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  • RISK  (20)
  • 1
    Keywords: Genetic ; colorectal ; RISK ; METABOLISM ; VARIABILITY
    Type of Publication: Book chapter
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  • 2
    Keywords: SUPPORT ; DISEASE ; RISK ; PROTEIN ; INDEX ; REDUCTION ; BODY-WEIGHT ; TRIAL ; HUMANS ; WOMEN ; OBESITY ; FAT ; C-REACTIVE PROTEIN ; TRENDS ; POSTMENOPAUSAL WOMEN ; exercise ; SERUM ; WEIGHT ; INTERLEUKIN-6 ; methods ; anthropometry ; OVERWEIGHT ; female ; INCREASED RISK ; BMI ; Aged ; Middle Aged ; WAIST CIRCUMFERENCE ; CONTROLLED-TRIAL ; WEIGHT-LOSS ; 3 ; INVESTIGATE ; C-REACTIVE-PROTEIN ; Abdominal ; *Exercise Therapy ; *Postmenopause ; AEROBIC EXERCISE ; C-Reactive Protein/*analysis ; Obesity/*physiopathology ; Serum Amyloid A Protein/analysis
    Abstract: PURPOSE: To investigate the effect of a yearlong moderate-intensity aerobic exercise intervention on C-reactive protein (CRP), serum amyloid A (SAA), and interleukin 6 (IL-6) among overweight or obese postmenopausal women. METHODS: In a randomized controlled trial, 115 postmenopausal, overweight or obese, sedentary women, aged 50-75 yr were randomized to an aerobic exercise intervention of moderate-intensity (60%-75% observed maximal HR), for 〉 or = 45 min x d(-1), 5 d x wk (n = 53), or to a 1-d x wk(-1) stretching control (n = 62), on an intent-to-treat basis. CRP, SAA, and IL-6 were measured at baseline, at 3 months, and at 12 months. RESULTS: From baseline to 12 months, CRP decreased 10% in exercisers and increased 12% in controls (P = 0.01); no effects were observed for SAA and IL-6. Among participants at baseline who were obese (body mass index (BMI) 〉 or = 30 kg x m(-2)) or had abdominal obesity (waist circumference (WC) 〉 or = 88 cm), exercise resulted in a more pronounced reduction in CRP (BMI 〉 or = 30 kg x m(-2), P = 0.002; WC 〉 or = 88 cm, P 〈 0.0001), borderline for SAA (BMI 〉 or = 30 kg x m(-2), P = 0.08; WC 〉 or = 88 cm, P = 0.04); no intervention effects were observed among women who did not have these characteristics. Overall, weight loss was minimal in the exercise intervention ( approximately 1.8 kg). Linear trends were observed between CRP and 12-month changes in aerobic fitness (Ptrend = 0.006), exercise adherence (Ptrend = 0.004), percentage body fat (Ptrend = 0.002), body weight (Ptrend = 0.002), WC (Ptrend = 0.02), and intra-abdominal fat (Ptrend = 0.03). CONCLUSIONS: A moderate-intensity exercise intervention reduced CRP for 12 months among women who were obese at baseline. These findings support the role of exercise in modulating inflammatory processes that are related to increased risk of chronic disease among obese women.
