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  • polymorphism  (7)
  • 1
    Keywords: CANCER ; MODEL ; PROSTATE ; DISEASE ; RISK ; GENE ; MARKER ; IMPACT ; BIOMARKERS ; ASSOCIATION ; LINKAGE ; polymorphism ; single nucleotide polymorphism ; SUSCEPTIBILITY ; VARIANTS ; STAGE ; IDENTIFICATION ; HEALTH ; SNP ; PROSTATE-CANCER ; MARKERS ; LINKAGE DISEQUILIBRIUM ; diabetes ; REPLICATION ; FUTURE ; DIABETES-MELLITUS ; ONCOLOGY ; VARIANT ; METAANALYSIS ; biomarker ; methods ; MULTIETHNIC COHORT ; LINKAGE-DISEQUILIBRIUM ; 8Q24 ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; genetic association ; SCAN ; Genetic ; COMMON VARIANTS ; Type ; single nucleotide ; RISK-ASSOCIATED LOCI
    Abstract: Background: Genome-wide association studies have identified multiple genetic variants associated with susceptibility to prostate cancer (PrCa). In the two-stage Cancer Genetic Markers of Susceptibility prostate cancer scan, a single-nucleotide polymorphism (SNP), rs10486567, located within intron 2 of JAZF1 gene on chromosome 7p15.2, showed a promising association with PrCa overall (P = 2.14 x 10(-6)), with a suggestion of stronger association with aggressive disease (P = 1.2 x 10(-7)). Methods: In the third stage of genome-wide association studies, we genotyped 106 JAZF1 SNPs in 10,286 PrCa cases and 9,135 controls of European ancestry. Results: The strongest association was observed with the initial marker rs10486567, which now achieves genome-wide significance [P = 7.79 x 10(-11); ORHET, 1.19 (95% confidence interval, 1.12-1.27); ORHOM, 1.37 (95% confidence interval, 1.20-1.56)]. We did not confirm a previous suggestion of a stronger association of rs10486567 with aggressive disease (P = 1.60 x 10(-4) for aggressive cancer, n = 4,597; P = 3.25 x 10(-8) for non-aggressive cancer, n = 4,514). Based on a multilocus model with adjustment for rs10486567, no additional independent signals were observed at chromosome 7p15.2. There was no association between PrCa risk and SNPs in JAZF1 previously associated with height (rs849140; P = 0.587), body stature (rs849141, tagged by rs849136; P = 0.171), and risk of type 2 diabetes and systemic lupus erythematosus (rs864745, tagged by rs849142; P = 0.657). Conclusion: rs10486567 remains the most significant marker for PrCa risk within JAZF1 in individuals of European ancestry. Impact: Future studies should identify all variants in high linkage disequilibrium with rs10486567 and evaluate their functional significance for PrCa. Cancer Epidemiol Biomarkers Prev; 19(5); 1349-55. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20406958
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  • 2
    Keywords: RECEPTOR ; CANCER ; COHORT ; RISK ; GENE ; MECHANISM ; MARKER ; RISK-FACTORS ; mechanisms ; BINDING ; CELL-LINES ; ASSOCIATION ; LINKAGE ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; prevention ; HEALTH ; WOMEN ; SNP ; risk factors ; prostate cancer ; PROSTATE-CANCER ; MARKERS ; cancer risk ; DATABASE ; REGION ; REGIONS ; LINKAGE DISEQUILIBRIUM ; nutrition ; POSTMENOPAUSAL WOMEN ; PROGRAM ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; LOCUS ; single-nucleotide ; BLOCKS ; DEHYDROEPIANDROSTERONE-SULFATE ; SEX-HORMONE LEVELS ; prospective ; RISK-FACTOR ; CANCER-RISK ; MULTIETHNIC COHORT ; ANDROGEN ; BASE-LINE CHARACTERISTICS ; CAG REPEAT POLYMORPHISM ; COMMON VARIANT ; LINKAGE-DISEQUILIBRIUM ; NURSES HEALTH ; POLYGLUTAMINE TRACTS ; POSSIBLE MECHANISMS ; RECEPTOR GENE ; SET ; VITAMIN-D-RECEPTOR
    Abstract: Introduction Androgens have been hypothesised to influence risk of breast cancer through several possible mechanisms, including their conversion to estradiol or their binding to the oestrogen receptor and/ or androgen receptor ( AR) in the breast. Here, we report on the results of a large and comprehensive study of the association between genetic variation in the AR gene and risk of breast cancer in the National Cancer Institute Breast and Prostate Cancer Cohort Consortium ( BPC3). Methods The underlying genetic variation was determined by first sequencing the coding regions of the AR gene in a panel of 95 advanced breast cancer cases. Second, a dense set of