Folate and carcinogenesis: evidence, mechanisms, and implications

Kim, Young–In

doi:10.1016/s0955-2863(98)00074-6

Cited by 502 publications

(426 citation statements)

References 186 publications

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“…However, not all animal studies support the protective role of folate supplementation in colorectal carcinogenesis. 4 In one study, dietary folate supplementation did not have a significant inhibitory effect on aberrant crypt foci, probably the earliest recognizable precursor lesion and a well established intermediate biomarker of colorectal carcinoma. In another study, folate supplementation significantly increased the size and multiplicity of colorectal tumors.…”

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confidence: 96%

“…Although it is well established that folic acid deficiency will retard the growth of established cancers, it does not necessarily follow that nonneoplastic folate-deficient tissues are less likely to undergo neoplastic transformation. 4 The roles of folate deficiency and supplementation in colorectal carcinogenesis have been studied extensively since Freudenheim et al 5 suggested this relationship. They found a lower risk of colorectal carcinoma in association with high dietary folate intake in a case-control study.…”

mentioning

confidence: 99%

“…In another study, folate supplementation significantly increased the size and multiplicity of colorectal tumors. 4 Some studies have shown that folate deficiency reduces the development of colorectal carcinoma in rats. 23 Cravo et al 24 concluded from a rat study that folate-deficient rats developed microscopic and macroscopic colorectal neoplasms after initiation of dimethylhydrazine, suggesting that folate deficiency affects an early phase of colorectal carcinogenesis.…”

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confidence: 99%

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Intake of dietary folate vitamers and risk of colorectal carcinoma

Konings

Goldbohm

Brants

et al. 2002

Cancer

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BACKGROUNDSeveral studies have reported inverse associations between folate intake and colorectal carcinoma risk. Few were prospective studies and none evaluated the association between the intake of individual folate vitamers and colorectal carcinoma risk.METHODSThe aim of the current study was to investigate the relationship between dietary folate intake and the risk of colorectal carcinoma in a large prospective cohort study in The Netherlands comprising 120,852 men and women aged 55–69 years. After 7.3 years of follow‐up, 760 colon and 411 rectal carcinoma cases were available for analysis. Data processing and analysis used the case–cohort approach. A new Dutch database was used to estimate intakes of total and individual folate vitamers.RESULTSAnalyses adjusted for age, energy intake, family history of colorectal carcinoma, alcohol, vitamin C, iron, and dietary fiber intake yielded an inverse association between colon carcinoma risk and total dietary folate intake (rate ratio [RR]highest vs. lowest quintile, men: 0.73; 95% confidence interval [CI], 0.46–1.17, P trend = 0.03; women: 0.68; 95% CI, 0.39–1.20, P trend = 0.18). An inverse association between rectal carcinoma and total dietary folate intake was found only among men (RR highest vs. lowest quintile, men: 0.66; 95% CI, 0.35–1.21, P trend = 0.03). Analyses showed no clear difference in colorectal carcinoma risk associated with intake of different folate vitamers.CONCLUSIONSDietary folate intake was related inversely to colon and male rectal carcinoma risk. Cancer 2002;95:1421–33. © 2002 American Cancer Society.DOI 10.1002/cncr.10866

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confidence: 99%

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Intake of dietary folate vitamers and risk of colorectal carcinoma

Konings

Goldbohm

Brants

et al. 2002

Cancer

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“…Collectively, the evidence from epidemiological, animal and human studies strongly suggests that folate status modulates the risk of developing cancers in selected tissue, the most notable of which is the colorectum (Kim, 1999). Folate depletion appears to enhance carcinogenesis, whereas folate supplementation may convey a protective effect (Kim, 1999).…”

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“…Folate depletion appears to enhance carcinogenesis, whereas folate supplementation may convey a protective effect (Kim, 1999). Recent studies suggest that folate may play an important role in the prevention of breast cancer, particularly among women consuming alcohol (Zhang, 2004).…”

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Investigation of systemic folate status, impact of alcohol intake and levels of DNA damage in mononuclear cells of breast cancer patients

et al. 2005

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Folate is required for DNA synthesis, repair and methylation. Low folate status has been implicated in carcinogenesis, possibly as a result of higher rate of genetic damage. The aim of this study is to compare folate status and levels of DNA damage between breast cancer and benign breast disease control patients. Fasting blood samples from 64 histologically confirmed untreated breast cancer patients (mean age 57 years) and 30 benign breast disease control patients (mean age 51 years) were obtained. Red cell folate (RCF) and plasma homocysteine were measured. Mononuclear cells (MNC) were isolated for genetic damage analysis using the basic alkaline comet assay. Results are expressed as tail moment. Data were log transformed as appropriate before analysis for normalisation purposes. The geometric mean (95% confidence interval) of RCF (ng ml À1 ) in breast cancer patients was 339.07 (333.3 -404.6) vs 379.5 (335.8 -505.2) in control patients (P ¼ 0.24). Corresponding plasma homocysteine concentrations (mmol l À1 ) were 11.9 (10.6 -16.4) vs 10.1 (9.3 -11.9) (P ¼ 0.073), respectively. The mean tail moment (s.d.) of DNA damage in MNC of breast cancer patients detected by the basic comet assay was 1.4 (0.66) vs -0.17 (0.79) in controls (Po0.0001, t-test), the modified comet assay 'endonuclease III (Endo III)' was 1.7 (0.70) vs 0.86 (0.81) (Po0.0001, t-test), and the modified comet assay 'formamidopyrimidine glycosylase (FPG)' was 1.6 (0.62) vs 0.99 (0.94) (Po0.0001, t-test). There was a significant negative correlation between RCF levels and DNA damage detected by modified comet assay 'FPG' (Pearson Correlation Coefficient r 2 ¼ À0.26, P ¼ 0.02) and DNA damage was found to be significantly higher in MNC of breast cancer patients compared to benign breast disease control patients. Breast cancer patients tended to have lower RCF levels and higher levels of plasma homocysteine, but these differences were not significant. The study provides preliminary evidence that reduced folate status may be implicated in the aetiology of breast cancer perhaps by increasing the in vivo level of genetic instability.

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B Vitamin and/or ω-3 Fatty Acid Supplementation and Cancer

Touvier¹

2012

Arch Intern Med

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Folate and carcinogenesis: evidence, mechanisms, and implications

Cited by 502 publications

References 186 publications

Intake of dietary folate vitamers and risk of colorectal carcinoma

Intake of dietary folate vitamers and risk of colorectal carcinoma

Investigation of systemic folate status, impact of alcohol intake and levels of DNA damage in mononuclear cells of breast cancer patients

B Vitamin and/or ω-3 Fatty Acid Supplementation and Cancer

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