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Br J Nutr. 2016 May;115(9):1643-60. doi: 10.1017/S0007114516000696.

Vitamin D and colorectal cancer: molecular, epidemiological and clinical evidence.

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1Department of Medical Oncology,Dana-Farber Cancer Institute and Harvard Medical School, 450 Brookline Avenue,Boston,MA 02215,USA.
3Department of Nutrition,Harvard T. H. Chan School of Public Health, 677 Huntington Avenue,Boston,MA 02115,USA.


In many cells throughout the body, vitamin D is converted into its active form calcitriol and binds to the vitamin D receptor (VDR), which functions as a transcription factor to regulate various biological processes including cellular differentiation and immune response. Vitamin D-metabolising enzymes (including CYP24A1 and CYP27B1) and VDR play major roles in exerting and regulating the effects of vitamin D. Preclinical and epidemiological studies have provided evidence for anti-cancer effects of vitamin D (particularly against colorectal cancer), although clinical trials have yet to prove its benefit. In addition, molecular pathological epidemiology research can provide insights into the interaction of vitamin D with tumour molecular and immunity status. Other future research directions include genome-wide research on VDR transcriptional targets, gene-environment interaction analyses and clinical trials on vitamin D efficacy in colorectal cancer patients. In this study, we review the literature on vitamin D and colorectal cancer from both mechanistic and population studies and discuss the links and controversies within and between the two parts of evidence.


25(OH)D 25-Hydroxyvitamin D; 25-Hydroxyvitamin D; CDK cyclin-dependent kinase; MPE molecular pathological epidemiology; P450 hydroxylases; VDR vitamin D receptor; Vitamin D supplementation; miR microRNA

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