markers from the public database was genotyped in a panel of 349 healthy women. The linkage disequilibrium relationships ( blocks) across the gene were then identified, and haplotypetagging single nucleotide polymorphisms ( htSNPs) were selected to capture the common genetic variation across the locus. The htSNPs were then genotyped in the nested breast cancer cases and controls from the Cancer Prevention Study II, European Prospective Investigation into Cancer and Nutrition, Multiethnic Cohort, Nurses' Health Study, and Women's Health Study cohorts ( 5,603 breast cancer cases and 7,480 controls). Results We found no association between any genetic variation ( SNP, haplotype, or the exon 1 CAG repeat) in the AR gene and risk of breast cancer, nor were any statistical interactions with known breast cancer risk factors observed. Conclusion Among postmenopausal Caucasian women, common variants of the AR gene are not associated with risk of breast cancer
    Type of Publication: Journal article published
    PubMed ID: 16987421
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  • 3
    Keywords: CANCER ; PROSTATE ; COMMON ; CT ; SUPPORT ; COHORT ; POPULATION ; RISK ; GENE ; ASSOCIATION ; LINKAGE ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; SUSCEPTIBILITY ; ALPHA ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; ENCODES ; HEALTH ; WOMEN ; SNP ; MEN ; prostate cancer ; PROSTATE-CANCER ; LINE ; REGION ; LINKAGE DISEQUILIBRIUM ; POPULATIONS ; POSTMENOPAUSAL WOMEN ; SINGLE ; DEFICIENCY ; ONCOLOGY ; ASSOCIATIONS ; SNPs ; CANCER SUSCEPTIBILITY ; METAANALYSIS ; biomarker ; INTERVAL ; HAPLOTYPE ; HAPLOTYPES ; single-nucleotide ; USA ; HORMONES ; STEROID-HORMONES ; odds ratio ; cancer research ; MULTIETHNIC COHORT ; PREDICT ; steroids ; postmenopausal ; block ; HORMONE-LEVELS ; EXONS ; GENETIC-VARIATION ; ANDROGEN RECEPTOR GENE ; BRAZILIAN PATIENTS ; SERUM ANDROGENS
    Abstract: CYP17 encodes cytochrome p450c17 alpha, which mediates activities essential for the production of sex steroids. Common germ line variation in the CYP17 gene has been related to inconsistent results in breast and prostate cancer, with most studies focusing on the nonsynonymous single nucleotide polymorphism (SNP) T27C (rs743572). We comprehensively characterized variation in CYP17 by direct sequencing of exons followed by dense genotyping across the 58 kb region around CYP17 in five racial/ethnic populations. Two blocks of strong linkage disequilibrium were identified and nine haplotype-tagging SNPs, including T27C, were chosen to predict common haplotypes (R-h(2) 〉= 0.85). These haplotype-tagging SNPs were genotyped in 8,138 prostate cancer cases and 9,033 controls, and 5,333 breast cancer cases and 7,069 controls from the Breast and Prostate Cancer Cohort Consortium. We observed borderline significant associations with prostate cancer for rs2486758 [TC versus TT, odds ratios (OR), 1.07; 95% confidence intervals (95% Cl), 1.00-1.14; CC versus TT, OR, 1.09; 95% CI, 0.95-1.26; P trend = 0.04] and rs6892 (AG versus AA, OR, 1.08; 95% CI, 1.00-1.15; GG versus AA, OR, 1.11; 95% CI, 0.95-1.30; P trend = 0.03). We also observed marginally significant associations with breast cancer for rs4919687 (GA versus GG, OR, 1.04; 95% CI, 0.97-1.12, AA versus GG, OR, 1.17; 95% CI, 1.03-1.34; P trend = 0.03) and rs4919682 (CT versus CC, OR, 1.04; 95% CI, 0.97-1.12; TT versus CC, OR, 1.16; 95% CI, 1.01-1.33; P trend = 0.04). Common variation at CYP17 was not associated with circulating sex steroid hormones in men or postmenopausal women. Our findings do not support the hypothesis that common germ line variation in CYP17 makes a substantial contribution to postmenopausal breast or prostate cancer susceptibility
    Type of Publication: Journal article published
    PubMed ID: 18006912
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  • 4
    Keywords: CANCER ; human ; PATHWAY ; PATHWAYS ; DISEASE ; EPIDEMIOLOGY ; POPULATION ; RISK ; GENE ; GENES ; TUMOR-NECROSIS-FACTOR ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY ; LYMPHOMA ; case-control studies ; INDIVIDUALS ; ALCOHOL-CONSUMPTION ; B-CELL LYMPHOMA ; FACTOR-ALPHA ; CYTOKINE ; case-control study ; case control studies ; single-nucleotide ; single-nucleotide polymorphism ; GENOTYPE DATA ; pooled analysis ; INTERLEUKIN-10 ; PROMOTER POLYMORPHISMS ; BIOLOGICAL IMPLICATIONS
