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  • case control studies  (19)
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  • 1
    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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  • 2
    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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  • 3
    Keywords: CANCER ; MODEL ; MODELS ; FOLLOW-UP ; RISK ; METABOLISM ; INDEX ; CARCINOGENESIS ; ASSOCIATION ; BREAST-CANCER ; NO ; hormone ; PLASMA ; NUMBER ; WOMEN ; OBESITY ; cancer risk ; ORAL-CONTRACEPTIVES ; cholesterol ; LIPOPROTEIN ; LOW-DENSITY-LIPOPROTEIN ; case-control studies ; ABNORMALITIES ; BODY ; DIABETES-MELLITUS ; EPIC ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; ENDOMETRIAL CANCER ; RELATIVE RISK ; REGRESSION-MODELS ; CLUSTER ; POSTMENOPAUSAL WOMEN ; MASS INDEX ; MASSES ; BODIES ; ONCOLOGY ; case control study ; case-control study ; REGRESSION ; ASSOCIATIONS ; ENDOMETRIAL ; RE ; INCREASE ; BODY-SIZE ; PHYSICAL-ACTIVITY ; LEVEL ; case control studies ; INTERVAL ; metabolic syndrome ; HORMONES ; prospective ; UNIT ; CANCER-RISK ; C-PEPTIDE ; SET ; case control ; LOGISTIC-REGRESSION ; BODY-MASS ; BODY-MASS-INDEX ; lipid ; HDL-CHOLESTEROL ; LOW-DENSITY ; SERUM-CHOLESTEROL
    Abstract: To clarify the role of metabolic factors in endometrial carcinogenesis, we conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), and examined the relation between prediagnostic plasma lipids, lipoproteins, and glucose, the metabolic syndrome (MetS; a cluster of metabolic factors) and endometrial cancer risk. Among pre- and postmenopausal women, 284 women developed endometrial cancer during follow-up. Using risk set sampling, 546 matched control subjects were selected. From conditional logistic regression models, high-density lipoprotein cholesterol (HDL-C) levels were inversely associated with risk body mass index (BMI)-adjusted relative risk (FR) for top versus bottom quartile 0.61 (95% confidence intervals (CI) 0.38-0.97), P-trend= 0.02). Glucose levels were positively associated with risk (BMI-adjusted RR top versus bottom quartile 1.69 (95% Cl 0.99-2.90), P-trend, = 0.03), which appeared stronger among postmenopausal women (BMI-adjusted RR top versus bottom tertile 2.61 (95% Cl 1.46-4.66), P-trend=0.0006, P-heterogeneity=0.13) and never-users of exogenous hormones (P-heterogeneity=0-005 for oral contraceptive (OC) use and 0.05 for hormone replacement therapy-use). The associations of HDL-C and glucose with risk were no longer statistically significant after further adjustment for obesity-related hormones. Plasma total cholesterol, Low-density lipoprotein cholesterol (LDL-C), and triglycerides were not significantly related to overall risk. The presence of MetS was associated with risk (RR 2.12 (95% CI 1.51-2.97)), which increased with the number of MetS factors (P-trend=0.02). An increasing number of MetS factors other than waist circumference, however, was marginally significantly associated with risk only in women with waist circumference above the median (P-interaction=0-01). None of the associations differed significantly by fasting status. These findings suggest that metabolic abnormalities and obesity may act synergistically to increase endometrial cancer risk
    Type of Publication: Journal article published
    PubMed ID: 17914105
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  • 4
    Keywords: CANCER ; BLOOD ; RISK ; ENZYMES ; GENE ; GENES ; ACTIVATION ; DNA ; CARCINOGENESIS ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; AGE ; CIGARETTE-SMOKING ; COUNTRIES ; GENOTYPES ; COLORECTAL CANCERS ; LINKAGE DISEQUILIBRIUM ; adenocarcinoma ; case-control studies ; TOBACCO ; GASTRIC-CANCER ; nutrition ; SMOKERS ; case-control study ; VARIANT ; TOBACCO-SMOKE ; GSTM1 ; GSTT1 ; gastric cancer ; S-TRANSFERASE M1 ; case control studies ; INTERVAL ; ENZYME ; GENETIC-POLYMORPHISM ; LOCUS ; FAMILY-HISTORY ; prospective ; ALLELE FREQUENCIES ; COMPOUND ; EPOXIDE HYDROLASE POLYMORPHISMS ; EUROPEAN COUNTRIES ; HIGH-INCIDENCE AREA ; INCREASED RISK ; NEVER SMOKERS ; odds ratio ; T1 NULL GENOTYPES ; tobacco smoke ; UNIT
