Dietary folate and colorectal cancer

Vecchia, Carlo La; Negri, Eva; Pelucchi, Claudio; Franceschi, Silvia

doi:10.1002/ijc.10720

Cited by 89 publications

(44 citation statements)

References 21 publications

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“…17 Other epidemiological studies have noted results generally in line with those of the present study, including null or inverse associations between intake or circulating levels of vitamin B12 and the risk of CRC or related endpoints, [12][13][14][15][16] and inverse associations for the risk of rectal cancer. 11,12 Several previous reports have related combinations of dietary factors involved in one-carbon metabolism to CRC risk, with results tending to support a cancer preventative effect of a ''high methyldonor'' diet, including, 11,15,16 or not including, [19][20][21][22][23] vitamin B12. Our findings, combining plasma vitamin B12 and folate (Table III) and total homocysteine concentrations (Table IV) did not support such an effect for colon cancer.…”

Section: Discussionmentioning

confidence: 99%

Plasma vitamin B12 concentrations and the risk of colorectal cancer: A nested case‐referent study

Dahlin

Guelpen

Hultdin

et al. 2008

Intl Journal of Cancer

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In this nested case-referent study, we related plasma concentrations of vitamin B12 to the risk of colorectal cancer, taking into consideration prediagnostic plasma folate and total homocysteine concentrations. Subjects were 226 cases and double matched referents from the population-based Northern Sweden Health and Disease Study. Follow-up times from recruitment to diagnosis ranged from 0.1 to 12.7 years, with a median of 4.2 years. Plasma vitamin B12 concentrations were inversely associated with the risk of rectal cancer: univariate odds ratio for the highest versus lowest quintile 0.34 (95% confidence interval (95% CI) 0.13-0.83), p trend 5 0.004. Risk estimates were attenuated slightly but remained statistically significant after adjustment for body mass index, current smoking, recreational and occupational physical activity, alcohol intake and prediagnostic plasma folate and total homocysteine concentrations: OR 0.30 (95% CI 0.08-0.99), p trend 5 0.025. The corresponding univariate and fully adjusted odds ratios for colon cancer were 1.25 (CI 0.66-2.36), p trend 5 0.185 and 1.42 (CI 0.67-3.05), p trend 5 0.113, respectively. The observed over-risk was attributable to left-sided colon cancer. Interaction analyses including vitamin B12, folate and homocysteine were in line with the results for vitamin B12 alone. In conclusion, these results suggest that increasing levels of plasma vitamin B12, alone or together with other factors involved in one-carbon metabolism, may reduce the risk of rectal cancer, whereas for colon cancer, the association appears to be less clear. ' 2007 Wiley-Liss, Inc.Key words: vitamin B12; cobalamin; colorectal cancer; risk factors; prospective Folate is a nutrient frequently discussed in the context of cancer etiology, particularly colorectal cancer (CRC).1 However, although functional folate status is highly dependent on vitamin B12 (cobalamin), few studies have addressed the potential role of vitamin B12 in colorectal tumorigenesis.Vitamin B12, found essentially only in animal products, acts as a coenzyme for methionine synthase, which mediates the methylation of homocysteine to methionine. Folate, in the form of 5-methyltetrahydrofolate (5-methylTHF) donates one-carbon groups for the reaction. Methionine is then converted to S-adenosylmethionine, which is responsible for methylation of DNA and other molecules. DNA methylation contributes to both genome stability and the regulation of gene expression, and is one of the principal mechanisms proposed for the putative involvement of one-carbon metabolism in carcinogenesis.1,2 The other main hypothesis is based on the critical role of folate, and thus vitamin B12, in DNA synthesis and repair.2 5,10-methylenetetrahydrofolate (5,10-methyleneTHF), which can be used for nucleotide synthesis, including the production of thymine from uracil, is converted to 5-methylTHF by methylenetetrahydrofolate reductase (MTHFR). However, since the MTHFR reaction is irreversible, 5-methylTHF must undergo a complete metabolic cycle, including the methionin...

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Section: Discussionmentioning

confidence: 99%

Plasma vitamin B12 concentrations and the risk of colorectal cancer: A nested case‐referent study

Dahlin

Guelpen

Hultdin

et al. 2008

Intl Journal of Cancer

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“…When several estimates were presented using different adjustments, 3,14,22,23 the fully adjusted ones were included. Where studies presented information for dietary and total folate intake separately, the estimates for both were abstracted.…”