    Abstract: Background Common genetic variants in immune and inflammatory response genes can affect the risk of developing non-Hodgkin lymphoma. We aimed to test this hypothesis using previously unpublished data from eight European, Canadian, and US case-control studies of the International Lymphoma Epidemiology Consortium (InterLymph). Methods We selected 12 single-nucleotide polymorphisms for analysis, on the basis of previous functional or association data, in nine genes that have important roles in lymphoid development, Th1/Th2 balance, and proinflammatory or anti-inflammatory pathways (IL1A, IL1RN, IL1B, IL2, IL6, IL10, TNF, LTA, and CARD15). Genotype data for one or more single-nucleotide polymorphisms were available for 3586 cases of non-Hodgkin lymphoma and for 4018 controls, and were assessed in a pooled analysis by use of a random-effects logistic regression model. Findings The tumour necrosis factor (TNF) -308G -〉 A polymorphism was associated with increased risk of nonHodgkin lymphoma (p for trend=0 . 005), particularly for diffuse large B-cell lymphoma, the main histological subtype (odds ratio 1 . 29 [95% CI 1 . 10-1 . 51] for GA and 1.65 [1 . 16-2 . 34] for AA, p for trend 〈 0 . 0001), but not for follicular lymphoma. The interleukin 10 (IL10) -3575T -〉 A polymorphism was also associated with increased risk of non-Hodgkin lymphoma (p for trend=0 . 02), again particularly for diffuse large B-cell lymphoma (p for trend=0 . 006). For individuals homozygous for the TNF -308A allele and carrying at least one IL 10 -3575A allele, risk of diffuse large B-cell lymphoma doubled (2 . 13 [1 . 37-3 . 32], p=0 . 00083). Interpretation Common polymorphisms in TNF and IL10, key cytokines for the inflammatory response and Th1/Th2 balance, could be susceptibility loci for non-Hodgkin lymphoma. Moreover, our results underscore the importance of consortia for investigating the genetic basis of chronic diseases like cancer
    Type of Publication: Journal article published
    PubMed ID: 16389181
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  • 5
    Keywords: CANCER ; PROSTATE ; COHORT ; RISK ; polymorphism ; POLYMORPHISMS ; BREAST ; breast cancer ; BREAST-CANCER ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; LEVEL ; IGFBP3 ; CANCER-RISK ; IGFBP-3 ; PREDICT ; IGF1 ; breast cancer risk ; CONSORTIUM
    Type of Publication: Journal article published
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  • 6
    Keywords: RECEPTOR ; CANCER ; CELLS ; proliferation ; CELL ; MODEL ; MODELS ; PATHWAY ; PROSTATE ; THERAPY ; DIAGNOSIS ; COHORT ; HISTORY ; RISK ; GENE ; GENES ; PROTEIN ; PROTEINS ; FAMILY ; IMPACT ; INDEX ; CARCINOGENESIS ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; BREAST ; breast cancer ; BREAST-CANCER ; NO ; STAGE ; PATTERNS ; family history ; WOMEN ; SNP ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; REGION ; REGIONS ; LINKAGE DISEQUILIBRIUM ; BINDING-PROTEINS ; body mass index ; POSTMENOPAUSAL WOMEN ; BINDING PROTEIN ; ANIMAL-MODELS ; BODIES ; IGF-I ; REGRESSION ; FAMILIES ; PATTERN ; THERAPIES ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; LEVEL ; analysis ; HAPLOTYPE ; HAPLOTYPES ; MASS ; ANIMAL-MODEL ; IGFBP3 ; FAMILY-HISTORY ; CANCER-RISK ; animal ; IGFBP-3 ; PREDICT ; animal model ; BINDING PROTEINS ; postmenopausal ; block ; IGF1 ; modification ; body mass ; animal models ; breast cancer risk ; CONSORTIUM ; NUCLEOTIDE ; hormone therapy ; effect modification ; MENOPAUSAL STATUS