    Type of Publication: Journal article published
    PubMed ID: 19568208
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  • 3
    Keywords: CANCER ; RISK ; GENE ; TUMORS ; BIOMARKERS ; ASSOCIATION ; polymorphism ; HEALTH ; colorectal cancer ; COLORECTAL-CANCER ; GENOTYPES ; COLON-CANCER ; microsatellite instability ; VARIANT ; C677T POLYMORPHISM ; SUBGROUPS ; COMMON MUTATION ; GENOMIC DNA METHYLATION ; Genetic ; single nucleotide ; ACID SUPPLEMENTATION ; FOLATE STATUS ; KIDNEY-TRANSPLANT RECIPIENTS ; METHYLENETETRAHYDROFOLATE REDUCTASE POLYMORPHISM ; MTHFR C677T ; PLASMA TOTAL HOMOCYSTEINE
    Abstract: Background: The MTHFR C677T TT genotype is associated with a 159% to 189% reduction in colorectal cancer risk, but it is not clear if other variants of the gene are associated with colorectal cancer risk. Methods: We used a tagSNP approach to comprehensively evaluate associations between variation in the MTHFR gene and colorectal cancer risk using a large family-based case-control study of 1,750 Population-based and 245 clinic-based families from the Colon Cancer Family Registry We assessed 22 TagSNPs, selected based on pairwise r(2) 〉 95%, using the Haploview Tagger and genotyped the TagSNPs on the Illumina GoldenGate or Sequenom platforms. The association between single nucleotide polymorphisms and colorectal cancer was assessed using log-additive, codominant, and recessive models. Results: From studying the population-based families, the C677T (rs1801133) and A1298C (rs1801131) polymorphisms were associated with a decreased colorectal cancer risk overall [odds ratio (OR), 0.81; 95% confidence interval (95% CI), 0.63-1.04; and OR, 0.82; 95% CI, 0.64-1.07, respectively]. The 677 TT genotype was associated with a decreased risk of microsatellite-stable/microsatellite-low tumors (OR, 0.69; 95% CI, 0.49-0.97) and an increased risk of rnicrosatellite-high tumors (OR, 2.22; 95% CI, 0.91-5.431, P-interaction = 0.01), as well as an increased risk of proximal cancers and a decreased risk of distal and rectal cancers (P-interaction = 0.02). No other single nucleotide polymorphism was associated with risk overall or within subgroups. Conclusion: The 677 TT and 1298 CC genotypes may each be associated with a decrease in colorectal cancer risk. We observed little evidence of additional genetic variability in the MTHFR gene relevant to colorectal cancer risk. Cancer Epidemiol Biomarkers Prev; 19(1); 89-100. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20056627
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  • 4
    Keywords: CANCER ; EXPRESSION ; tumor ; RISK ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; RNA ; SAMPLE ; SAMPLES ; TISSUE ; INDEX ; BIOMARKERS ; BIOLOGY ; CYCLE ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; prevention ; gene expression ; HUMANS ; ASSAY ; WOMEN ; REPRODUCIBILITY ; risk factors ; NECROSIS-FACTOR-ALPHA ; cancer risk ; REGION ; FAT ; INDIVIDUALS ; BIOPSY ; TNF-ALPHA ; ADIPOSE-TISSUE ; POSTMENOPAUSAL WOMEN ; leptin ; EXTRACTION ; mRNA ; INTERLEUKIN-6 ; LEVEL ; biomarker ; methods ; ASSAYS ; OVERWEIGHT ; female ; RELEVANCE ; CANCER-RISK ; NECROSIS ; AGREEMENT ; colorectal ; SHORT-TERM ; Adiponectin ; AROMATASE ; INSIGHT ; Abdominal ; Adiponectin/biosynthesis/genetics ; Aromatase/biosynthesis/genetics ; Biopsy/methods ; Breast Neoplasms/*genetics/pathology ; Colorectal Neoplasms/*genetics/pathology ; Interleukin-6/biosynthesis/genetics ; Leptin/biosynthesis/genetics ; Obesity/*complications/genetics/pathology ; Overweight/complications/genetics/pathology ; Pilot Projects ; RNA,Messenger/analysis ; Subcutaneous Fat/metabolism/*pathology/surgery ; Tumor Markers,Biological/*analysis/genetics ; Tumor Necrosis Factor-alpha/biosynthesis/genetics
    Abstract: Examination of adipose tissue biology may provide important insight into mechanistic links for the observed association between higher body fat and risk of several types of cancer, in particular colorectal and breast cancer. We tested two different methods of obtaining adipose tissue from healthy individuals. Ten overweight or obese (body mass index, 25-40 kg/m(2)), postmenopausal women were recruited. Two subcutaneous abdominal adipose tissue samples were obtained per individual (i.e., right and left lower abdominal regions) using two distinct methods (method A: 14-gauge needle with incision, versus method B: 16-gauge needle without incision). Gene expression was examined at the mRNA level for leptin, adiponectin, aromatase, interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in flash-frozen tissue, and at the protein level for leptin, adiponectin, IL-6, and TNF-alpha following short-term culture. Participants preferred biopsy method A and few participants reported any of the usual minor side effects. Gene expression was detectable for leptin, adiponectin, and aromatase, but was below detectable limits for IL-6 and TNF-alpha. For detectable genes, relative gene expression in adipose tissue obtained by methods A and B was similar for adiponectin (r = 0.64, P = 0.06) and leptin (r = 0.80, P = 0.01), but not for aromatase (r = 0.37,P = 0.34). Protein levels in tissue culture supernatant exhibited good intra-assay agreement [coefficient of variation (CV), 1-10%], with less agreement for intraindividual agreement (CV, 17-29%) and reproducibility, following one freeze-thaw cycle (CV, 〉14%). Subcutaneous adipose tissue biopsies from healthy, overweight individuals provide adequate amounts for RNA extraction, gene expression, and other assays of relevance to cancer prevention research.