    Abstract: Metabolizing enzymes, which often display genetic polymorphisms, are involved in the activation of compounds present in tobacco smoke that may be relevant to gastric carcinogenesis. We report the results of a study looking at the association between risk of gastric adenocarcinoma and polymorphisms in genes CYP1A1, CYP1A2, EPHX1, and GSTT1. A nested case-control study was carried out within the European Prospective Investigation into Cancer and Nutrition, developed in 10 European countries. The study includes 243 newly diagnosed cases of histologically confirmed gastric adenocarcinoma and 946 controls matched by center, age, sex, and date of blood collection. Genotypes were determined in nuclear DNA from WBCs. We found an increased risk of gastric cancer for homozygotes for C (histidine) variant in Y113H of EPHX1 (odds ratio, 1.91; 95% confidence interval, 1.19-3.07) compared with subjects with TC/TT. There was also a significant increased risk for smokers carrying at least one variant allele A in Ex7+129C 〉 A (m4) of CYP1A1 and never smokers with null GSTT1 and allele A in the locus -3859G 〉 A of CYP1A2. Most of these genes are involved in the activation and detoxification of polycyclic aromatic hydrocarbons, suggesting a potential role of these compounds in gastric carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 17164366
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  • 5
    Keywords: CANCER ; carcinoma ; FOLLOW-UP ; COHORT ; cohort study ; RISK ; SITE ; INFECTION ; ASSOCIATION ; antibodies ; WOMEN ; MEN ; COUNTRIES ; DIET ; STOMACH ; adenocarcinoma ; case-control studies ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; CALIBRATION ; case-control study ; INCREASE ; case control studies ; HELICOBACTER-PYLORI INFECTION ; prospective ; Helicobacter pylori ; intake ; FOODS
    Abstract: It is considered that fruit and vegetable (F&V) protect against oesophagus and gastric cancer (GC). However, 2 recent meta-analyses suggest that the strength of association on GC seems to he weaker for vegetables than for fruit and weaker in cohort than in case-control studies. No evidence exists from cohort studies about adenocarcinoma of oesophagus (ACO). In 521,457 men and women participating in the EPIC cohort in 10 European countries, information of diet and lifestyle was collected at baseline. After an average of 6.5 years of follow-up, a total of 330 GC and 65 ACO, confirmed and classified by a panel of pathologists, was used for the analysis. We examined the relation between F&V intake and GC and ACO. A calibration study in a sub-sample was used to control diet measurement errors. In a sub-sample of cases and a random sample of controls, antibodies against Helicobacter pylori (Hp) were measured and interactions with F&V were examined in a nested case-control study. We observed no association with total vegetable intake or specific groups of vegetables and GC risk, except for the intestinal type, where a negative association is possible regarding total vegetable (calibrated HR 0.66; 95% CI 0.35-1.22 per 100 g increase) and onion and garlic intake (calibrated HR 0.70; 95% CI 0.38-1.29 per 10 g increase). No evidence of association between fresh fruit intake and GC risk was observed. We found a negative but non significant association between citrus fruit intake and the cardia site (calibrated HR 0.77; 95% CI 0.47-1.22 per 100 g increase) while no association was observed with the non-cardia site. Regarding ACO, we found a non significant negative association for vegetable intake and for citrus intake (calibrated HRs 0.72; 95% Cl 0.32-1.64 and 0.77; 95% CI 0.46-1.28 per 100 and 50 g increase, respectively). It seems that lip infection does not modify the effect of F&V intake. Our study supports a possible protective role of vegetable intake in the intestinal type of GC and the ACO. Citrus fruit consumption may have a role in the protection against cardia GC and ACO. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16380980
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  • 6
