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Wei Zheng - One of the best experts on this subject based on the ideXlab platform.

  • pufa levels in erythrocyte membrane phospholipids are differentially associated with Colorectal Adenoma risk
    British Journal of Nutrition, 2017
    Co-Authors: Samara Rifkin, Martha J Shrubsole, Reid M Ness, Wei Zheng, Qiuyin Cai, Walter E Smalley, Larry L Swift, Harvey J Murff
    Abstract:

    Dietary intake of PUFA has been associated with Colorectal neoplasm risk; however, results from observational studies have been inconsistent. Most prior studies have utilised self-reported dietary measures to assess fatty acid exposure which might be more susceptible to measurement error and biases compared with biomarkers. The purpose of this study was to determine whether erythrocyte phospholipid membrane PUFA percentages are associated with Colorectal Adenoma risk. We included data from 904 Adenoma cases and 835 polyp-free controls who participated in the Tennessee Colorectal Polyp Study, a large colonoscopy-based case-control study. Erythrocyte membrane PUFA percentages were measured using GC. Conditional logistic regression was used to calculate adjusted OR for risk of Colorectal Adenomas with erythrocyte membrane PUFA. Higher erythrocyte membrane percentages of arachidonic acid was associated with an increased risk of Colorectal Adenomas (adjusted OR 1·66; 95 % CI 1·05, 2·62, P trend=0·02) comparing the highest tertile to the lowest tertile. The effect size for arachidonic acid was more pronounced when restricting the analysis to advanced Adenomas only. Higher erythrocyte membrane EPA percentages were associated with a trend towards a reduced risk of advanced Colorectal Adenomas (P trend=0·05). Erythrocyte membrane arachidonic acid percentages are associated with an increased risk of Colorectal Adenomas.

  • evaluation of pro inflammatory markers plasma c reactive protein and urinary prostaglandin e2 metabolite in Colorectal Adenoma risk
    Molecular Carcinogenesis, 2016
    Co-Authors: James R Davenport, Reid M Ness, Wei Zheng, Qiuyin Cai, Walter E Smalley, Ginger L Milne, Zhiguo Zhao
    Abstract:

    C-reactive protein (CRP) is a pro-inflammatory protein with potential as a biomarker in predicting colon cancer risk. However, little is known regarding its association with risk of Colorectal Adenomas, particularly by subtypes. We conducted a colonoscopy-based matched case-control study to assess whether elevated plasma CRP levels may be associated with Colorectal Adenoma risk and further whether this association may be modified by urinary prostaglandin E2 metabolite (PGE-M), a biomarker of systemic prostaglandin E2 production. Included in the study were 226 cases with a single small tubular Adenoma, 198 cases with multiple small tubular Adenomas, 283 cases with at least one advanced Adenoma, and 395 polyp-free controls. No apparent association between CRP level and risk of single small tubular Adenomas was found (ptrend  = 0.59). A dose-response relationship with CRP level was observed for risk of either multiple small tubular Adenomas (OR = 2.01, 95%CI = 1.10-3.68 for the highest versus lowest tertile comparison; ptrend = 0.03) or advanced Adenomas (OR = 1.81, 95%CI = 1.10-2.96 for the highest versus lowest tertile comparison; ptrend  = 0.02). In a joint analysis of CRP level and PGE-M, risk of multiple or advanced Adenoma was greatest among those with highest levels of both CRP and PGE-M in comparison to those with low CRP and low PGE-M (OR = 3.72, 95%CI = 1.49-9.72). Our results suggest that elevated CRP, particularly in the context of concurrent elevated PGE-M, may be a biomarker of multiple or advanced Adenoma risk in a screening age population. © 2015 Wiley Periodicals, Inc.

  • abstract 1674 two phase study of kcnj1 polymorphisms calcium magnesium and Colorectal Adenoma risk results from the tennessee Colorectal polyp study
    Cancer Research, 2012
    Co-Authors: Martha J Shrubsole, Reid M Ness, Todd L Edwards, Xinqing Deng, Waltersmalley E Smalley, Jirong Long, Zhi Chen, Wei Zheng
    Abstract:

    Background: Previous studies generated inconsistent results on the associations between intakes of calcium and magnesium with risk of Colorectal Adenoma and cancer. It is possible that some of the inconsistency is due to a modifying effect by genetic polymorphisms involved in calcium and magnesium homeostasis. The KCNJ1 gene encodes the Inward-rectifier potassium channel (ROMK). ROMK plays an essential role in the homeostasis of potassium, which is critical for the reabsorption of calcium and magnesium. Objectives: We hypothesize that common variants in KCNJ1 may modify the associations between intakes of calcium and/or magnesium and risk of Colorectal Adenoma risk. Methods: Included were participants of the Tennessee Colorectal Polyp Study (TCPS), a colonoscopy-based case control study conducted in Nashville, TN. In the phase I study, genotyping was performed using the Affymetrix Human Mapping 500K array set in 958 Colorectal Adenoma cases and 909 controls and 13 tagging single-nucleotide polymorphisms (SNPs) in the KCNJ1 gene were evaluated. SNPs identified as significant in phase I were genotyped in phase II in an independent set (860 cases and 3083 controls). Results: In phase I, 1 tagging SNP was significantly associated with Adenoma risk and 8 SNPs were interacted significantly with calcium or magnesium intake in risk of Colorectal Adenoma. In phase II, only 1 of the 9 SNPs significantly interacted with calcium and magnesium intakes in relation to Colorectal Adenoma although the genotype per se was not directly associated with the risk. In combined analysis, the p value for the interaction between the SNP and calcium intake was 0.00015 and it remained statistically significant after Bonferroni correction for multiple comparisons. In stratified analyses by levels of calcium and magnesium (above or below RDA levels), we found Adenoma risk significantly increased for those who with at least 1 variant allele and whose intake levels of calcium and magnesium were below the RDA levels, with ORs (95% CI) of 1.35 (1.10, 1.67) and 1.43 (1.08, 1.89) respectively, compared to those who did not possess the variant allele. The corresponding ORs (95% CI) increased to 1.84 (1.33, 2.53) and 2.30 (1.53, 3.46), respectively, multiple Adenomas versus controls. Conclusions: In this two-stage analysis, we found no overall association of Adenoma with KCNJ1 genotype. However, common KCNJ1 variants significantly interacted with intakes of calcium and magnesium in risk of Colorectal Adenoma, particular for multiple Adenomas. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1674. doi:1538-7445.AM2012-1674