    Type of Publication: Journal article published
    PubMed ID: 19139016
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  • 5
    Keywords: CANCER ; tumor ; MODEL ; PATHWAY ; PATHWAYS ; EXPOSURE ; RISK ; ENZYMES ; GENE ; GENES ; DNA ; colon ; SEQUENCE ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; DNA-REPAIR ; MUTATION ; REPAIR ; CIGARETTE-SMOKING ; colorectal cancer ; smoking ; COLORECTAL-CANCER ; DAMAGE ; COLON-CANCER ; INSTABILITY ; microsatellite instability ; MUTATIONS ; DNA-DAMAGE ; PHENOTYPE ; CARCINOGENS ; SMOKERS ; DNA repair ; EXCISION-REPAIR ; BRAF ; TP53 ; colon cancer ; VARIANT ; XRCC1 ; DNA damage ; INCREASED RISK ; population-based ; colorectal ; base excision repair ; REPAIR GENES ; CONFIDENCE ; INSIGHT ; TP53 mutation
    Abstract: DNA repair enzymes function in major pathways to reverse DNA damage, including base excision repair (BER). Missense polymorphisms in BER repair genes may contribute to differences in DNA repair capacity, specific mutations, and susceptibility to cancer in the presence of exposure to carcinogens such as cigarette smoking. In a study of 1,604 incident colon cancer cases and 1,969 matched population-based controls genotyped for BER variants OGG1 (S326C) and XRCC1 (R194W, R280H, and R399Q), we found no associations with colon cancer overall. However, a 2-fold increased risk of BRAF V600E tumor mutation was observed in current and former cigarette smokers homozygous for the OGG1 polymorphism (odds ratio, 2.2; 95% confidence interval, 1.02-4.9, recessive model); similar associations were not observed for microsatellite instability, CpG island methylator phenotype, KRAS2 mutations, or TP53 mutations. The XRCC1 R194W polymorphism was associated with a modest increased risk of TP53 tumor mutations in those who regularly smoked cigarettes (odds ratio, 1.4; 95% confidence interval, 1.02-1.9). These findings point to the importance of studying tumor mutations when examining DNA repair polymorphisms and cigarette smoke exposure to identify potentially relevant associations with colorectal cancer.
