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  • BREAST  (12)
  • 1
    Keywords: ENERGIES ; CANCER ; Germany ; human ; MODEL ; MODELS ; FOLLOW-UP ; COHORT ; EPIDEMIOLOGY ; RISK ; RISK-FACTORS ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; TRIAL ; hormone ; HEALTH ; ENERGY ; AGE ; WOMEN ; HORMONE REPLACEMENT THERAPY ; OBESITY ; risk factors ; COUNTRIES ; cancer risk ; RISK FACTOR ; EPIC ; EPIC study ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; POSTMENOPAUSAL WOMEN ; MASS INDEX ; PH ; WEIGHT ; body weight ; fat distribution ; HEIGHT ; ADIPOSITY ; breast neoplasm ; HORMONE-REPLACEMENT THERAPY ; METAANALYSIS
    Abstract: The evidence for anthropometric factors influencing breast cancer risk is accumulating, but uncertainties remain concerning the role of fat distribution and potential effect modifiers. We used data from 73,542 premenopausal and 103,344 postmenopausal women from 9 European countries, taking part in the EPIC study. RRs from Cox regression models were calculated, using measured height, weight, BMI and waist and hip circumferences; categorized by cohort wide quintiles; and expressed as continuous variables, adjusted for study center, age and other risk factors. During 4.7 years of follow-up, 1,879 incident invasive breast cancers were identified. In postmenopausal women, current HRT modified the body size-breast cancer association. Among nonusers, weight, BMI and hip circumference were positively associated with breast cancer risk (all P-trend less than or equal to 0.002); obese women (BMI 〉 30) had a 31% excess risk compared to women with BMI 〈 25. Among HRT users, body measures were inversely but nonsignificantly associated with breast cancer. Excess breast cancer risk with HRT was particularly evident among lean women. Pooled RRs per height increment of 5 cm were 1.05 (95% CI 1.00-1.16) in premenopausal and 1.10 (95% CI 1.05-1.16) in postmenopausal women. Among premenopausal women, hip circumference was the only other measure significantly related to breast cancer (P-trend = 0.03), after accounting for BMI. In postmenopausal women not taking exogenous hormones, general obesity is a significant predictor of breast cancer, while abdominal fat assessed as waist-hip ratio or waist circumference was not related to excess risk when adjusted for BMI. Among premenopausal women, weight and BMI showed nonsignificant inverse associations with breast cancer. (C) 2004 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15252848
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  • 2
    Keywords: RECEPTOR ; CANCER ; GROWTH ; GROWTH-FACTOR ; proliferation ; tumor ; CELL-PROLIFERATION ; PATHWAY ; RISK ; GENE ; GENES ; PROTEIN ; TUMORS ; RELEASE ; PATIENT ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; COLORECTAL-CANCER ; PROSTATE-CANCER ; cancer risk ; case-control studies ; SOMATOSTATIN ; CANCER PATIENTS ; nutrition ; FACTOR-I ; BINDING PROTEIN ; SERUM ; SINGLE ; IGF-I ; BINDING-PROTEIN ; case-control study ; ASSOCIATIONS ; RE ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; cell proliferation ; development ; GROWTH-FACTOR-I ; BINDING PROTEIN-3 ; LEVEL ; case control studies ; GENOTYPE DATA ; FACTOR (IGF)-I ; PREMENOPAUSAL WOMEN ; IGFBP3 ; insulin-like growth factor ; PLASMA-LEVELS ; SERUM-LEVELS
    Abstract: Insulin-like growth factor-I (IGF-I) stimulates cell proliferation and can enhance the development of tumors in different organs. Epidemiologic studies have shown that an elevated level of circulating IGF-I is associated to increased risk of breast cancer as well as other cancers. Genetic variants affecting the release or biological action of growth hormone (GH), the main stimulator of IGF-I production, may predict circulating levels of IGF-I and have an effect on cancer risk. We tested this hypothesis with a large case-control study of 807 breast cancer patients and 1,588 matched control subjects nested within the European Prospective Investigation into Cancer and Nutrition. We genotyped 22 common single nucleotide polymorphisms in 10 genes involved in GH production and action (GHRH, GHRHR, SST, SSTR1-SSTR5, POU1F1, and GH1), and in parallel, we measured serum levels of IGF-I and IGFBP-3, its major binding protein, in samples of cases and controls. SST and SSTR2 polymorphisms showed weak but statistically significant associations with breast cancer risk. SSTR5 polymorphisms were associated with IGF-I levels, whereas one polymorphism in GHRHR and one in POU1F1 were associated with IGFBP-3 levels. Our conclusion is that common genetic variation in the GH synthesis pathway, as measured by single nucleotide polymorphisms selected in the present study, is not a major determinant of IGF-I and IGFBP-3 circulating levels, and it does not play a major role in altering breast cancer risk