  • urinary prostaglandin e2 metabolite and risk for Colorectal Adenoma
    Cancer Prevention Research, 2012
    Co-Authors: Martha J Shrubsole, Reid M Ness, Zhi Chen, Qiuyin Cai, Walter E Smalley, Wanqing Wen, Ginger L Milne, Wei Zheng
    Abstract:

    COX-2 is upregulated in most Colorectal cancers. Most of the COX-2 tumor-inducing effects are believed to be mediated through overproduction of prostaglandin E(2) (PGE(2)), which can be measured using a urinary metabolite of PGE(2), PGE-M. Urinary PGE-M was assessed in a case-control study of Colorectal Adenoma. Included in the analysis were 224 cases with at least one advanced Adenoma, 152 cases with multiple small tubular Adenomas, 300 cases with only a single small tubular Adenoma, and 364 polyp-free controls. There were no statistical differences in PGE-M levels between controls and cases with a single small tubular Adenoma. However, cases with either an advanced Adenoma or multiple small tubular Adenomas had more than 25% higher levels of PGE-M than controls. Participants with the highest quartile level of PGE-M were approximately 2.5-fold more likely to have advanced or multiple small tubular Adenoma in comparison with those with the lowest level of PGE-M [OR = 2.53; 95% confidence interval (CI), 1.54-4.14; P(trend) < 0.001]. The association was strongest among women. PGE-M level was associated with increased risk for multiple or advanced Adenoma but not single small Adenoma. Our study suggests that PGE-M may be a useful risk marker for assessing the risk of harboring clinically more important versus less important Colorectal neoplasia.

  • abstract 3763 calcium intake cabp1 polymorphisms and the risk of Colorectal Adenoma results from tennessee Colorectal polyp study
    Cancer Research, 2011
    Co-Authors: Martha J Shrubsole, Reid M Ness, Todd L Edwards, Xinqing Deng, Waltersmalley E Smalley, Jirong Long, Wei Zheng
    Abstract:

    Background: High calcium consumption may confer a reduced risk of Colorectal Adenoma and cancer. This effect could differ by polymorphisms in the genes involved in calcium regulation. The calcium binding protein 1(CABP1) gene encodes a calbindin-D9k protein, an important component of calcium mediated cellular signal transduction. CABP1 express primarily in intestine, and increased levels of Calbindin-D9k in intestine were found to be correlated with calcium hyperabsorption. A recent study found that deletion of CABP1 and another gene had a significant effect on calcium processing under calcium-deficient conditions. These findings suggest the variations in CABP1 expression in intestine may explain some of the variability in calcium absorption. However, so far no study has evaluated genetic variations in CABP1 with the risk of Colorectal Adenoma. Objectives: In the current study, we first screened whether CABP1 variants or their interactions with calcium intake were associated with urinary calcium among 256 normal controls. Further, single-nucleotide polymorphisms (SNPs) were evaluated for their independent association and interactions with calcium intake in relation to Colorectal Adenoma risk. Methods: Included in the study were 958 Adenoma cases and 909 controls from the Tennessee Colorectal Polyp Study (TCPS), an ongoing colonoscopy-based case-control study conducted in Nashville, TN. Genotyping was performed using the Affymetrix Human Mapping 500K array set. Seven tagging SNPs in CABP1 were analyzed. Linear regression models were used to estimate the association between genotypes and urinary calcium level. Multivariate unconditional logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (CI). Multiplicative interactions for gene-diet interactions were evaluated in logistic regression models by using likelihood ratio tests. Results: Although no SNPs were observed to be associated with urinary calcium levels, one SNP (rs7956304) was found to be significantly associated with risk of Adenoma. In comparison to participants with the GG genotype, participants with GA had higher risk of Colorectal Adenoma (OR=1.29, 95% CI 1.03-1.61, P=0.027), while participants with the AA genotype had no appreciable difference in risk (OR=0.82, 95% CI 0.50-1.35, P=0.428). This SNP was not observed to interact with calcium intake. Conclusions: These findings suggest that genetic variations in CABP1 may affect the risk of Colorectal Adenoma. To the best of our knowledge, this study is the first to evaluate CABP1 polymorphisms in relation to the risk of Adenoma. Our finding of a significant association is promising; however, the finding should be confirmed in future studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3763. doi:10.1158/1538-7445.AM2011-3763

Edward Giovannucci - One of the best experts on this subject based on the ideXlab platform.

  • glucosamine and chondroitin supplements and risk of Colorectal Adenoma and serrated polyp
    Cancer Epidemiology Biomarkers & Prevention, 2020
    Co-Authors: Dong Hoon Lee, Edward Giovannucci, Yin Cao, Mingyang Song, Xuehong Zhang, Chao Cao, Xiaoyu Zong, Kelli Oconnell
    Abstract:

    Background: Studies have shown an inverse association between use of glucosamine and chondroitin supplements and Colorectal cancer risk. However, the association with the precursor lesion, Colorectal Adenoma and serrated polyp, has not been examined. Methods: Analyses include 43,163 persons from the Nurses9 Health Study (NHS), Health Professionals Follow-up Study (HPFS), and NHS2 who reported on glucosamine/chondroitin use in 2002 and who subsequently underwent ≥1 lower gastrointestinal endoscopy. By 2012, 5,715 conventional (2,016 high-risk) Adenomas were detected, as were 4,954 serrated polyps. Multivariable logistic regression for clustered data was used to calculate OR and 95% confidence intervals (CI). Results: Glucosamine/chondroitin use was inversely associated with high risk and any conventional Adenoma in NHS and HPFS: in the pooled multivariable-adjusted model, glucosamine + chondroitin use at baseline was associated with a 26% (OR = 0.74; 95% CI, 0.60–0.90; Pheterogeneity = 0.23) and a 10% (OR = 0.90; 95% CI, 0.81–0.99; Pheterogeneity = 0.36) lower risk of high-risk Adenoma and overall conventional Adenoma, respectively. However, no association was observed in NHS2, a study of younger women (high-risk Adenoma: OR = 1.09; 95% CI, 0.82–1.45; overall conventional Adenoma: OR = 1.00; 95% CI, 0.86–1.17), and effect estimates pooled across all three studies were not significant (high-risk: OR = 0.83; 95% CI, 0.63–1.10; Pheterogeneity = 0.03; overall conventional Adenoma: OR = 0.93; 95% CI, 0.85–1.02; Pheterogeneity = 0.31). No associations were observed for serrated polyps. Conclusions: Glucosamine/chondroitin use was associated with lower risks of high-risk and overall conventional Adenoma in older adults; however, this association did not hold in younger women, or for serrated polyps. Impact: Our study suggests that glucosamine and chondroitin may act on early Colorectal carcinogenesis in older adults.