Section: Data Extraction and Classificationmentioning

confidence: 99%

Folate intake and colorectal cancer risk: A meta‐analytical approach

SanJoaquin

Allen

Couto

et al. 2004

Intl Journal of Cancer

311

198

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Adequate consumption of folate may reduce the risk of colorectal cancer. We performed a meta-analysis of 7 cohort and 9 casecontrol studies that examined the association between folate consumption and colorectal cancer risk. In cohort studies, the association between folate consumption and colorectal cancer risk was stronger for dietary folate (folate from foods alone; relative risk for high vs. low intake ‫؍‬ 0.75; 95% CI ‫؍‬ 0.64 -0.89) than for total folate (folate from foods and supplements; relative risk for high vs. low intake ‫؍‬ 0.95; 95% CI ‫؍‬ 0.81-1.11) and there was no significant heterogeneity between studies. There was significant heterogeneity between case-control studies. These results offer some support for the hypothesis that folate has a small protective effect against colorectal cancer but confounding by other dietary factors cannot be ruled out. © 2004 Wiley-Liss, Inc. Key words: colorectal cancer; folate; folic acid; meta-analysis In Europe and most of the industrialized world, colorectal cancer (CRC) is the third most common cancer in men after lung and prostate cancer and the second most common in women after breast cancer. 1 There is experimental evidence suggesting that folate, a vitamin found mostly in vegetables and cereals, may reduce the risk of CRC. 2 An inadequate intake of folate may increase the risk of CRC by various mechanisms, including hypomethylation of DNA, which interferes with gene expression and impairs DNA repair, or by uracil misincorporation leading to DNA breaks and instability. The epidemiologic data, however, are not consistent; to date, 5 3-7 out of 7 3-9 prospective investigations and 7 10 -16 out of 11 case-control studies 10 -20 have found a relatively low risk for CRC in association with a relatively high intake of folate. No intervention studies have investigated the effect of folate supplementation on CRC risk, although the one trial with adenomatous polyps as an endpoint found a nonsignificant reduction in colorectal adenoma recurrence after 2 years in those receiving a folate supplement compared to placebo. 21 The aim of this study is to conduct a metaanalysis of published data to provide an overall estimate of the association of dietary and total folate (folate from food and supplements) with CRC risk. Material and methods Search strategyWe conducted electronic searches of the PubMed database, which includes articles back to the 1950s and up to January 2004, using both MeSH headings and text words including the terms "folate," "folic acid," "colorectal," "colon," "rectum," "bowel," "cancer" and exploded variants. All full articles that matched the inclusion criteria were retrieved and the reference lists in those articles were hand-searched for other relevant publications. Inclusion criteriaWe sought to identify all published English-language articles that provided estimates of risk (with 95% confidence intervals) of cancer of the colon and/or rectum in relation to dietary or total folate intake. Two studies that did not show confidence intervals for...

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“…Folate is a key B vitamin required for 1-carbon metabolism and is critical for DNA methylation, synthesis, and repair (Jemal et al, 2007). Deficiency of folate has been suggested to increase the risk of colorectal cancer because folate deficiency results in irregular DNA methylation and imbalance in DNA precursors (Eichholzer et al, 2001;La Vecchia et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Impact of methylenetetrahydrofolate reductase polymorphisms and folate intake on the risk of gastric cancer and their association with Helicobacter pylori infection and tumor site

Chen¹,

Yuan²,

Duan³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Folic acid and methylenetetrahydrofolate reductase (MTHFR) may both affect the development of human cancer. We conducted a population-based case-control study in a Chinese population to investigate the potential role of folate intake and MTHFR gene polymorphisms in gastric cancer, and their interaction with infection by Helicobacter pylori and tumor location. A total of 767 patients with newly diagnosed gastric cancer and 775 controls were selected for this study. Genotyping of MTHFR C677T and A1298C was conducted by TaqMan assays using the ABI Prism 7911HT Sequence Detection System, and information 9719 MTHFR and folate and gastric cancer risk ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (4): 9718-9726 (2014) on folate intake was collected by questionnaire. Compared with the CC genotype of MTHFR C677T, the TT genotype was significantly associated with a decreased risk of gastric cancer when the analysis was adjusted for other potential risk factors. We found a marginal significantly decreased risk of gastric cancer for individuals carrying the T allele [adjusted odds ratio (OR) = 0.83; 95% confidence interval (CI) = 0.65-1.01]. We detected an inverse relationship between folate intake and risk of gastric cancer, and the adjusted ORs (95%CI) for moderate and high folate intake were 0.97 (0.74-1.25) and 0.64 (0.49-0.87), respectively. Moreover, H. pylori infection, folate intake, and location of the tumor showed a significant interaction with the MTHFR C677T polymorphism. Our study suggests a protective role of MTHFR 677TT and high folate intake against gastric cancer, and the effect of the MTHFR C677T genotype may differ by H. pylori infection, folate consumption, and tumor site.

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Dietary folate and colorectal cancer

Cited by 89 publications

References 21 publications

Plasma vitamin B12 concentrations and the risk of colorectal cancer: A nested case‐referent study

Plasma vitamin B12 concentrations and the risk of colorectal cancer: A nested case‐referent study

Folate intake and colorectal cancer risk: A meta‐analytical approach

Impact of methylenetetrahydrofolate reductase polymorphisms and folate intake on the risk of gastric cancer and their association with Helicobacter pylori infection and tumor site

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