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  • 1
    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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  • 2
    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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  • 3
    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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  • 4
    Abstract: Folate status is an important predictor of colorectal cancer risk. Common genetic variants in genes involved in regulating cellular folate levels might also predict risk, but there are limited data on this issue. We conducted a family-based case-control association study of variants in four genes involved in folate uptake and distribution: FOLR1, FPGS, GGH and SLC19A1, using 1,750 population-based and 245 clinic-based cases of pathologically confirmed colorectal cancer and their unaffected relatives participating in the Colon Cancer Family Registries. Standardized questionnaires, administered to all participants, collected information on risk factors and diet. Standard molecular techniques were used to determine microsatellite instability (MSI) status on cases. tagSNPs (n = 29) were selected based on coverage as assessed by pairwise r2. We found no evidence that tagSNPs in these genes were associated with risk of colorectal cancer. For the SLC19A1-rs1051266 (G80A, Arg27His) missense polymorphism, the A/A genotype was not associated with risk of colorectal cancer using population-based (OR = 1.00; 95% CI = 0.81-1.23) or clinic-based (OR = 0.75; 95% CI = 0.44-1.29) families compared to the G/A and G/G genotypes. We found no evidence that the association between any tagSNP and CRC risk was modified by multivitamin use, folic acid use and dietary folate intake and total folate intake. The odds ratios were similar, irrespective of MSI status, tumor subsite and family history of colorectal cancer. In conclusion, we found no significant evidence that genetic variants in FOLR1, GGH, FPGS and SLC19A1 are associated with the risk of colorectal cancer.
    Type of Publication: Journal article published
    PubMed ID: 20037791
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Icarus 101 (1993), S. 71-83 
    ISSN: 0019-1035
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 0022-4731
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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