  • Dietary marine n-3 fatty acids in relation to risk of distal Colorectal Adenoma in women. Cancer Epidemiol Biomarkers Prev
    2016
    Co-Authors: Walter C. Willett, Charles S. Fuchs, Edward Giovannucci
    Abstract:

    Epidemiologic studies of dietary marine n-3 fatty acids and risk of Colorectal cancer have been inconsistent, and their relation to risk of Colorectal Adenoma has not been evaluated in detail. We examined dietary marine n-3 fatty acids and the ratio of marine n-3 to total n-6 fatty acids (n-3/ n-6 ratio) in relation to risk of Adenoma of the distal colon or rectum among 34,451 U.S. women who were initially free of Colorectal cancer or polyps, who completed a semiquan-titative food frequency questionnaire in 1980, and who underwent endoscopy from 1980 to 1998. We documented 1,719 distal Colorectal Adenoma cases (705 large Adenomas, 897 small Adenomas, 1,280 distal colon Adenomas, and 505 rectal Adenomas) during 18 years of follow-up. Neither dietary marine n-3 fatty acids nor n-3/n-6 ratio were associated with risk of total distal Colorectal Adenoma after adjustment for age and established risk factors [multivar-iable relative risk (RR) for extreme quintiles of dietary marine n-3 fatty acids = 1.04; 95 % confidence interval (95% CI), 0.84-1.27, P trend = 0.66; RR for extreme quintiles of n-3/ n-6 ratio = 1.02; 95 % CI, 0.83-1.25; Ptrend = 0.86]. Similarly, no significant associations were observed separately for distal colon or rectal Adenoma. However, higher intake of dietary marine n-3 fatty acids was nonsignificantly but suggestively inversely associated with large Adenoma (RR, 0.74; 95 % CI, 0.54-1.01; Ptrend = 0.16) but directly associated with small Adenoma (RR, 1.36; 95 % CI, 1.02-1.81; Ptrend = 0.09). Our findings do not support the hypothesis that a higher intake of marine n-3 fatty acids or a higher n-3/n-6 ratio reduces the risk of distal Colorectal Adenoma but are suggestive that higher intake may reduce the progression of small Adenomas to large Adenomas. (Cancer Epidemiol Biomarkers Prev 2005;14(4):835–41

  • assessing individual risk for high risk Colorectal Adenoma at first time screening colonoscopy
    International Journal of Cancer, 2015
    Co-Authors: Yin Cao, Charles S. Fuchs, Andrew T Chan, Bernard Rosner, Rulla M Tamimi, Edward Giovannucci
    Abstract:

    Assessing risk of Colorectal Adenoma at first-time colonoscopy that are of higher likelihood of developing advanced neoplasia during surveillance could help tailor first-line Colorectal cancer screening. We developed prediction models for high-risk Colorectal Adenoma (at least one Adenoma ≥1 cm, or with advanced histology, or ≥3 Adenomas) among 4,881 asymptomatic white men and 17,970 women who underwent colonoscopy as their first-time screening for Colorectal cancer in two prospective US studies using logistic regressions. C-statistics and Hosmer-Lemeshow tests were used to evaluate discrimination and calibration. Ten-fold cross-validation was used for internal validation. A total of 330 (6.7%) men and 678 (3.8%) women were diagnosed with high-risk Adenoma at first-time screening colonoscopy. The model for men included age, family history of Colorectal cancer, BMI, smoking, sitting watching TV/VCR, regular aspirin/NSAID use, physical activity, and a joint term of multivitamin and alcohol. For women, the model included age, family history of Colorectal cancer, BMI, smoking, alcohol, beef/pork/lamb as main dish, regular aspirin/NSAID, calcium, and oral contraceptive use. The C-statistic of the model for men was 0.67 and 0.60 for women (0.64 and 0.57 in cross-validation). Both models calibrated well. The predicted risk of high-risk Adenoma for men in the top decile was 15.4% vs. 1.8% for men in the bottom decile (Odds Ratio [OR] = 9.41), and 6.6% vs. 2.1% for women (OR = 3.48). In summary, we developed and internally validated an absolute risk assessment tool for high-risk Colorectal Adenoma among the US population that may provide guidance for first-time Colorectal cancer screening.

  • long term use of multivitamins and risk of Colorectal Adenoma in women
    British Journal of Cancer, 2014
    Co-Authors: Jennifer Massa, Walter C. Willett, Edward Giovannucci, Eunyoung Cho, Endel J Orav
    Abstract:

    Use of multivitamins may reduce the risk of Colorectal Adenoma, but the duration of use needed is unclear. We prospectively examined years of multivitamin use and risk of Colorectal Adenoma among 43 641 women who had a first endoscopy between 1991 and 2007 in the Nurses’ Health Study II. Use of multivitamins was assessed through biennial questionnaires since 1989. We documented 2277 Colorectal Adenoma cases. Reporting multivitamin use at any time during the study period compared with never reporting its use was associated with a reduced risk of Adenoma (multivariable relative risk (RR)=0.86, 95% confidence interval (CI): 0.76–0.97). There was no clear trend with duration of multivitamin use: years of use compared with never use, ⩽4 years (RR=0.84, 95% CI: 0.74–0.96), 5–9 years (RR=0.89, 95% CI: 0.77, 1.02), 10–14 years (RR=0.86, 95% CI: 0.74, 1.01), 15–19 years (RR=0.85, 95% CI: 0.70, 1.02), and 20–26 years (RR=0.80, 95% CI: 0.64, 1.01); (P trend=0.87). The strongest associations (years of use vs never user) were for size of Adenoma: large (⩾1 cm) <4 years (RR=0.75, 95% CI: 0.58–0.96) and in alcohol users (⩾1.4 g per day) 20–26 years (RR=0.67, 95% CI: 0.49–0.91). Our findings suggest that use of multivitamins is associated with lower risk of Colorectal Adenoma, even with relatively short duration of use.

