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Dietary folate and APC mutations in sporadic colorectal cancer.
J Nutr 2006; 136(12):3015-21JN

Abstract

Folate deficiency has been associated with colorectal cancer risk and may be involved in colorectal carcinogenesis through increased chromosome instability, gene mutations, and aberrant DNA methylation. Within the Netherlands Cohort Study on diet and cancer, we investigated the associations between dietary folate intake and colorectal cancer risk with (APC(+)) and without (APC(-)) truncating APC mutations, accounting for hMLH1 expression and K-ras mutations. In total, 528 cases and 4200 subcohort members were available for data analyses of the study cohort (n = 120,852) from a follow-up period between 2.3 and 7.3 y after baseline. Adjusted gender-specific incidence rate ratios (RR) over tertiles of folate intake were calculated in case-cohort analyses for colon and rectal cancer. Although relatively high folate intake was not associated with overall colorectal cancer risk, it reduced the risk of APC(-)colon tumors in men (RR 0.58, 95% CI 0.32-1.05, P(trend) = 0.06 for the highest vs. lowest tertile of folate intake). In contrast, it was positively associated with APC(+) colon tumors in men (highest vs. lowest tertile: RR 2.77, 95% CI 1.29-5.95, P(trend) = 0.008) and was even stronger when the lack of hMLH1 expression and K-ras mutations were excluded (RR 3.99, 95% CI 1.43-11.14, P(trend) = 0.007). Such positive associations were not observed among women; nor was folate intake associated with rectal cancer when APC mutation status was taken into account. Relatively high folate consumption reduced the risk of APC(-) colon tumors, but folate intake was positively associated with APC(+) colon tumors among men. These opposite results may indicate that folate enhances colorectal carcinogenesis through a distinct APC mutated pathway.

Authors+Show Affiliations

Research Institute Growth and Development (GROW), Department of Epidemiology, Maastricht University, Maastricht, The Netherlands. stefan.devogel@epid.unimaas.nlNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17116713

Citation

de Vogel, Stefan, et al. "Dietary Folate and APC Mutations in Sporadic Colorectal Cancer." The Journal of Nutrition, vol. 136, no. 12, 2006, pp. 3015-21.
de Vogel S, van Engeland M, Lüchtenborg M, et al. Dietary folate and APC mutations in sporadic colorectal cancer. J Nutr. 2006;136(12):3015-21.
de Vogel, S., van Engeland, M., Lüchtenborg, M., de Bruïne, A. P., Roemen, G. M., Lentjes, M. H., ... Weijenberg, M. P. (2006). Dietary folate and APC mutations in sporadic colorectal cancer. The Journal of Nutrition, 136(12), pp. 3015-21.
de Vogel S, et al. Dietary Folate and APC Mutations in Sporadic Colorectal Cancer. J Nutr. 2006;136(12):3015-21. PubMed PMID: 17116713.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary folate and APC mutations in sporadic colorectal cancer. AU - de Vogel,Stefan, AU - van Engeland,Manon, AU - Lüchtenborg,Margreet, AU - de Bruïne,Adriaan P, AU - Roemen,Guido M J M, AU - Lentjes,Marjolein H F M, AU - Goldbohm,R Alexandra, AU - van den Brandt,Piet A, AU - de Goeij,Anton F P M, AU - Weijenberg,Matty P, PY - 2006/11/23/pubmed PY - 2007/1/24/medline PY - 2006/11/23/entrez SP - 3015 EP - 21 JF - The Journal of nutrition JO - J. Nutr. VL - 136 IS - 12 N2 - Folate deficiency has been associated with colorectal cancer risk and may be involved in colorectal carcinogenesis through increased chromosome instability, gene mutations, and aberrant DNA methylation. Within the Netherlands Cohort Study on diet and cancer, we investigated the associations between dietary folate intake and colorectal cancer risk with (APC(+)) and without (APC(-)) truncating APC mutations, accounting for hMLH1 expression and K-ras mutations. In total, 528 cases and 4200 subcohort members were available for data analyses of the study cohort (n = 120,852) from a follow-up period between 2.3 and 7.3 y after baseline. Adjusted gender-specific incidence rate ratios (RR) over tertiles of folate intake were calculated in case-cohort analyses for colon and rectal cancer. Although relatively high folate intake was not associated with overall colorectal cancer risk, it reduced the risk of APC(-)colon tumors in men (RR 0.58, 95% CI 0.32-1.05, P(trend) = 0.06 for the highest vs. lowest tertile of folate intake). In contrast, it was positively associated with APC(+) colon tumors in men (highest vs. lowest tertile: RR 2.77, 95% CI 1.29-5.95, P(trend) = 0.008) and was even stronger when the lack of hMLH1 expression and K-ras mutations were excluded (RR 3.99, 95% CI 1.43-11.14, P(trend) = 0.007). Such positive associations were not observed among women; nor was folate intake associated with rectal cancer when APC mutation status was taken into account. Relatively high folate consumption reduced the risk of APC(-) colon tumors, but folate intake was positively associated with APC(+) colon tumors among men. These opposite results may indicate that folate enhances colorectal carcinogenesis through a distinct APC mutated pathway. SN - 0022-3166 UR - https://www.unboundmedicine.com/medline/citation/17116713/Dietary_folate_and_APC_mutations_in_sporadic_colorectal_cancer_ L2 - https://academic.oup.com/jn/article-lookup/doi/10.1093/jn/136.12.3015 DB - PRIME DP - Unbound Medicine ER -