    Keywords: CANCER ; FOLLOW-UP ; COHORT ; POPULATION ; RISK ; INFECTION ; CARCINOGENESIS ; ASSOCIATION ; WOMEN ; MEN ; cancer risk ; DOSE-RESPONSE ; DIETARY ; adenocarcinoma ; ADENOCARCINOMAS ; case-control studies ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; case-control study ; DIETARY FACTORS ; ASSOCIATIONS ; INCREASE ; case control studies ; INTERVAL ; prospective ; MEAT INTAKE ; RED MEAT ; JAPANESE ; Helicobacter pylori ; N-NITROSO COMPOUNDS
    Abstract: Background. Dietary factors are thought to have an important role in gastric and esophageal carcinogenesis, but evidence from cohort studies for such a role is lacking. We examined the risks of gastric cancer and esophageal adenocarcinoma associated with meat consumption within the European Prospective Investigation Into Cancer and Nutrition (EPIC) cohort. Methods: A total of 521 457 men and women aged 35-70 years in 10 European countries participated in the EPIC cohort. Dietary and lifestyle information was collected at recruitment. Cox proportional hazard models were used to examine associations between meat intake and risks of cardia and gastric noncardia cancers and esophageal adenocarcinoma. Data from a calibration substudy were used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. In a nested case-control study, we examined interactions between Helicobacter pylori infection status (i.e., plasma H. pylori antibodies) and meat intakes. All statistical tests were two-sided. Results: During a mean follow-up of 6.5 years, 330 gastric adenocarcinoma and 65 esophageal adenocarcinomas were diagnosed. Gastric noncardia cancer risk was statistically significantly associated with intakes of total meat (calibrated HR per 100-g/day increase = 3.52, 95%, CI = 1.96 to 6.34), red meat (calibrated HR per 50-g/day increase = 1.73; 95% CI = 1.03 to 2.88), and processed meat (calibrated HR per 50-g/day increase = 2.45; 95% CI = 1.43 to 4.21). The association between the risk of gastric noncardia cancer and total meat intake was especially large in H. pylori-infected subjects (odds ratio per 100-g/day increase = 5.32; 95% CI = 2.10 to 13.4). Intakes of total, red, or processed meat were not associated with the risk of gastric cardia cancer. A positive but non-statistically significant association was observed between esophageal adenocarcinoma cancer risk and total and processed meat intake in the calibrated model. In this study population, the absolute risk of development of gastric adenocarcinoma within 10 years for a study subject aged 60 years was 0.26% for the lowest quartile of total meat intake and 0.33% for the highest quartile of total meat intake. Conclusion: Total, red, and processed meat intakes were associated with an increased risk of gastric noncardia cancer, especially in H. pylori antibody-positive subjects, but not with cardia gastric cancer
    Type of Publication: Journal article published
    PubMed ID: 16507831
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  • 7
    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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  • 8
    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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  • 9
    Keywords: APOPTOSIS ; CANCER ; proliferation ; BLOOD ; CELL ; CELL-PROLIFERATION ; Germany ; MODEL ; MODELS ; COHORT ; RISK ; RISKS ; SITE ; PROTEIN ; PROTEINS ; colon ; BINDING ; ASSOCIATION ; NO ; resistance ; NUMBER ; AGE ; WOMEN ; colorectal cancer ; OBESITY ; COLORECTAL-CANCER ; COUNTRIES ; RATES ; cancer risk ; BINDING-PROTEINS ; DIET ; case-control studies ; DIABETES-MELLITUS ; EPIC ; nutrition ; FACTOR-I ; REGRESSION-MODELS ; physical activity ; BINDING PROTEIN ; insulin ; SERUM ; IGF-I ; ONCOLOGY ; BINDING-PROTEIN ; case-control study ; REGRESSION ; ASSOCIATIONS ; secretion ; BODY-SIZE ; PHYSICAL-ACTIVITY ; LEVEL ; biomarker ; case control studies ; pancreatic ; BLOOD-GLUCOSE ; INSULIN-RESISTANCE ; rectum ; USA ; prospective ; rectal cancer ; prospective study ; CANCERS ; CANCER-RISK ; C-PEPTIDE ; IGFBP-1 ; colorectal ; BINDING PROTEINS ; LOGISTIC-REGRESSION ; IGFBP-2 ; FACTOR BINDING PROTEIN-1 ; IGF ; insulin resistance ; GROWTH-FACTOR (IGF)-I