  • effect of combined folic acid vitamin b6 and vitamin b12 on Colorectal Adenoma
    Journal of the National Cancer Institute, 2012
    Co-Authors: Yiqing Song, Edward Giovannucci, Joann E Manson, Imin Lee, Nancy R Cook, Ligi Paul, Jacob Selhub, Shumin M Zhang
    Abstract:

    Results The risk of Colorectal Adenoma was similar among participants receiving treatment (24.3%, 180 of 741 participants) vs placebo (24.0%, 175 of 729 participants) (multivariable adjusted relative risk = 1.00, 95% confidence interval = 0.83 to 1.20). Treatment was not associated with the risk of Adenoma when data were analyzed by subsite, size, stage, and the number of Adenomas. There was no statistically significant effect modification by alcohol intake, history of cancer or Adenoma, or baseline plasma levels or intakes of folate, vitamin B6, or vitamin B12. Conclusion Our results indicate no statistically significant effect of combined folic acid, vitamin B6, and vitamin B12 treatment on Colorectal Adenoma among women at high risk for cardiovascular disease. J Natl Cancer Inst 2012;104:1562–1575 Folate, vitamin B6, and vitamin B12 are essential cofactors that play important roles in one-carbon metabolism, which is required for the maintenance of intracellular DNA synthesis and methylation. Data from both in vitro and animal studies have suggested a protective effect of B vitamins against Colorectal carcinogenesis (1,2), although the results have been somewhat mixed and the complex mechanisms have not yet been fully elucidated. Observational evidence, though not entirely consistent, has suggested that blood levels of folate or vitamin B6 are inversely related to the risk of Colorectal neoplasia. Some, but not all prospective studies have suggested a 20%–40% reduction in the risk of Colorectal cancer or Adenoma in those with the highest intake of folate compared with those with the lowest intake (1–3). A recent meta-analysis of nine prospective studies showed a 10% reduction in Colorectal cancer in individuals with the highest vitamin B6 intake compared with those

Reid M Ness - One of the best experts on this subject based on the ideXlab platform.

  • pufa levels in erythrocyte membrane phospholipids are differentially associated with Colorectal Adenoma risk
    British Journal of Nutrition, 2017
    Co-Authors: Samara Rifkin, Martha J Shrubsole, Reid M Ness, Wei Zheng, Qiuyin Cai, Walter E Smalley, Larry L Swift, Harvey J Murff
    Abstract:

    Dietary intake of PUFA has been associated with Colorectal neoplasm risk; however, results from observational studies have been inconsistent. Most prior studies have utilised self-reported dietary measures to assess fatty acid exposure which might be more susceptible to measurement error and biases compared with biomarkers. The purpose of this study was to determine whether erythrocyte phospholipid membrane PUFA percentages are associated with Colorectal Adenoma risk. We included data from 904 Adenoma cases and 835 polyp-free controls who participated in the Tennessee Colorectal Polyp Study, a large colonoscopy-based case-control study. Erythrocyte membrane PUFA percentages were measured using GC. Conditional logistic regression was used to calculate adjusted OR for risk of Colorectal Adenomas with erythrocyte membrane PUFA. Higher erythrocyte membrane percentages of arachidonic acid was associated with an increased risk of Colorectal Adenomas (adjusted OR 1·66; 95 % CI 1·05, 2·62, P trend=0·02) comparing the highest tertile to the lowest tertile. The effect size for arachidonic acid was more pronounced when restricting the analysis to advanced Adenomas only. Higher erythrocyte membrane EPA percentages were associated with a trend towards a reduced risk of advanced Colorectal Adenomas (P trend=0·05). Erythrocyte membrane arachidonic acid percentages are associated with an increased risk of Colorectal Adenomas.

  • evaluation of pro inflammatory markers plasma c reactive protein and urinary prostaglandin e2 metabolite in Colorectal Adenoma risk
    Molecular Carcinogenesis, 2016
    Co-Authors: James R Davenport, Reid M Ness, Wei Zheng, Qiuyin Cai, Walter E Smalley, Ginger L Milne, Zhiguo Zhao
    Abstract:

    C-reactive protein (CRP) is a pro-inflammatory protein with potential as a biomarker in predicting colon cancer risk. However, little is known regarding its association with risk of Colorectal Adenomas, particularly by subtypes. We conducted a colonoscopy-based matched case-control study to assess whether elevated plasma CRP levels may be associated with Colorectal Adenoma risk and further whether this association may be modified by urinary prostaglandin E2 metabolite (PGE-M), a biomarker of systemic prostaglandin E2 production. Included in the study were 226 cases with a single small tubular Adenoma, 198 cases with multiple small tubular Adenomas, 283 cases with at least one advanced Adenoma, and 395 polyp-free controls. No apparent association between CRP level and risk of single small tubular Adenomas was found (ptrend  = 0.59). A dose-response relationship with CRP level was observed for risk of either multiple small tubular Adenomas (OR = 2.01, 95%CI = 1.10-3.68 for the highest versus lowest tertile comparison; ptrend = 0.03) or advanced Adenomas (OR = 1.81, 95%CI = 1.10-2.96 for the highest versus lowest tertile comparison; ptrend  = 0.02). In a joint analysis of CRP level and PGE-M, risk of multiple or advanced Adenoma was greatest among those with highest levels of both CRP and PGE-M in comparison to those with low CRP and low PGE-M (OR = 3.72, 95%CI = 1.49-9.72). Our results suggest that elevated CRP, particularly in the context of concurrent elevated PGE-M, may be a biomarker of multiple or advanced Adenoma risk in a screening age population. © 2015 Wiley Periodicals, Inc.