    Type of Publication: Journal article published
    PubMed ID: 16214911
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  • 3
    Keywords: CANCER ; BLOOD ; MODEL ; MODELS ; COHORT ; RISK ; RISKS ; PATIENT ; RISK-FACTORS ; BINDING ; CYCLE ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; WOMEN ; risk factors ; cancer risk ; case-control studies ; EPIC ; nutrition ; ESTRADIOL ; SERUM ; SINGLE ; DEFICIENCY ; case-control study ; ASSOCIATIONS ; RE ; MAMMARY-GLAND ; ESTROGEN ; case control studies ; INTERVAL ; TESTS ; RANDOMIZED CONTROLLED-TRIAL ; PREMENOPAUSAL WOMEN ; SERUM-LEVELS ; ADRENAL ANDROGENS ; ESTROGEN PLUS PROGESTIN ; FEMALE NOBLE RATS ; HEALTHY POSTMENOPAUSAL WOMEN ; HORMONE LEVELS ; ONE-YEAR PERIOD ; REPLACEMENT THERAPY
    Abstract: Background. Contrasting etiologic hypotheses about the role of endogenous sex steroids in breast cancer development among premenopausal women implicate ovarian androgen excess and progesterone deficiency, estrogen excess, estrogen and progesterone excess, and both an excess or lack of adrenal androgens (dehydroepiandrosterone [DHEA] or its sulfate [DHEAS]) as risk factors. We conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort to examine associations among premenopausal serum concentrations of sex steroids and subsequent breast cancer risk. Methods: Levels of DHEAS, (Delta 4-)androstenedione, testosterone, and sex hormone binding globulin (SHBG) were measured in single prediagnostic serum samples from 370 premenopausal women who subsequently developed breast cancer (case patients) and from 726 matched cancer-free control subjects. Levels of progesterone, estrone, and estradiol were also measured for the 285 case patients and 555 matched control subjects who had provided information about the day of menstrual cycle at blood donation. Conditional logistic regression models were used to estimate relative risks of breast cancer by quartiles of hormone concentrations. All statistical tests were two-sided. Results: Increased risks of breast cancer were associated with elevated serum concentrations of testosterone (odds ratio [OR] for highest versus lowest quartile = 1.73, 95% confidence interval [CI] = 1.16 to 2.57; P-trend =.01), androstenedione (OR for highest versus lowest quartile = 1.569 95% CI = 1.05 to 2.32; P-trend =.01), and DHEAS (OR for highest versus lowest quartile = 1.48, 95% CI = 1.02 to 2.14; P-trend =.10) but not SHBG. Elevated serum progesterone concentrations were associated with a statistically significant reduction in breast cancer risk (OR for highest versus lowest quartile = 0.61, 95% CI = 0.38 to 0.98; P-trend =.06). The absolute risk of breast cancer for women younger than 40 followed up for 10 years was estimated at 2.6% for those in the highest quartile of serum testosterone versus 1.5% for those in the lowest quartile; for the highest and lowest quartiles of progesterone, these estimates were 1.7% and 2.6%, respectively. Breast cancer risk was not statistically significantly associated with serum levels
    Type of Publication: Journal article published
    PubMed ID: 15900045
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  • 4
    Keywords: CANCER ; BLOOD ; EXPOSURE ; RISK ; BINDING ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; HEALTH ; WOMEN ; DIETARY ; UNITED-STATES ; ALCOHOL ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; EPIC ; nutrition ; QUESTIONNAIRE ; IMMUNOASSAYS ; immunoassay ; LIFE-STYLE FACTORS ; dehydroepiandrosterone ; POSTMENOPAUSAL WOMEN ; SERUM ; ONCOLOGY ; RE ; EPIC PROJECT ; LEVEL ; methods ; PREMENOPAUSAL WOMEN ; SERUM-LEVELS ; alcohol consumption ; PREMENOPAUSAL ; prospective ; BINDING GLOBULIN ; CIRCULATING LEVELS ; intake ; steroids ; HORMONE CONCENTRATIONS ; alcohol intake ; ESTRADIOL LEVELS ; post-menopausal women ; pre-menopausal ; SERUM HORMONE CONCENTRATIONS ; sex steroids
