESR2), progesterone receptor (PGR), aromatase cytochrome 450 enzyme (CYP19A1), and 17 beta-hydroxysteroid dehydrogenase type 2 gene (HSD17B2).OBJECTIVESSeveral lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control by evaluating genetic variation in estrogen receptors (ESR1 and ESR2), progesterone receptor (PGR), aromatase cytochrome 450 enzyme (CYP19A1), and 17 beta-hydroxysteroid dehydrogenase type 2 gene (HSD17B2).We included 158 incident cases of colorectal cancer and 563 randomly chosen control subjects from 28,345 women in the Women's Health Study aged 45 or older who provided blood samples and had no history of cancer or cardiovascular disease at baseline in 1993. All cases and controls were Caucasians of European descent. A total of 63 tagging and putative functional SNPs in the 5 genes were included for analysis. Unconditional logistic regression was used to estimate odds ratio (ORs) and 95% confidence intervals (CIs).METHODSWe included 158 incident cases of colorectal cancer and 563 randomly chosen control subjects from 28,345 women in the Women's Health Study aged 45 or older who provided blood samples and had no history of cancer or cardiovascular disease at baseline in 1993. All cases and controls were Caucasians of European descent. A total of 63 tagging and putative functional SNPs in the 5 genes were included for analysis. Unconditional logistic regression was used to estimate odds ratio (ORs) and 95% confidence intervals (CIs).There was no association between variation in ESR1, ESR2, PGR, CYP19A1 and HSD17B2 and colorectal cancer risk after correction for multiple comparisons (p values after correction > or =0.25). There was also no association with any of the haplotypes examined (p > or = 0.15) and no evidence of joint effects of variants in the 5 genes (p > or = 0.51).RESULTSThere was no association between variation in ESR1, ESR2, PGR, CYP19A1 and HSD17B2 and colorectal cancer risk after correction for multiple comparisons (p values after correction > or =0.25). There was also no association with any of the haplotypes examined (p > or = 0.15) and no evidence of joint effects of variants in the 5 genes (p > or = 0.51).Our data offer insufficient support for an association between variation in ESR1, ESR2, PGR, CYP19A1, and HSD17B2 and risk for developing colorectal cancer.CONCLUSIONOur data offer insufficient support for an association between variation in ESR1, ESR2, PGR, CYP19A1, and HSD17B2 and risk for developing colorectal cancer.
Objectives Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex hormones affect colorectal cancer development remain unknown. We sought to determine whether the association may be under genetic control by evaluating genetic variation in estrogen receptors (ESR1 and ESR2), progesterone receptor (PGR), aromatase cytochrome 450 enzyme (CYP19A1), and 17 beta-hydroxysteroid dehydrogenase type 2 gene (HSD17B2). Methods We included 158 incident cases of colorectal cancer and 563 randomly chosen control subjects from 28,345 women in the Women’s Health Study aged 45 or older who provided blood samples and had no history of cancer or cardiovascular disease at baseline in 1993. All cases and controls were Caucasians of European descent. A total of 63 tagging and putative functional SNPs in the 5 genes were included for analysis. Unconditional logistic regression was used to estimate odds ratio (ORs) and 95% confidence intervals (CIs). Results There was no association between variation in ESR1, ESR2, PGR, CYP19A1 and HSD17B2 and colorectal cancer risk after correction for multiple comparisons ( p values after correction ≥0.25). There was also no association with any of the haplotypes examined ( p  ≥ 0.15) and no evidence of joint effects of variants in the 5 genes ( p  ≥ 0.51). Conclusion Our data offer insufficient support for an association between variation in ESR1, ESR2, PGR, CYP19A1, and HSD17B2 and risk for developing colorectal cancer.
Author Manson, JoAnn E.
Lee, I-Min
Giovannucci, Edward
Cook, Nancy R.
Zhang, Shumin M.
Lin, Jennifer
Zee, Robert Y. L.
Liu, Kuang-Yu
Buring, Julie E.
AuthorAffiliation 2 Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
3 Department of Epidemiology, Harvard School of Public Health, Boston, MA
1 Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
5 Department of Ambulatory Care and Prevention, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
4 Department of Nutrition, Harvard School of Public Health, Boston, MA
AuthorAffiliation_xml – name: 2 Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
– name: 4 Department of Nutrition, Harvard School of Public Health, Boston, MA
– name: 1 Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
– name: 3 Department of Epidemiology, Harvard School of Public Health, Boston, MA
– name: 5 Department of Ambulatory Care and Prevention, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
Author_xml – sequence: 1
  fullname: Lin, Jennifer
– sequence: 2
  fullname: Zee, Robert Y. L
– sequence: 3
  fullname: Liu, Kuang-Yu
– sequence: 4
  fullname: Zhang, Shumin M
– sequence: 5
  fullname: Lee, I-Min
– sequence: 6
  fullname: Manson, JoAnn E
– sequence: 7
  fullname: Giovannucci, Edward
– sequence: 8
  fullname: Buring, Julie E
– sequence: 9
  fullname: Cook, Nancy R
BackLink https://www.ncbi.nlm.nih.gov/pubmed/20148360$$D View this record in MEDLINE/PubMed
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Issue 6
Keywords Estrogen receptors
Sex hormone genes
Progesterone receptor
CYP19A1
Colorectal cancer
HSD17B2
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Snippet Objectives Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which...
Objectives Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which...
Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which sex...
Objectives: Several lines of evidence have suggested that female hormones may lower the risk for developing colorectal cancer. However, the mechanisms by which...
SourceID pubmedcentral
proquest
pubmed
crossref
springer
jstor
fao
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 897
SubjectTerms Aged
Ambulatory care
Biomedical and Life Sciences
Biomedicine
Breast cancer
Cancer Research
Cardiovascular disease
Colorectal cancer
colorectal neoplasms
Colorectal Neoplasms - genetics
CYP19A1
Cytochrome
Dehydrogenases
Disease prevention
Endocrine therapy
Enzymes
Epidemiology
Estradiol Dehydrogenases
Estradiol Dehydrogenases - genetics
Estrogen receptors
Estrogens
Ethnicity
Ethnicity - genetics
Female
Females
Genes
Genetic loci
Genetic Variation
Genetic Variation - genetics
genetics
Gonadal Steroid Hormones
Gonadal Steroid Hormones - genetics
Haplotypes
Health care
Hematology
Hormones
Hospitals
HSD17B2
Humans
Logistic Models
Middle Aged
Odds Ratio
Oncology
Original Paper
Polymorphism, Single Nucleotide
Postmenopause
Preventive medicine
Progesterone receptor
Public Health
Receptors
Receptors, Estrogen
Receptors, Estrogen - genetics
Receptors, Progesterone
Receptors, Progesterone - genetics
Receptors, Steroid
Receptors, Steroid - genetics
Risk Factors
Sex hormone genes
Sex hormones
Steroids
Tumors
White People
White People - genetics
Womens health
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Title Genetic variation in sex-steroid receptors and synthesizing enzymes and colorectal cancer risk in women
URI https://www.jstor.org/stable/40645686
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Volume 21
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