  • abstract 1674 two phase study of kcnj1 polymorphisms calcium magnesium and Colorectal Adenoma risk results from the tennessee Colorectal polyp study
    Cancer Research, 2012
    Co-Authors: Martha J Shrubsole, Reid M Ness, Todd L Edwards, Xinqing Deng, Waltersmalley E Smalley, Jirong Long, Zhi Chen, Wei Zheng
    Abstract:

    Background: Previous studies generated inconsistent results on the associations between intakes of calcium and magnesium with risk of Colorectal Adenoma and cancer. It is possible that some of the inconsistency is due to a modifying effect by genetic polymorphisms involved in calcium and magnesium homeostasis. The KCNJ1 gene encodes the Inward-rectifier potassium channel (ROMK). ROMK plays an essential role in the homeostasis of potassium, which is critical for the reabsorption of calcium and magnesium. Objectives: We hypothesize that common variants in KCNJ1 may modify the associations between intakes of calcium and/or magnesium and risk of Colorectal Adenoma risk. Methods: Included were participants of the Tennessee Colorectal Polyp Study (TCPS), a colonoscopy-based case control study conducted in Nashville, TN. In the phase I study, genotyping was performed using the Affymetrix Human Mapping 500K array set in 958 Colorectal Adenoma cases and 909 controls and 13 tagging single-nucleotide polymorphisms (SNPs) in the KCNJ1 gene were evaluated. SNPs identified as significant in phase I were genotyped in phase II in an independent set (860 cases and 3083 controls). Results: In phase I, 1 tagging SNP was significantly associated with Adenoma risk and 8 SNPs were interacted significantly with calcium or magnesium intake in risk of Colorectal Adenoma. In phase II, only 1 of the 9 SNPs significantly interacted with calcium and magnesium intakes in relation to Colorectal Adenoma although the genotype per se was not directly associated with the risk. In combined analysis, the p value for the interaction between the SNP and calcium intake was 0.00015 and it remained statistically significant after Bonferroni correction for multiple comparisons. In stratified analyses by levels of calcium and magnesium (above or below RDA levels), we found Adenoma risk significantly increased for those who with at least 1 variant allele and whose intake levels of calcium and magnesium were below the RDA levels, with ORs (95% CI) of 1.35 (1.10, 1.67) and 1.43 (1.08, 1.89) respectively, compared to those who did not possess the variant allele. The corresponding ORs (95% CI) increased to 1.84 (1.33, 2.53) and 2.30 (1.53, 3.46), respectively, multiple Adenomas versus controls. Conclusions: In this two-stage analysis, we found no overall association of Adenoma with KCNJ1 genotype. However, common KCNJ1 variants significantly interacted with intakes of calcium and magnesium in risk of Colorectal Adenoma, particular for multiple Adenomas. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1674. doi:1538-7445.AM2012-1674

  • urinary prostaglandin e2 metabolite and risk for Colorectal Adenoma
    Cancer Prevention Research, 2012
    Co-Authors: Martha J Shrubsole, Reid M Ness, Zhi Chen, Qiuyin Cai, Walter E Smalley, Wanqing Wen, Ginger L Milne, Wei Zheng
    Abstract:

    COX-2 is upregulated in most Colorectal cancers. Most of the COX-2 tumor-inducing effects are believed to be mediated through overproduction of prostaglandin E(2) (PGE(2)), which can be measured using a urinary metabolite of PGE(2), PGE-M. Urinary PGE-M was assessed in a case-control study of Colorectal Adenoma. Included in the analysis were 224 cases with at least one advanced Adenoma, 152 cases with multiple small tubular Adenomas, 300 cases with only a single small tubular Adenoma, and 364 polyp-free controls. There were no statistical differences in PGE-M levels between controls and cases with a single small tubular Adenoma. However, cases with either an advanced Adenoma or multiple small tubular Adenomas had more than 25% higher levels of PGE-M than controls. Participants with the highest quartile level of PGE-M were approximately 2.5-fold more likely to have advanced or multiple small tubular Adenoma in comparison with those with the lowest level of PGE-M [OR = 2.53; 95% confidence interval (CI), 1.54-4.14; P(trend) < 0.001]. The association was strongest among women. PGE-M level was associated with increased risk for multiple or advanced Adenoma but not single small Adenoma. Our study suggests that PGE-M may be a useful risk marker for assessing the risk of harboring clinically more important versus less important Colorectal neoplasia.

  • abstract 3763 calcium intake cabp1 polymorphisms and the risk of Colorectal Adenoma results from tennessee Colorectal polyp study
    Cancer Research, 2011
    Co-Authors: Martha J Shrubsole, Reid M Ness, Todd L Edwards, Xinqing Deng, Waltersmalley E Smalley, Jirong Long, Wei Zheng
    Abstract:

    Background: High calcium consumption may confer a reduced risk of Colorectal Adenoma and cancer. This effect could differ by polymorphisms in the genes involved in calcium regulation. The calcium binding protein 1(CABP1) gene encodes a calbindin-D9k protein, an important component of calcium mediated cellular signal transduction. CABP1 express primarily in intestine, and increased levels of Calbindin-D9k in intestine were found to be correlated with calcium hyperabsorption. A recent study found that deletion of CABP1 and another gene had a significant effect on calcium processing under calcium-deficient conditions. These findings suggest the variations in CABP1 expression in intestine may explain some of the variability in calcium absorption. However, so far no study has evaluated genetic variations in CABP1 with the risk of Colorectal Adenoma. Objectives: In the current study, we first screened whether CABP1 variants or their interactions with calcium intake were associated with urinary calcium among 256 normal controls. Further, single-nucleotide polymorphisms (SNPs) were evaluated for their independent association and interactions with calcium intake in relation to Colorectal Adenoma risk. Methods: Included in the study were 958 Adenoma cases and 909 controls from the Tennessee Colorectal Polyp Study (TCPS), an ongoing colonoscopy-based case-control study conducted in Nashville, TN. Genotyping was performed using the Affymetrix Human Mapping 500K array set. Seven tagging SNPs in CABP1 were analyzed. Linear regression models were used to estimate the association between genotypes and urinary calcium level. Multivariate unconditional logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (CI). Multiplicative interactions for gene-diet interactions were evaluated in logistic regression models by using likelihood ratio tests. Results: Although no SNPs were observed to be associated with urinary calcium levels, one SNP (rs7956304) was found to be significantly associated with risk of Adenoma. In comparison to participants with the GG genotype, participants with GA had higher risk of Colorectal Adenoma (OR=1.29, 95% CI 1.03-1.61, P=0.027), while participants with the AA genotype had no appreciable difference in risk (OR=0.82, 95% CI 0.50-1.35, P=0.428). This SNP was not observed to interact with calcium intake. Conclusions: These findings suggest that genetic variations in CABP1 may affect the risk of Colorectal Adenoma. To the best of our knowledge, this study is the first to evaluate CABP1 polymorphisms in relation to the risk of Adenoma. Our finding of a significant association is promising; however, the finding should be confirmed in future studies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3763. doi:10.1158/1538-7445.AM2011-3763

Wen Yi Huang - One of the best experts on this subject based on the ideXlab platform.