    Type of Publication: Journal article published
    PubMed ID: 19959686
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  • 6
    Keywords: CANCER ; tumor ; RISK ; TISSUE ; TUMORS ; DNA ; MARKER ; SEQUENCE ; SEQUENCES ; ASSOCIATION ; AGE ; WOMEN ; colorectal cancer ; etiology ; MEN ; OBESITY ; COLORECTAL-CANCER ; MARKERS ; RISK FACTOR ; COLON-CANCER ; microsatellite instability ; MISMATCH REPAIR ; PHENOTYPE ; body mass index ; LIFE-STYLE ; GENETIC INSTABILITY ; RECTAL-CANCER ; ONCOLOGY ; case-control study ; REGRESSION ; ASSOCIATIONS ; SIBLINGS ; MATRIX METALLOPROTEINASES ; WEIGHT ; BODY-MASS INDEX ; population-based ; EXPANSION ; WAIST CIRCUMFERENCE ; WEIGHT CHANGE ; journals
    Abstract: Being overweight or obese is an established risk factor for colorectal cancer, more so for men than for women. Approximately 10%-20% of colorectal tumors display microsatellite instability (MSI), defined as the expansion or contraction of small repeated sequences in the DNA of tumor tissue relative to nearby normal tissue. We evaluated associations between overweight or obesity and colorectal cancer risk, overall and by tumor MSI status. The study included 1794 case subjects with incident colorectal cancer who were identified through population-based cancer registries and 2684 of their unaffected sex-matched siblings as control subjects. Recent body mass index (BMI), BMI at age 20 years, and adult weight change were derived from self-reports of height and weight. Tumor MSI status, assessed at as many as 10 markers, was obtained for 69.7% of the case subjects and classified as microsatellite (MS)-stable (0% of markers unstable; n = 913), MSI-low (〉 0% but 〈 30% of markers unstable; n = 149), or MSI-high (〉= 30% of markers unstable; n = 188). Multivariable conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). All statistical tests were two-sided. Recent BMI, modeled in 5 kg/m(2) increments, was positively associated with risk of colorectal cancer for men and women combined (OR = 1.24; 95% CI = 1.15 to 1.34), for women only (OR = 1.20; 95% CI = 1.10 to 1.32), and for men only (OR = 1.30; 95% CI = 1.15 to 1.47). There was no interaction with sex (P = .22). Recent BMI, per 5 kg/m(2), was positively associated with the risk of MS-stable (OR = 1.38; 95% CI = 1.24 to 1.54) and MSI-low (OR = 1.33; 95% CI = 1.04 to 1.72) colorectal tumors, but not with the risk of MSI-high tumors (OR = 1.05; 95% CI = 0.84 to 1.31). The increased risk of colorectal cancer associated with a high BMI might be largely restricted to tumors that display the more common MS-stable phenotype, suggesting further that colorectal cancer etiology differs by tumor MSI status
    Type of Publication: Journal article published
    PubMed ID: 20208017
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  • 7
    Keywords: CANCER ; tumor ; Germany ; MODEL ; MODELS ; DIAGNOSIS ; INFORMATION ; EXPOSURE ; RISK ; PATIENT ; FAMILY ; IMPACT ; prognosis ; BIOMARKERS ; colon ; ASSOCIATION ; 5-FLUOROURACIL ; ACID ; prevention ; PROGRESSION ; HEALTH ; DESIGN ; WOMEN ; colorectal cancer ; MEN ; COLORECTAL-CANCER ; COLON-CANCER ; CANCER-PATIENTS ; PREVALENCE ; CANCER PATIENTS ; QUESTIONNAIRE ; SMOKERS ; VEGETABLES ; LIFE-STYLE ; exercise ; ONCOLOGY ; REGISTRY ; REGRESSION ; ASSOCIATIONS ; colon cancer ; FAS ; biomarker ; MULTIETHNIC COHORT ; colorectal ; RANDOMIZED CLINICAL-TRIAL ; VITAMIN ; VEGETABLE INTAKE ; FOLATE ; DIETARY-SUPPLEMENTS
    Abstract: Background: Supplement use among cancer patients is high, and folic acid intake in particular may adversely affect the progression of colorectal cancer. Few studies have evaluated the use of folic acid-containing supplements (FAS) and its predictors in colorectal cancer patients. Objective: To assess the use of FAS, change in use, and its predictors after colorectal cancer diagnosis. Design: We used logistic regression models to investigate predictors of FAS use and its initiation after colorectal cancer diagnosis in 1,092 patients recruited through the Colon Cancer Family Registry. Results: The prevalence of FAS use was 35.4% before and 55.1% after colorectal cancer diagnosis (P = 0.004). Women were more likely than men to use FAS after diagnosis [ odds ratio (OR), 1.47; 95% confidence interval (95% CI), 1.14-1.89], as were those consuming more fruit (P-trend 〈 0.0001) or vegetables (P-trend = 0.001), and U. S. residents (P 〈 0.0001). Less likely to use FAS after diagnosis were nonwhite patients (OR, 0.66; 95% CI, 0.45-0.97), current smokers (OR, 0.67; 95% CI, 0.46-0.96), and those with higher meat intake (P-trend = 0.03). Predictors of FAS initiation after diagnosis were generally similar to those of FAS use after diagnosis, although associations with race and vegetable intake were weaker and those with exercise stronger. Conclusions: Our analysis showed substantial increases in the use of FAS after diagnosis with colorectal cancer, with use or initiation more likely among women, Caucasians, U. S. residents, and those with a health-promoting life-style. Impact: Studies of cancer prognosis that rely on prediagnostic exposure information may result in substantial misclassification. Cancer Epidemiol Biomarkers Prev; 19(8); 2023-34. (C) 2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20696661