    Abstract: IGF-1 has been shown to promote proliferation of normal epithelial breast cells, and the IGF pathway has also been linked to mammary carcinogenesis in animal models. We comprehensively examined the association between common genetic variation in the IGF1, IGFBP1, and IGFBP3 genes in relation to circulating IGF-I and IGFBP-3 levels and breast cancer risk within the NCI Breast and Prostate Cancer Cohort Consortium (BPC3). This analysis included 6,912 breast cancer cases and 8,891 matched controls (n = 6,410 for circulating IGF-I and 6,275 for circulating IGFBP-3 analyses) comprised primarily of Caucasian women drawn from six large cohorts. Linkage disequilibrium and haplotype patterns were characterized in the regions surrounding IGF1 and the genes coding for two of its binding proteins, IGFBP1 and IGFBP3. In total, thirty haplotype-tagging single nucleotide polymorphisms (htSNP) were selected to provide high coverage of common haplotypes; the haplotype structure was defined across four haplotype blocks for IGF1 and three for IGFBP1 and IGFBP3. Specific IGF1 SNPs individually accounted for up to 5% change in circulating IGF-I levels and individual IGFBP3 SNPs were associated up to 12% change in circulating IGFBP-3 levels, but no associations were observed between these polymorphisms and breast cancer risk. Logistic regression analyses found no associations between breast cancer and any htSNPs or haplotypes in IGF1, IGFBP1, or IGFBP3. No effect modification was observed in analyses stratified by menopausal status, family history of breast cancer, body mass index, or postmenopausal hormone therapy, or for analyses stratified by stage at diagnosis or hormone receptor status. In summary, the impact of genetic variation in IGF1 and IGFBP3 on circulating IGF levels does not appear to substantially influence breast cancer risk substantially among primarily Caucasian postmenopausal women
    Type of Publication: Journal article published
    PubMed ID: 18596909
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  • 7
    Keywords: CANCER ; GROWTH ; proliferation ; PATHWAY ; PROSTATE ; COHORT ; DISEASE ; HISTORY ; RISK ; GENE ; GENES ; FAMILY ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; STAGE ; AGE ; OVARIAN-CANCER ; SNP ; MEN ; PROSTATE-CANCER ; FACTOR-I ; CELL-MIGRATION ; PHOSPHOINOSITIDE 3-KINASE ; signaling ; ONCOLOGY ; REGRESSION ; ASSOCIATIONS ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; GROWTH-FACTOR-I ; BINDING PROTEIN-3 ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; PHOSPHATIDYLINOSITOL 3-KINASE ; FACTOR (IGF)-I ; pooled analysis ; FAMILY-HISTORY ; INCREASED RISK ; CANCER-RISK ; genetic association ; single nucleotide ; REGULATORY SUBUNIT
    Abstract: The phosphatidylinositol 3-kinase (PI3K) pathway regulates various cellular processes, including cellular proliferation and intracellular trafficking, and may affect prostate carcinogenesis. Thus, we explored the association between single-nucleotide polymorphisms (SNP) in PI3K genes and prostate cancer. Pooled data from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium were examined for associations between 89 SNPs in PI3K genes (PIK3C2B, PIK3AP1, PIK3C2A, PIK3CD, and PIK3R3) and prostate cancer risk in 8,309 cases and 9,286 controls. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using logistic regression. SNP rs7556371 in PIK3C2B was significantly associated with prostate cancer risk [ORper (allele), 1.08 (95% CI, 1.03-1.14); P-trend = 0.0017] after adjustment for multiple testing (P-adj = 0.024). Simultaneous adjustment of rs7556371 for nearby SNPs strengthened the association [ORper (allele), 1.21 (95% CI, 1.09-1.34); P-trend = 0.0003]. The adjusted association was stronger for men who were diagnosed before the age of 65 years [ORper (allele), 1.47 (95% CI, 1.20-1.79); P-trend = 0.0001] or had a family history [ORper (allele) = 1.57 (95% CI, 1.11-2.23); P-trend = 0.0114], and was strongest in those with both characteristics [ORper (allele) = 2.31 (95% CI, 1.07-5.07), P-interaction = 0.005]. Increased risks were observed among men in the top tertile of circulating insulin-like growth factor-I (IGF-I) levels [ORper (allele) = 1.46 (95% CI, 1.04-2.06); P-trend = 0.075]. No differences were observed with disease aggressiveness (Gleason grade = 8 or stage T-3/T-4 or fatal). In conclusion, we observed a significant association between PIK3C2B and prostate cancer risk, especially for familial, early-onset disease, which may be attributable to IGF-dependent PI3K signaling. Cancer Res; 70(6); 2389-96. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20197460
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