  • abstract lb 158 weight change in adulthood and Colorectal Adenoma incidence in the prostate lung Colorectal and ovarian cancer screening trial
    Cancer Research, 2020
    Co-Authors: Sonja I Berndt, Wen Yi Huang, Andrew T Kunzmann, Cari M Kitahara, Kathryn Hughes Barry
    Abstract:

    Obesity is a known risk factor for Colorectal cancer, but the influence of weight change during one9s lifetime on Colorectal Adenoma, precursor to Colorectal cancer, is less understood. We prospectively investigated the association between weight change in different time periods in adulthood and the risk of Colorectal Adenoma. We included 1,041 incident distal Colorectal Adenoma cases (negative on baseline trial flexible sigmoidoscopy screen and positive on follow-up trial sigmoidoscopy screen 3-5 years later) and 16,394 controls (negative on both trial screens) from the screening arm of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. We required participants to have no history of Colorectal polyps, other colon comorbidities or cancer. Using self-reported weight data at trial baseline, we estimated odds ratios (OR) and 95% confidence intervals (95% CI) for early-late (age 20-baseline, i.e. ages 55-74), early-middle (age 20-50) and middle-late (age 50-baseline) adulthood weight change with Colorectal Adenoma using logistic regression. We defined the weight stable group (referent) as weight loss 1 to ≤2, >2 to ≤3 and >3 kg/5 years. We adjusted models for starting BMI (age 20 or 50), age, sex, race, smoking and other factors including diet. Compared to weight stable participants, weight loss in early-late adulthood was inversely associated with Colorectal Adenoma (OR=0.6, 95% confidence interval (CI): 0.3-0.9); results were similar for early-middle adulthood (OR=0.5, 95% CI: 0.3-0.8), but less pronounced for middle-late adulthood (OR=0.8, 95% CI: 0.7-1.0). Early-late adulthood weight gain of >3 kg/5 years was associated with higher odds of Adenoma (OR=1.3, 95% CI: 1.1-1.6); results were similar for middle-late adulthood (OR=1.2, 95% CI: 1.0-1.4), but less pronounced for early-middle adulthood (OR=1.1, 95% CI: 0.9-1.3). We observed some evidence of a stronger association for men than women (for early-late adulthood weight gain >3 kg/5 years, OR for men=1.4, 95% CI: 1.1-1.8; OR for women=1.1, 95% CI: 0.8-1.5), although the interaction was not statistically significant (p-int=0.65). When we stratified by starting BMI, we observed a significantly decreased risk of Colorectal Adenoma with weight loss from early-late adulthood among those who were overweight/obese at age 20 (OR=0.4, 95% CI: 0.2-0.9). Findings suggest that weight loss in adulthood for those who are overweight/obese is associated with a reduced risk of Colorectal Adenoma. In addition, our results suggest that a modest rate of weight gain in adulthood of >3 kg/5 years is associated with an increased risk of Colorectal Adenoma. These findings underscore the importance of healthy weight maintenance in adulthood in preventing Colorectal Adenoma. Citation Format: Shisi He, Sonja I. Berndt, Andrew T. Kunzmann, Cari M. Kitahara, Wen-Yi Huang, Kathryn Hughes Barry. Weight change in adulthood and Colorectal Adenoma incidence in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr LB-158.

  • Research Article A Prospective Evaluation of C-reactive Protein Levels and Colorectal Adenoma
    2016
    Co-Authors: Marc J Gunter, Arthur Schatzkin, Wen Yi Huang, A J. Cross, Frank Z. Stanczyk, Mark Purdue, Xiaonan Xue, Robert Schoen, Paul J. Limburg, Rashmi Sinha
    Abstract:

    Background: Inflammation is hypothesized to play a role in Colorectal tumorigenesis. Circulating levels of C-reactive protein (CRP), a serologic marker of the inflammatory response, have been positively associated with Colorectal cancer development in some studies; however, there are limited data on the relation of CRP with Colorectal Adenomas, established precursors of Colorectal cancer. Methods: A nested case–control investigation of CRP levels and incident Colorectal Adenoma was conducted in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, a randomized trial of 154,942 individuals designed to test the efficacy of flexible sigmoidoscopy on Colorectal cancermortality when performed once, and then repeated 3 to 5 years later. Serum CRP levels were measured in baseline blood specimens from participants who were free of polyps in the left-sided colorectum at the baseline screening procedure, butwhowere found at the subsequent screen to have at least one Colorectal Adenoma (n 356), and in a set of polyp-free, frequency-matched controls (n 396). Results: In a multivariable logistic regression model that included established Colorectal Adenoma risk factors, a 1-unit increase in log CRP level was associated with a 15 % reduction in risk of developing Colorectal Adenoma (OR 0.85, 95 % CI, 0.75–0.98, Ptrend 0.01). This association did not differ according to body size, smoking behavior, gender, use of nonsteroidal antiinflammatory drugs, or Adenoma location. Conclusions: High circulating CRP levels may be protective against Colorectal Adenoma development. Impact: Though at contrast with mechanistic data on inflammation and Colorectal tumorigenesis, this finding is not inconsistent with prior results on CRP and Colorectal Adenoma and warrants further investigation. Cancer Epidemiol Biomarkers Prev; 20(3); 537–44. 2011 AACR

  • A prospective evaluation of C-reactive protein levels and Colorectal Adenoma development
    2016
    Co-Authors: Marc J Gunter, Arthur Schatzkin, Wen Yi Huang, A J. Cross, Frank Z. Stanczyk, Mark Purdue, Xiaonan Xue, Robert Schoen, Paul J. Limburg, Rashmi Sinha
    Abstract:

    Background Inflammation is hypothesized to play a role in Colorectal tumorigenesis. Circulating levels of C-reactive protein (CRP), a serologic marker of the inflammatory response, have been positively associated with Colorectal cancer development in some studies; however, there are limited data on the relation of CRP with Colorectal Adenomas, established precursors of Colorectal cancer. Methods A nested case-control investigation of CRP levels and incident Colorectal Adenoma was conducted in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, a randomized trial of 154,942 individuals designed to test the efficacy of flexible sigmoidoscopy on Colorectal cancer mortality when performed once, and then repeated 3-5 years later. Serum CRP levels were measured in baseline blood specimens from participants who were free of polyps in the left-sided colorectum at the baseline screening procedure, but who were found at the subsequen