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  • 8
    Keywords: carcinoma ; RISK ; GENOME ; DISCOVERY ; smoking ; COLORECTAL-CANCER ; molecular epidemiology ; HETEROGENEITY ; SCIENCE ; ENVIRONMENTAL-FACTORS
    Abstract: Cancer research is drawing on the human genome project to develop new molecular-targeted treatments. This is an exciting but insufficient response to the growing, global burden of cancer, particularly as the projected increase in new cases in the coming decades is increasingly falling on developing countries. The world is not able to treat its way out of the cancer problem. However, the mechanistic insights from basic science can be harnessed to better understand cancer causes and prevention, thus underpinning a complementary public health approach to cancer control. This manuscript focuses on how new knowledge about the molecular and cellular basis of cancer, and the associated high-throughput laboratory technologies for studying those pathways, can be applied to population-based epidemiological studies, particularly in the context of large prospective cohorts with associated biobanks to provide an evidence base for cancer prevention. This integrated approach should allow a more rapid and informed translation of the research into educational and policy interventions aimed at risk reduction across a population.
    Type of Publication: Journal article published
    PubMed ID: 25515230
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  • 9
    Keywords: CANCER ; EXPRESSION ; ALGORITHM ; SUPPORT ; DISEASE ; RISK ; ENZYMES ; PROTEIN ; DRUG ; MARKER ; colon ; ASSOCIATION ; LINKAGE ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; FREQUENCIES ; ADENOMAS ; HUMANS ; PROMOTER ; SNP ; GENOTYPES ; COLON-CANCER ; case-control studies ; C-REACTIVE PROTEIN ; INDIVIDUALS ; inflammation ; SINGLE ; ADULT ; ADULTS ; case control study ; case-control study ; colon cancer ; VARIANT ; SNPs ; CARDIOVASCULAR-DISEASE ; interaction ; methods ; EUROPEANS ; GENOTYPE ; HAPLOTYPE ; HAPLOTYPES ; female ; Male ; INCREASED RISK ; Aged ; Middle Aged ; colorectal ; Genetic ; genetic variation ; CONFIDENCE ; HYPERPLASTIC POLYPS ; C-REACTIVE-PROTEIN ; *Haplotypes ; *Polymorphism,Single Nucleotide ; Anti-Inflammatory Agents,Non-Steroidal/*metabolism/therapeutic use ; Aryl Hydrocarbon Hydroxylases/genetics/metabolism ; C-Reactive Protein/*genetics/metabolism ; Colorectal Neoplasms/enzymology/*genetics/pathology ; Glucuronosyltransferase/genetics/metabolism ; Hyperplastic polyp ; Intestinal Polyps/enzymology/*genetics/pathology
    Abstract: INTRODUCTION: C-reactive protein (CRP) is a nonspecific marker of inflammation linked to cardiovascular disease and possibly colon cancer. Polymorphisms in CRP have been associated with differential CRP concentrations among healthy adults, with some evidence for functional effects on CRP expression. METHODS: A linkage disequilibrium-based tag single nucleotide polymorphism (SNP)-selection algorithm identified six tagSNPs for Europeans (-821A〉G, -390C〉T/A, 90A〉T, 838G〉C, 2043G〉A, and 4363C〉A), defining six haplotypes with more than 1% frequency. In a case-control study of adenomatous (n=491) or hyperplastic (n=184) polyps versus polyp-free controls (n=583) we investigated these SNPs in relation to colorectal polyp risk. RESULTS: Individuals with 838 GC or CC genotypes had a modestly, although not statistically significantly, increased risk of adenomas (odds ratio: 1.4 95% confidence interval: 0.9-2.1) and a nearly 2-fold increased risk of concurrent adenomas and hyperplastic polyps (odds ratio: 2.0 95% confidence interval: 1.1-3.6). Increased risk for concurrent adenomas and hyperplastic polyps was also observed for haplotype ACACAC. No other main associations were detected. Risk of adenomas associated with 2043G〉A differed with nonsteroidal anti-inflammatory drug (NSAID) use. Among NSAID nonusers, there was a suggestion that the GA or AA genotypes were associated with decreased risk of adenomas; this was not seen among NSAID users (P interaction=0.03). We also observed interactions between UGT1A1 [TA](7) promoter repeat polymorphism and CRP tagSNPs -390C〉T/A and 90A〉T, in which only the homozygous variant CRP genotype was associated with increased risk of adenoma among those with the UGT1A1 6rpt/6rpt genotype (P interaction=0.02 and 0.04 for -390C〉T/A and 90A〉T, respectively). CONCLUSION: These results provide limited support for associations between genetic variation in CRP and colorectal polyp risk. The observed interactions should be evaluated further.