    Abstract: Objective Women with a moderate intake of alcohol have higher concentrations of sex steroids in serum, and higher risk of developing breast cancer, compared to non-drinkers. In the present study, we investigate the relationships between alcohol consumption and serum levels of sex steroids and sex-hormone binding globulin (SHBG) in 790 pre- and 1,291 post-menopausal women, who were part of the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods Serum levels of testosterone (T), androstenedione (Delta(4)), dehydroepiandrosterone sulphate (DHEAS), estrone (E-1), estradiol (E-2) and SHBG were measured by direct immunoassays. Free T (fT) and free E-2 (fE(2)) were calculated according to mass action laws. Current alcohol intake exposure to alcohol was assessed from dietary questionnaires. Results Pre-menopausal women who consumed more than 25 g/day of alcohol had about 30% higher DHEAS, T and fT, 20% higher Delta(4) and about 40% higher E-1, concentrations compared to women who were non-consumers. E-2, fE(2) and SHBG concentrations showed no association with current alcohol intake. In post-menopausal women, DHEAS, fT, T, Delta(4), and E-1 concentrations were between 10% and 20% higher in women who consumed more than 25 g/day of alcohol compared to non-consumers. E-2 or fE(2) were not associated with alcohol intake at all. SHBG levels were about 15% lower in alcohol consumers compared to non-consumers. Conclusion This study supports the hypothesis of an influence of alcohol intake on sex hormone concentrations in blood
    Type of Publication: Journal article published
    PubMed ID: 16933054
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  • 5
    Keywords: CANCER ; GROWTH ; GROWTH-FACTOR ; BLOOD ; DENSITY ; COHORT ; NEW-YORK ; RISK ; GENE ; SAMPLE ; SAMPLES ; TISSUE ; primary ; RISK-FACTORS ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; BREAST ; breast cancer ; BREAST-CANCER ; CARE ; DESIGN ; WOMEN ; SNP ; risk factors ; PROSTATE-CANCER ; cancer risk ; RECRUITMENT ; BINDING-PROTEINS ; NETHERLANDS ; POSTMENOPAUSAL WOMEN ; menopause ; SERUM ; ONCOLOGY ; RE ; INCREASE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; GROWTH-FACTOR-I ; ALLELES ; LEVEL ; methods ; HAPLOTYPE ; GENOTYPE DATA ; USA ; PREMENOPAUSAL ; prospective study ; mammographic density ; RISK-FACTOR ; CANCER-RISK ; CIRCULATING LEVELS ; MULTIETHNIC COHORT ; Insulin-Like Growth Factor I ; NOV ; postmenopausal ; quantitative ; block ; breast density ; IGF1 ; breast cancer risk ; NUCLEOTIDE ; APOLIPOPROTEIN-E ISOFORMS ; Prospect-EPIC
    Abstract: Introduction High breast density is one of the strongest known risk factors for developing breast cancer. Insulin-like growth factor I (IGF-I) is a strong mitogen and has been suggested to increase breast cancer risk by increasing the amount of dense tissue in the female breast. Objectives We wanted to investigate the effect of common variation in the IGF-1 gene on serum IGF-I levels and on breast density. Design and methods Mammograms and blood samples of 1,928 premenopausal participants of the Dutch Prospect-EPIC cohort were collected at baseline. Using a haplotype tagging approach, 16 single nucleotide polymorphisms (SNP) from three blocks covering the IGF-1 gene were genotyped in all study participants. Breast density was assessed using a quantitative computer-assisted method. For a subgroup of women, who went through menopause within 5 years after recruitment (n = 656), premenopausal IGF-I levels and additionally postmenopausal breast density were determined. False positive report probabilities (FPRP) for statistically significant relations were calculated using the Wacholder method. Results The minor alleles of five SNPs in block 3 were significantly associated with elevated levels of IGF-I (rs9989002, rs2033178, rs7136446, rs978458, rs6220; P-values: 0.01-0.04). The same SNPs were related with modestly higher percent breast density before menopause and-in the subgroup of women that became postmenopausal during follow-up-with a modestly higher percent breast density after menopause. The most significant result, i.e. the relation between rs6220 and IGF-I levels, had an FPRP 〈 0.5 assuming prior probabilities of 0.01 and higher. Conclusion Common genetic variation in the IGF-1 gene is related to circulating levels of IGF-I, but the relationship with breast density is indecisive
