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  • COLORECTAL-CANCER  (5)
  • 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: RECEPTOR ; CANCER ; tumor ; Germany ; MODEL ; MODELS ; CT ; DEATH ; RISK ; GENE ; GENES ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; ACID ; NUMBER ; colorectal cancer ; COLORECTAL-CANCER ; COLON-CANCER ; LINKAGE DISEQUILIBRIUM ; FATTY-ACIDS ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; nutrition ; ARACHIDONIC-ACID ; PPAR-GAMMA ; signaling ; ONCOLOGY ; REGRESSION ; FRAMEWORK ; VARIANT ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; HAPLOTYPE ; prospective ; fish consumption ; GENOME-WIDE ASSOCIATION ; GENETIC-VARIATION ; Genetic ; POPULATION STRATIFICATION ; COMMON POLYMORPHISMS ; single nucleotide ; ASPIRIN-INTOLERANT ASTHMA ; METABOLIZING GENES ; PROSTAGLANDIN-E
    Abstract: Colorectal cancer (CRC) is the third most common malignant tumor and the fourth leading cause of cancer death worldwide. The crucial role of fatty acids for a number of important biological processes suggests a more in-depth analysis of inter-individual differences in fatty acid metabolizing genes as contributing factor to colon carcinogenesis. We examined the association between genetic variability in 43 fatty acid metabolism-related genes and colorectal risk in 1225 CRC cases and 2032 controls participating in the European Prospective Investigation into Cancer and Nutrition study. Three hundred and ninety two single-nucleotide polymorphisms were selected using pairwise tagging with an r(2) cutoff of 0.8 and a minor allele frequency of 〉 5%. Conditional logistic regression models were used to estimate odds ratios and corresponding 95% confidence intervals. Haplotype analysis was performed using a generalized linear model framework. On the genotype level, hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD), phospholipase A2 group VI (PLA2G6) and transient receptor potential vanilloid 3 were associated with higher risk for CRC, whereas prostaglandin E receptor 2 (PTGER2) was associated with lower CRC risk. A significant inverse association (P 〈 0.006) was found for PTGER2 GGG haplotype, whereas HPGD AGGAG and PLA2G3 CT haplotypes were significantly (P 〈 0.001 and P = 0.003, respectively) associated with higher risk of CRC. Based on these data, we present for the first time the association of HPGD variants with CRC risk. Our results support the key role of prostanoid signaling in colon carcinogenesis and suggest a relevance of genetic variation in fatty acid metabolism-related genes and CRC risk
    Type of Publication: Journal article published
    PubMed ID: 20042636
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  • 3
    Keywords: COLORECTAL-CANCER ; DNA methylation ; ALCOHOL-CONSUMPTION ; CALIBRATION ; RECALL ; EPIC PROJECT ; COGNITIVE IMPAIRMENT ; NEURAL-TUBE DEFECTS ; FOLIC-ACID FORTIFICATION ; VITAMIN-B-12 STATUS
    Abstract: Folate plays an important role in the synthesis and methylation of DNA as a cofactor in one-carbon metabolism. Inadequate folate intake has been linked to adverse health events. However, comparable information on dietary folate intake across European countries has never been reported. The objective of the present study was to describe the dietary folate intake and its food sources in ten countries in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. A cross-sectional analysis was conducted in 36 034 participants (aged 35-74 years) who completed a single 24 h dietary recall using a computerised interview software program, EPIC-Soft (R) (International Agency for Research on Cancer, Lyon). Dietary folate intake was estimated using the standardised EPIC Nutrient DataBase, adjusted for age, energy intake, weight and height and weighted by season and day of recall. Adjusted mean dietary folate intake in most centres ranged from 250 to 350 mu g/d in men and 200 to 300 mu g/d in women. Folate intake tended to be lower among current smokers and heavier alcohol drinkers and to increase with educational level, especially in women. Supplement users (any types) were likely to report higher dietary folate intake in most centres. Vegetables, cereals and fruits, nuts and seeds were the main contributors to folate intake. Nonetheless, the type and pattern of consumption of these main food items varied across the centres. These first comparisons of standardised dietary folate intakes across different European populations show moderate regional differences (except the UK health conscious group), and variation by sex, educational level, smoking and alcohol-drinking status, and supplement use.
    Type of Publication: Journal article published
    PubMed ID: 22040523
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  • 4
    Keywords: BREAST-CANCER ; COLORECTAL-CANCER ; PROSTATE-CANCER ; STOMACH ; DIETARY-INTAKE ; EPIDEMIOLOGIC EVIDENCE ; HELICOBACTER-PYLORI INFECTION ; MEAT CONSUMPTION ; NUTRIENT INTAKE PATTERNS ; PROSPECTIVE COHORT
    Abstract: BACKGROUND: Epidemiologic data suggest that diet is a risk factor in the etiology of gastric cancer. However, the role of dietary fatty acids, a modifiable risk factor, remains relatively unexplored. OBJECTIVE: The objective of this study was to determine the association of plasma phospholipid fatty acid concentrations, as biomarkers of exogenous and endogenously derived fatty acids, with the risk of gastric adenocarcinoma in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition-Europe Gastric Cancer (EPIC-EURGAST). DESIGN: Fatty acids were measured by gas chromatography in prediagnostic plasma phospholipids from 238 cases matched to 626 controls by age, sex, study center, and date of blood donation. Conditional logistic regression models adjusted for Helicobacter pylori infection status, BMI, smoking, physical activity, education, and energy intake were used to estimate relative cancer risks. RESULTS: Positive risk associations for gastric cancer were observed in the highest compared with the lowest quartiles of plasma oleic acid (OR: 1.72; 95% CI: 1.01, 2.94), di-homo-gamma-linolenic acid (OR: 1.92; 95% CI: 1.10, 3.35), alpha-linolenic acid (OR: 3.20; 95% CI: 1.70, 6.06), and the ratio of MUFAs to saturated fatty acids, as an indicator of stearoyl-CoA desaturase-1 enzyme activity (OR: 1.40; 95% CI: 0.81, 2.43). An inverse risk association was observed with the ratio of linoleic to alpha-linolenic acid (OR: 0.37; 95% CI: 0.20, 0.66). CONCLUSION: These data suggest that a specific prediagnostic plasma phospholipid fatty acid profile, characterized mainly by high concentrations of oleic acid, alpha-linolenic acid, and di-homo-gamma-linolenic acid, which presumably reflect both a complex dietary pattern and altered fatty acid metabolism, may be related to increased gastric cancer risk.
    Type of Publication: Journal article published
    PubMed ID: 21993438
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  • 5
    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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