  • iron homeostasis and distal Colorectal Adenoma risk in the prostate lung Colorectal and ovarian cancer screening trial
    Cancer Prevention Research, 2011
    Co-Authors: Amanda J Cross, Richard B. Hayes, Rashmi Sinha, Wen Yi Huang, Meredith Yeager, Xiaonan Xue, Richard J Wood, Marc J Gunter
    Abstract:

    Red meat consumption has been positively associated with Colorectal cancer; however, the biologic mechanism underlying this relationship is not understood. Red meat is a major source of iron, which may play a role in Colorectal carcinogenesis via increased crypt cell proliferation, cytotoxicity, and endogenous N-nitrosation. In a nested case-control study within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we prospectively evaluated multiple iron exposure parameters, including dietary intake and serum measures of iron, ferritin, transferrin, total iron binding capacity (TIBC), and unsaturated iron binding capacity (UIBC) in relation to incident Colorectal Adenoma in 356 cases and 396 matched, polyp-free controls. We also investigated variation in eight key genes involved in iron homeostasis in relation to Colorectal Adenoma in an additional series totaling 1,126 cases and 1,173 matched controls. We observed a positive association between red meat intake and Colorectal Adenoma (odds ratio comparing extreme quartiles [ORq4-q1] = 1.59, 95% confidence interval [CI]: 1.02-2.49, P-trend = 0.03). Serum TIBC and UIBC were inversely associated with Colorectal Adenoma (ORq4-q1 = 0.57, 95% CI: 0.37-0.88, P-trend = 0.03; and ORq4-q1 = 0.62, 95% CI: 0.40-0.95, P-trend = 0.04, respectively). Colorectal Adenoma was not associated with serum ferritin, iron, or transferrin saturation, or with polymorphisms in genes involved in iron homeostasis. Serum TIBC and UIBC, parameters which have a reciprocal relationship with overall iron load, were inversely related to Colorectal Adenoma, suggesting that individuals with lower iron status have a reduced risk of Colorectal Adenoma.

  • polymorphisms in the Adenomatous polyposis coli apc gene and advanced Colorectal Adenoma risk
    European Journal of Cancer, 2010
    Co-Authors: Hui Lee Wong, Richard B. Hayes, Ulrike Peters, Arthur Schatzkin, Robert S Bresalier, Wen Yi Huang, Ellen M Velie, Lawrence C Brody
    Abstract:

    Abstract While germline mutations in the Adenomatous polyposis coli ( APC ) gene cause the hereditary colon cancer syndrome (familial Adenomatous polyposis (FAP)), the role of common germline APC variants in sporadic Adenomatous polyposis remains unclear. We studied the association of eight APC single nucleotide polymorphisms (SNPs), possibly associated with functional consequences, and previously identified gene–environment (dietary fat intake and hormone replacement therapy (HRT) use) interactions, in relation to advanced Colorectal Adenoma in 758 cases and 767 sex- and race-matched controls, randomly selected from the screening arm of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Cases had at least one verified advanced Adenoma of the distal colon; controls, a negative sigmoidoscopy. We did not observe an association between genotypes for any of the eight APC SNPs and advanced distal Adenoma risk ( P global gene-based =0.92). Frequencies of identified common haplotypes did not differ between cases and controls ( P global haplotype test =0.97). However, the risk for advanced distal Adenoma was threefold higher for one rare haplotype (cases: 2.7%; controls: 1.6%) (odds ratio (OR)=3.27; 95% confidence interval (CI)=1.08–9.88). The genetic association between D1822V and advanced distal Adenoma was confined to persons consuming a high-fat diet ( P interaction =0.03). Similar interactions were not observed with HRT use. In our large, nested case-control study of advanced distal Adenoma and clinically verified Adenoma-free controls, we observed no association between specific APC SNPs and advanced Adenoma. Fat intake modified the APC D1822V-Adenoma association, but further studies are warranted.

Rashmi Sinha - One of the best experts on this subject based on the ideXlab platform.

  • Research Article A Prospective Evaluation of C-reactive Protein Levels and Colorectal Adenoma
    2016
    Co-Authors: Marc J Gunter, Arthur Schatzkin, Wen Yi Huang, A J. Cross, Frank Z. Stanczyk, Mark Purdue, Xiaonan Xue, Robert Schoen, Paul J. Limburg, Rashmi Sinha
    Abstract:

    Background: Inflammation is hypothesized to play a role in Colorectal tumorigenesis. Circulating levels of C-reactive protein (CRP), a serologic marker of the inflammatory response, have been positively associated with Colorectal cancer development in some studies; however, there are limited data on the relation of CRP with Colorectal Adenomas, established precursors of Colorectal cancer. Methods: A nested case–control investigation of CRP levels and incident Colorectal Adenoma was conducted in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, a randomized trial of 154,942 individuals designed to test the efficacy of flexible sigmoidoscopy on Colorectal cancermortality when performed once, and then repeated 3 to 5 years later. Serum CRP levels were measured in baseline blood specimens from participants who were free of polyps in the left-sided colorectum at the baseline screening procedure, butwhowere found at the subsequent screen to have at least one Colorectal Adenoma (n 356), and in a set of polyp-free, frequency-matched controls (n 396). Results: In a multivariable logistic regression model that included established Colorectal Adenoma risk factors, a 1-unit increase in log CRP level was associated with a 15 % reduction in risk of developing Colorectal Adenoma (OR 0.85, 95 % CI, 0.75–0.98, Ptrend 0.01). This association did not differ according to body size, smoking behavior, gender, use of nonsteroidal antiinflammatory drugs, or Adenoma location. Conclusions: High circulating CRP levels may be protective against Colorectal Adenoma development. Impact: Though at contrast with mechanistic data on inflammation and Colorectal tumorigenesis, this finding is not inconsistent with prior results on CRP and Colorectal Adenoma and warrants further investigation. Cancer Epidemiol Biomarkers Prev; 20(3); 537–44. 2011 AACR

  • A prospective evaluation of C-reactive protein levels and Colorectal Adenoma development
    2016
    Co-Authors: Marc J Gunter, Arthur Schatzkin, Wen Yi Huang, A J. Cross, Frank Z. Stanczyk, Mark Purdue, Xiaonan Xue, Robert Schoen, Paul J. Limburg, Rashmi Sinha
    Abstract:

    Background Inflammation is hypothesized to play a role in Colorectal tumorigenesis. Circulating levels of C-reactive protein (CRP), a serologic marker of the inflammatory response, have been positively associated with Colorectal cancer development in some studies; however, there are limited data on the relation of CRP with Colorectal Adenomas, established precursors of Colorectal cancer. Methods A nested case-control investigation of CRP levels and incident Colorectal Adenoma was conducted in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, a randomized trial of 154,942 individuals designed to test the efficacy of flexible sigmoidoscopy on Colorectal cancer mortality when performed once, and then repeated 3-5 years later. Serum CRP levels were measured in baseline blood specimens from participants who were free of polyps in the left-sided colorectum at the baseline screening procedure, but who were found at the subsequen

  • meat related mutagen exposure xenobiotic metabolizing gene polymorphisms and the risk of advanced Colorectal Adenoma and cancer
    Carcinogenesis, 2012
    Co-Authors: Anne M J Gilsing, Joel L Weissfeld, Barry I Graubard, Amanda J Cross, Sonja I Berndt, Elizabeth H Ruder, L Ferrucci, Laura Burdett, Rashmi Sinha
    Abstract:

    Meat mutagens, including heterocyclic amines (HCAs), polycyclic aromatic hydrocarbons (PAHs) and N-nitroso compounds (NOCs), may be involved in Colorectal carcinogenesis depending on their activation or detoxification by phase I and II xenobiotic metabolizing enzymes (XME). Using unconditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI), we examined the intake of five meat mutagens and >300 single nucleotide polymorphisms (SNPs) in 18 XME genes in relation to advanced Colorectal Adenoma (1205 cases and 1387 controls) and Colorectal cancer (370 cases and 401 controls) within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Dietary intake of meat mutagens was assessed using a food frequency questionnaire with a detailed meat-cooking module. An interaction was observed between 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) intake and the NAT1 polymorphism rs6586714 in the Adenoma study (P interaction = 0.001). Among individuals carrying a GG genotype, high MeIQx intake was associated with a 43% increased risk of Adenoma (95% CI 1.11–1.85, P trend = 0.07), whereas the reverse was observed among carriers of the A variant (OR = 0.50, 95% CI 0.30–0.84, P trend = 0.01). In addition, we observed some suggestive (P < 0.05) modifying effects for SNPs in other XME genes (UGT1A, CYP2E1, EPHX1, AHR and GSTM3), but these were not significant after adjustment for multiple testing. This large and comprehensive study of XME genes, meat mutagens and the risk of Colorectal tumours found that a NAT1 polymorphism modified the association between MeIQx intake and Colorectal Adenoma risk.

  • iron homeostasis and distal Colorectal Adenoma risk in the prostate lung Colorectal and ovarian cancer screening trial
    Cancer Prevention Research, 2011
    Co-Authors: Amanda J Cross, Richard B. Hayes, Rashmi Sinha, Wen Yi Huang, Meredith Yeager, Xiaonan Xue, Richard J Wood, Marc J Gunter
    Abstract:

    Red meat consumption has been positively associated with Colorectal cancer; however, the biologic mechanism underlying this relationship is not understood. Red meat is a major source of iron, which may play a role in Colorectal carcinogenesis via increased crypt cell proliferation, cytotoxicity, and endogenous N-nitrosation. In a nested case-control study within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we prospectively evaluated multiple iron exposure parameters, including dietary intake and serum measures of iron, ferritin, transferrin, total iron binding capacity (TIBC), and unsaturated iron binding capacity (UIBC) in relation to incident Colorectal Adenoma in 356 cases and 396 matched, polyp-free controls. We also investigated variation in eight key genes involved in iron homeostasis in relation to Colorectal Adenoma in an additional series totaling 1,126 cases and 1,173 matched controls. We observed a positive association between red meat intake and Colorectal Adenoma (odds ratio comparing extreme quartiles [ORq4-q1] = 1.59, 95% confidence interval [CI]: 1.02-2.49, P-trend = 0.03). Serum TIBC and UIBC were inversely associated with Colorectal Adenoma (ORq4-q1 = 0.57, 95% CI: 0.37-0.88, P-trend = 0.03; and ORq4-q1 = 0.62, 95% CI: 0.40-0.95, P-trend = 0.04, respectively). Colorectal Adenoma was not associated with serum ferritin, iron, or transferrin saturation, or with polymorphisms in genes involved in iron homeostasis. Serum TIBC and UIBC, parameters which have a reciprocal relationship with overall iron load, were inversely related to Colorectal Adenoma, suggesting that individuals with lower iron status have a reduced risk of Colorectal Adenoma.

  • meat intake preparation methods mutagens and Colorectal Adenoma recurrence
    Carcinogenesis, 2007
    Co-Authors: Maria Elena Martinez, Rashmi Sinha, Elizabeth T Jacobs, Eri L Ashbeck, Pete Lance, David S. Alberts, Patricia A Thompso
    Abstract:

    Red meat intake has been shown to be associated with higher risk of Colorectal cancer. Though the exact mechanisms responsible for this association remain unknown, several tumorigenic properties of meat have been proposed. One well-supported biologic mechanism is elevated exposure to the genotoxic formation of heterocyclic amines (HCAs), which occur when meat is cooked at high temperatures for a long period of time. We prospectively assessed the relation between type of meat, meat preparation method, doneness, a metric of HCAs and other mutagens and Colorectal Adenoma recurrence among 869 participants in a chemoprevention trial of ursodeoxycholic acid. Unconditional logistic regression analyses were used to estimate odds ratios (ORs) and associated 95% confidence intervals (CIs). Most meat variables assessed were positively but weakly associated with recurrence of any Adenoma. In contrast, recurrence of advanced or multiple Adenomas was more strongly associated with a number of the meat exposure variables evaluated. For recurrence of advanced lesions, significant associations were detected among individuals in the highest when compared with the lowest tertile of intake for pan-fried red meat (OR = 1.85; 95% CI = 1.10-3.13) and well/very well done red meat (OR = 1.71; 95% CI = 1.02-2.86). Significant positive associations were shown for recurrence of multiple Adenomas and the following variables: processed meat (OR = 1.83; 95% CI = 1.10-3.04), pan-fried red meat (OR = 1.63; 95% CI = 1.01-2.61), well/very well done red meat (OR = 1.68; 95% CI = 1.03-2.74), 2-amino-3,4,8-trimethylimidazo[4,5,-f]quinoxaline (OR = 1.74; 95% CI = 1.07-2.82) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (OR = 1.68; 95% CI = 1.03-2.75). Our results support a meat mutagen exposure hypothesis as a potential mechanism for recurrence of clinically significant Adenomatous polyps.