    Type of Publication: Journal article published
    PubMed ID: 19077918
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  • 10
    Keywords: CANCER ; tumor ; MODEL ; PATHWAY ; POPULATION ; RISK ; GENE ; GENES ; METABOLISM ; FAMILY ; IMPACT ; CARCINOGENESIS ; BIOMARKERS ; colon ; ASSOCIATION ; polymorphism ; single nucleotide polymorphism ; HEALTH ; SNP ; colorectal cancer ; COLORECTAL-CANCER ; cancer risk ; RISK FACTOR ; COLON-CANCER ; genotyping ; INSTABILITY ; microsatellite instability ; pathology ; DIHYDROFOLATE-REDUCTASE GENE ; ONCOLOGY ; REGISTRY ; REGRESSION ; colon cancer ; biomarker ; methods ; HAPLOTYPE ; METHIONINE SYNTHASE ; population-based ; CANCER-RISK ; colorectal ; GENETIC-VARIATION ; RANDOMIZED CLINICAL-TRIAL ; Genetic ; single nucleotide ; METHYLENETETRAHYDROFOLATE-REDUCTASE ; FOLATE ; BLOOD-CELL FOLATE ; DIETARY-FOLATE ; PAIR DELETION POLYMORPHISM ; TOTAL HOMOCYSTEINE CONCENTRATIONS ; UNMETABOLIZED FOLIC-ACID
    Abstract: Background: Folate-associated one-carbon metabolism (FOCM) may play an important role in colorectal carcinogenesis. Variation in FOCM genes may explain some of the underlying risk of colorectal cancer. Methods: This study utilized data from 1,805 population-based colorectal cancer cases and 2,878 matched sibling controls from the Colon Cancer Family Registry. We used a comprehensive haplotype tagging single nucleotide polymorphism (tagSNP) approach to select 395 tagSNPs in 15 genes involved in folate and vitamin B-12 metabolism. Genotyping was done using the Illumina GoldenGate or Sequenom platforms. Risk factor and dietary data were collected using self-completed questionnaires. Microsatellite instability (MSI) status was determined using standard techniques, and tumor subsite was obtained from pathology reports. The association between SNPs and colorectal cancer was assessed using conditional logistic regression with sibships as the matching factor and assuming a log additive or codominant model. Results: In the log additive model, two linked (r(2) = 0.99) tagSNPs in the DHFR gene (rs1677693 and rs1643659) were associated with a significant decrease in colorectal cancer risk after correction for multiple testing (odds ratio, 0.87; 95% confidence interval, 0.71-0.94; P = 0.029; and odds ratio, 0.87; 95% confidence interval, 0.71-0.95; P = 0.034 for rs1677693 and rs1643659, respectively). These two linked (r(2) = 0.99) tagSNPs and one tagSNP in the MTR gene (rs4659744) were significantly associated with reduced colorectal cancer risk only among individuals not using multivitamin supplements. Conclusions: Overall, we found only moderate evidence that genetic variation in 15 folate pathway genes may affect colorectal cancer risk except in non-multivitamin users. Impact: This study suggests that multivitamin supplement use may modify the association between folate pathway genes and colorectal cancer risk in a post-folic-acid-supplemented population. Cancer Epidemiol Biomarkers Prev; 19(7); 1812-21. (C) 2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20615890
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