    Type of Publication: Journal article published
    PubMed ID: 18064566
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  • 6
    Keywords: CANCER ; MODEL ; MODELS ; THERAPY ; EXPOSURE ; RISK ; RISKS ; METABOLISM ; tumour ; BINDING ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; prevention ; WOMEN ; cancer risk ; RELIABILITY ; case-control studies ; body mass index ; nutrition ; OSTEOPOROSIS ; ESTRADIOL ; dehydroepiandrosterone ; POSTMENOPAUSAL WOMEN ; MASSES ; SERUM ; ONCOLOGY ; case control study ; case-control study ; RE ; DHEA ; development ; LEVEL ; case control studies ; INTERVAL ; ADJUSTMENT ; MASS ; SERUM-LEVELS ; REPLACEMENT THERAPY ; COLLABORATIVE REANALYSIS ; DEHYDROEPIANDROSTERONE-SULFATE ; PREMENOPAUSAL ; SEX-HORMONE LEVELS ; TESTOSTERONE ; URINARY ANDROGENS
    Abstract: Considerable experimental and epidemiological evidence suggests that elevated endogenous sex steroids - notably androgens and oestrogens - promote breast tumour development. In spite of this evidence, postmenopausal androgen replacement therapy with dehydroepiandrosterone (DHEA) or testosterone has been advocated for the prevention of osteoporosis and improved sexual wellbeing. We have conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition. Levels of DHEA sulphate (DHEAS), (Delta 4-androstenedione), testosterone, oestrone, oestradiol and sex-hormone binding globulin (SHBG) were measured in prediagnostic serum samples of 677 postmenopausal women who subsequently developed breast cancer and 1309 matched control subjects. Levels of free testosterone and free oestradiol were calculated from absolute concentrations of testosterone, oestradiol and SHBG. Logistic regression models were used to estimate relative risks of breast cancer by quintiles of hormone concentrations. For all sex steroids the androgens as well as the oestrogens - elevated serum levels were positively associated with breast cancer risk, while SHBG levels were inversely related to risk. For the androgens, relative risk estimates (95% confidence intervals) between the top and bottom quintiles of the exposure distribution were: DHEAS 1.69 (1.23-2.33), androstenedione 1.94 (1.40-2.69), testosterone 1.85 (1.33-2.57) and free testosterone 2.50 (1.76-3.55). For the oestrogens, relative risk estimates were: oestrone 2.07 (1.42-3.02), oestradiol 2.28 (1.61-3.23) and free oestradiol (odds ratios 2.13 (1,52-2.98)). Adjustments for body mass index or other potential confounding factors did not substantially alter any of these relative risk estimates. Our results have shown that, among postmenopausal women, not only elevated serum oestrogens but also serum androgens are associated with increased breast cancer risk. Since DHEAS and androstenedione are largely of adrenal origin in postmenopausal women, our results indicated that elevated adrenal androgen synthesis is a risk factor for breast cancer. The results from this study caution against the use of DHEA(S), or other androgens, for postmenopausal androgen replacement therapy
    Type of Publication: Journal article published
    PubMed ID: 16322344
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  • 7
    Keywords: CANCER ; BLOOD ; COHORT ; cohort studies ; RISK ; TIME ; BINDING ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; WOMEN ; OBESITY ; cancer risk ; case-control studies ; BODY ; EPIC ; nutrition ; POSTMENOPAUSAL WOMEN ; insulin ; MASS INDEX ; SERUM ; case-control study ; RE ; INCREASE ; WEIGHT ; WAIST ; ESTROGEN ; LEVEL ; case control studies ; metabolic syndrome ; OVERWEIGHT ; HORMONES ; BMI ; EXTENT ; CANCER-RISK ; BODY-FAT DISTRIBUTION ; hip ; steroids ; FREE ESTRADIOL