    Abstract: Western style diets and lifestyles are associated with increasing rates of obesity, diabetes and insulin resistance. Higher circulating insulin levels may modulate cell proliferation and apoptosis either directly or indirectly by increasing the bioactivity of IGF-I and decreasing the bioactivity of some of its binding proteins. The objective of this study was to determine the association of increasing levels of serum C-peptide, a biomarker of pancreatic insulin secretion, and IGF binding proteins (IGFBP) -1 and -2 with colorectal cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), a large cohort involving 10 Western European countries. A total of 1,078 colorectal cancer cases were matched (age, date of blood donation, fasting status, gender, study center) to an equal number of control subjects. Relative cancer risks were estimated using conditional logistic regression models. Serum C-peptide concentration was positively associated with an increased colorectal cancer risk for the highest versus the lowest quintile (OR = 1.56, 95% CI = 1.16-2.09, p(trend) 〈 0.01), which was slightly attenuated after adjustment for BMI and physical activity (OR = 1.37, 95% CI = 1.00-1.88, p(trend) = 0.10). When stratified by anatomical site, the cancer risk was stronger in the colon (OR 1.67, 95% CI = 1.14-2.46, p(trend) 〈 0.01) than in the rectum (OR 1.42, 95% CI = 0.90-2.25, p(trend) = 0.35). The cancer risk estimates were not heterogeneous by gender or fasting status. No clear colorectal cancer risk associations were observed for IGFBP-1 or -2. This large prospective study confirms that hyperinsulinemia, as determined by C-peptide levels, is associated with an increased colorectal cancer risk. (C) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17372899
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  • 10
    Keywords: CANCER ; tumor ; MODEL ; MODELS ; cohort study ; RISK ; TUMORS ; CARCINOGENESIS ; ASSOCIATION ; PATTERNS ; REDUCED RISK ; COUNTRIES ; FIBER ; DIETARY ; adenocarcinoma ; ADENOCARCINOMAS ; case-control studies ; CARDIA ; CONSUMPTION ; FRUIT ; GASTRIC-CANCER ; nutrition ; STOMACH-CANCER ; RELATIVE RISK ; dietary fiber ; nutrient intake ; ONCOLOGY ; case control study ; case-control study ; ASSOCIATIONS ; gastric cancer ; case control studies ; INTERVAL ; SUBTYPES ; USA ; UNIT ; CANCER-RISK ; gastric ; ESOPHAGEAL ; cereal fiber
    Abstract: Numerous case-control studies suggest dietary fiber may reduce risk of gastric cancer, but this has not been confirmed prospectively. A previous case-control study reported reduced risk of gastric cardia adenocarcinomas associated with cereal fiber, but not with fruit or vegetable fiber. To date, different food sources of fiber have not been examined with respect to noncardia tumors or diverse histologic sub-types. This study prospectively examines associations between fiber from different food sources and incident gastric adenocarcinomas (GC) among more than 435,000 subjects from 10 countries participating in the European Prespective Investigation into Cancer and Nutrition study. Subjects aged 25-70 years completed dietary questionnaires in 1992-98, and were followed up for a median of 6.7 years. About 312 incident GCs were observed. The relative risk of GC was estimated based on cohort-wide sex-specific fiber intake quartiles using proportional hazards models to estimate hazards ratios (HRs) and 95% confidence intervals (CIs). Intakes of cereal fiber, but not total, fruit or vegetable fiber, were associated with reduced GC risk [adjusted HR for the highest vs. lowest quartile of cereal fiber 0.69, 0.48-0.99]. There was a strong inverse association for diffuse [HR 0.43, 0.22-0.86], but not intestinal type [HR 0.98, 0.54-1.80] tumors. Associations for cardia vs. noncardia tumors were similar to those for overall GC, although cardia associations did not reach significance. Cereal fiber consumption may help to reduce risk of GC, particularly diffuse type tumors. Further study on different food sources of fiber in relation to GC risk is warranted to confirm these relationships
    Type of Publication: Journal article published
    PubMed ID: 17582605
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