    Abstract: In a large case-control study on breast cancer risk and serum hormone concentrations, nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, we examined to what extent the relationship of excess body weight with breast cancer risk may be explained by changes in sex steroids. Height, weight, waist and hip circumferences, and serum measurements of testosterone [T], androstenedione [Delta(4)], dehydroepiandrosterone sulphate [DHEAS], estradiol [E-2], estrone [E-1] and sex-hormone binding globulin [SHBG] were available for 613 breast cancer cases, and 1,139 matched controls, who were all menopausal at the time of blood donation. Free T [fT] and free E-2 [fE(2)] were calculated using mass action equations. Breast cancer risk was related to body mass index (BMI) (RR = 1.11 [0.99-1.25], per 5 kg/m(2) increase in BMI), and waist (RR = 1.12 [1.02-1.24], per 10 cm increase) and hip circumferences (RR = 1.14 [1.02-1.27], per 10 cm increase). The increase in breast cancer risk associated with adiposity was substantially reduced after adjustment for any estrogens, especially for fE(2) (from 1.11 [0.99-1.25] to 0.99 [0.87-1.12], from 1.12 [1.02-1.24] to 1.02 [0.92-1.14] and from 1.14 [1.02-1.27] to 1.05 [0.93-1.18] for BMI, waist and hip circumferences, respectively). A modest attenuation in excess risk was observed after adjustment for fT, but the remaining androgens had little effect on the association of body adiposity with breast cancer. Our data indicate that the relationship of adiposity with breast cancer in postmenopausal women could be partially explained by the increases in endogenous estrogens, and by a decrease in levels of SHBG. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16385576
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  • 8
    Keywords: CANCER ; BLOOD ; MODEL ; MODELS ; COHORT ; RISK ; TISSUE ; MARKER ; RATS ; CONTRAST ; BINDING ; BREAST ; breast cancer ; BREAST-CANCER ; AGE ; WOMEN ; REDUCED RISK ; cancer risk ; GLUCOSE ; EPIC ; nutrition ; POSTMENOPAUSAL WOMEN ; insulin ; SERUM ; IGF-I ; REGRESSION ; RE ; INCREASE ; WEIGHT ; GROWTH-FACTOR-I ; LEVEL ; INTERVAL ; pancreatic ; INSULIN-RESISTANCE ; SERUM-LEVELS ; MAMMARY-CARCINOMA ; prospective ; CANCER-RISK ; C-PEPTIDE ; steroids ; FREE ESTRADIOL ; HEPATIC EXTRACTION ; PLASMA-INSULIN ; SEX-HORMONES
    Abstract: It has been hypothesized that chronic hyperinsulinemia, a major metabolic consequence of physical inactivity and excess weight, might increase breast cancer risk by direct effects on breast tissue or indirectly by increasing bioavailable levels of testosterone and estradiol. Within the European Prospective Investigation into Cancer and Nutrition (EPIC), we measured serum levels of C-peptide-a marker for pancreatic insulin secretion-in a total of 1,141 incident cases of breast cancer and 2,204 matched control subjects. Additional measurements were made of serum sex hormone binding globulin (SHBG) and sex steroids. Conditional logistic regression models were used to estimate breast cancer risk for different levels of C-peptide. C-peptide was inversely correlated with SHBG and hence directly correlated with free testosterone among both pre and postmenopausal women. C-peptide and free estradiol also correlated positively, but only among postmenopausal women. Elevated serum C-peptide levels were associated with a nonsignificant reduced risk of breast cancer diagnosed up to the age of 50 years [odds ratio (OR) = 0.70, (95% confidence interval (CI), 0.39-1.24); P-trend = 0.05]. By contrast, higher levels of C-peptide were associated with an increase of breast cancer risk among women above 60 years of age, however only among those women who had provided a blood sample under nonfasting conditions [OR = 2.03, (95% CI, 1.20-3.43); P-trend = 0.011. Our results do not support the hypothesis that chronic hyperinsulinemia generally increases breast cancer risk, independently of age. Nevertheless, among older, postmenopausal women, 6yperinsulinemia might contribute to increasing breast cancer risk. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16572422
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  • 9
    Keywords: RECEPTOR ; CANCER ; GROWTH ; GROWTH-FACTOR ; Germany ; RISK ; GENE ; GENES ; PROTEIN ; LIGAND ; INDEX ; CARCINOGENESIS ; CELL-LINES ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; STIMULATION ; NUMBER ; cancer risk ; case-control studies ; EPIC ; nutrition ; FOOD ; FOOD-INTAKE ; insulin ; BODIES ; ONCOLOGY ; case-control study ; RE ; VARIANT ; INCREASE ; HEIGHT ; GROWTH-FACTOR-I ; LEVEL ; CANCER DEVELOPMENT ; single-nucleotide polymorphism ; MASS ; BODY-MASS INDEX ; IGFBP3 ; prospective ; CANCER-RISK ; CIRCULATING LEVELS ; ENGLAND ; IGFBP-3 ; FACTOR-BINDING ; body mass ; breast cancer risk ; European Prospective Investigation into Cancer ; genetic variants ; DES-ACYL GHRELIN ; EXTREMELY OBESE CHILDREN ; GROWTH-HORMONE SECRETAGOGUE ; HEALTHY NORMAL-WEIGHT ; LEU72MET POLYMORPHISM ; PLASMA GHRELIN ; PREPROGHRELIN ISOFORM
    Abstract: Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor, has two major functions: the stimulation of the growth hormone production and the stimulation of food intake. Accumulating evidence also suggests a role of ghrelin in cancer development. We conducted a case-control study on 1359 breast cancer cases and 2389 matched controls, nested within the European Prospective Investigation into Cancer and Nutrition, to examine the association of common genetic variants in the genes coding for ghrelin (GHRL) and its receptor (GHSR) with anthropometric measures, circulating insulin growth factor I (IGF-I) and insulin-like growth factor-binding protein 3 and breast cancer risk. Pair-wise tagging was used to select the 15 polymorphisms that represent the majority of common genetic variants across the GHRL and GHSR genes. A significant increase in breast cancer risk was observed in carriers of the GHRL rs171407-G allele (odds ratio: 1.2; 95% confidence interval: 1.0-1.4; P = 0.02). The GHRL single-nucleotide polymorphism rs375577 was associated with a 5% increase in IGF-I levels (P = 0.01). A number of GHRL and GHSR polymorphisms were associated with body mass index (BMI) and height (P between 〈 0.01 and 0.04). The false-positive report probability (FPRP) approach suggests that these results are noteworthy (FPRP 〈 0.20). The results presented here add to a growing body of evidence that GHRL variations are associated with BMI. Furthermore, we have observed evidence for association of GHRL polymorphisms with circulating IGF-I levels and with breast cancer risk. These associations, however, might also be due to chance findings and further large studies are needed to confirm our results
    Type of Publication: Journal article published
    PubMed ID: 18650939
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  • 10
    Keywords: CANCER ; GROWTH ; proliferation ; RISK ; GENE ; GENES ; PROTEIN ; PROTEINS ; PATIENT ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; BREAST ; breast cancer ; BREAST-CANCER ; WOMEN ; COLORECTAL-CANCER ; PROSTATE-CANCER ; cancer risk ; FACTOR-I ; SERUM ; IGF-I ; RE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; CANDIDATE GENES ; GROWTH-FACTOR-I ; LEVEL ; case control studies ; single-nucleotide ; GENOTYPE DATA ; FACTOR (IGF)-I ; PREMENOPAUSAL WOMEN ; PLASMA-LEVELS ; SERUM-LEVELS ; ALPHA-5-BETA-1 INTEGRIN ; C-PEPTIDE ; IGFALS ; IGFBP-1 ; IGFBP-3 ; MULTIETHNIC COHORT
    Abstract: Insulin-like growth factor I (IGF-1) stimulates cell proliferation and can enhance the development of tumours in different organs. Epidemiological studies have shown that an elevated level of circulating IGF-1 is associated with increased risk of breast cancer, as well as of other cancers. Most of circulating IGF-I is bound to an acid-labile subunit and to one of six insulin-like growth factor binding proteins (IGFBPs), among which the most important are IGFBP-3 and IGFBP-1. Polymorphisms of the IGF1 gene and of genes encoding for the major IGF-1 carriers may predict circulating levels of IGF-1 and have an impact on cancer risk. We tested this hypothesis with a case - control study of 807 breast cancer patients and 1588 matched control subjects, nested within the European Prospective Investigation into Cancer and Nutrition. We genotyped 23 common single nucleotide polymorphisms in IGF1, IGFBP1, IGFBP3 and IGFALS, and measured serum levels of IGF-1 and IGFBP-3 in samples of cases and controls. We found a weak but significant association of polymorphisms at the 50 end of the IGF1 gene with breast cancer risk, particularly among women younger than 55 years, and a strong association of polymorphisms located in the 50 end of IGFBP3 with circulating levels of IGFBP-3, which confirms previous findings. Common genetic variation in these candidate genes does not play a major role in altering breast cancer risk in Caucasians
    Type of Publication: Journal article published
    PubMed ID: 16404426
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