No Interaction between Polymorphisms Related to Vitamin A Metabolism and Vitamin A Intake in Relation to Colorectal Cancer in a Prospective Danish Cohort

Vibeke Andersen, Ulrich Halekoh, Torsten Bohn, Anne Tjønneland, Ulla Vogel, Tine Iskov Kopp

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Resumé

Although vitamin A is essential for gut immune cell trafficking (paramount for the intestinal immune system), epidemiological studies on the role of vitamin A in colorectal cancer (CRC) aetiology are conflicting. By using functional polymorphisms, gene-environment (GxE) interaction analyses may identify the biological effects (or "mechanism of action") of environmental factors on CRC aetiology. Potential interactions between dietary or supplemental vitamin A intake and genetic variation in the vitamin A metabolic pathway genes related to risk of CRC were studied. We used a nested case-cohort design within the Danish "Diet, Cancer and Health" cohort, with prospectively collected lifestyle information from 57,053 participants, and the Cox proportional hazard models and likelihood ratio test. No statistically significant associations between the selected polymorphisms and CRC, and no statistically significant interactions between vitamin A intake and the polymorphisms were found. In conclusion, no support of an involvement of vitamin A in CRC aetiology was found.

OriginalsprogEngelsk
Artikelnummer1428
TidsskriftNutrients
Vol/bind11
Udgave nummer6
Antal sider15
ISSN2072-6643
DOI
StatusUdgivet - 25. jun. 2019

Fingeraftryk

colorectal neoplasms
vitamin A
Colorectal Neoplasms
genetic polymorphism
metabolism
etiology
Gene-Environment Interaction
genotype-environment interaction
Metabolic Networks and Pathways
Proportional Hazards Models
epidemiological studies
lifestyle
immune system
biochemical pathways
Epidemiologic Studies
Immune System
mechanism of action
digestive system
Diet
genetic variation

Citer dette

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title = "No Interaction between Polymorphisms Related to Vitamin A Metabolism and Vitamin A Intake in Relation to Colorectal Cancer in a Prospective Danish Cohort",
abstract = "Although vitamin A is essential for gut immune cell trafficking (paramount for the intestinal immune system), epidemiological studies on the role of vitamin A in colorectal cancer (CRC) aetiology are conflicting. By using functional polymorphisms, gene-environment (GxE) interaction analyses may identify the biological effects (or {"}mechanism of action{"}) of environmental factors on CRC aetiology. Potential interactions between dietary or supplemental vitamin A intake and genetic variation in the vitamin A metabolic pathway genes related to risk of CRC were studied. We used a nested case-cohort design within the Danish {"}Diet, Cancer and Health{"} cohort, with prospectively collected lifestyle information from 57,053 participants, and the Cox proportional hazard models and likelihood ratio test. No statistically significant associations between the selected polymorphisms and CRC, and no statistically significant interactions between vitamin A intake and the polymorphisms were found. In conclusion, no support of an involvement of vitamin A in CRC aetiology was found.",
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No Interaction between Polymorphisms Related to Vitamin A Metabolism and Vitamin A Intake in Relation to Colorectal Cancer in a Prospective Danish Cohort. / Andersen, Vibeke; Halekoh, Ulrich; Bohn, Torsten; Tjønneland, Anne; Vogel, Ulla; Kopp, Tine Iskov.

I: Nutrients, Bind 11, Nr. 6, 1428, 25.06.2019.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - No Interaction between Polymorphisms Related to Vitamin A Metabolism and Vitamin A Intake in Relation to Colorectal Cancer in a Prospective Danish Cohort

AU - Andersen, Vibeke

AU - Halekoh, Ulrich

AU - Bohn, Torsten

AU - Tjønneland, Anne

AU - Vogel, Ulla

AU - Kopp, Tine Iskov

PY - 2019/6/25

Y1 - 2019/6/25

N2 - Although vitamin A is essential for gut immune cell trafficking (paramount for the intestinal immune system), epidemiological studies on the role of vitamin A in colorectal cancer (CRC) aetiology are conflicting. By using functional polymorphisms, gene-environment (GxE) interaction analyses may identify the biological effects (or "mechanism of action") of environmental factors on CRC aetiology. Potential interactions between dietary or supplemental vitamin A intake and genetic variation in the vitamin A metabolic pathway genes related to risk of CRC were studied. We used a nested case-cohort design within the Danish "Diet, Cancer and Health" cohort, with prospectively collected lifestyle information from 57,053 participants, and the Cox proportional hazard models and likelihood ratio test. No statistically significant associations between the selected polymorphisms and CRC, and no statistically significant interactions between vitamin A intake and the polymorphisms were found. In conclusion, no support of an involvement of vitamin A in CRC aetiology was found.

AB - Although vitamin A is essential for gut immune cell trafficking (paramount for the intestinal immune system), epidemiological studies on the role of vitamin A in colorectal cancer (CRC) aetiology are conflicting. By using functional polymorphisms, gene-environment (GxE) interaction analyses may identify the biological effects (or "mechanism of action") of environmental factors on CRC aetiology. Potential interactions between dietary or supplemental vitamin A intake and genetic variation in the vitamin A metabolic pathway genes related to risk of CRC were studied. We used a nested case-cohort design within the Danish "Diet, Cancer and Health" cohort, with prospectively collected lifestyle information from 57,053 participants, and the Cox proportional hazard models and likelihood ratio test. No statistically significant associations between the selected polymorphisms and CRC, and no statistically significant interactions between vitamin A intake and the polymorphisms were found. In conclusion, no support of an involvement of vitamin A in CRC aetiology was found.

U2 - 10.3390/nu11061428

DO - 10.3390/nu11061428

M3 - Journal article

VL - 11

JO - Nutrients

JF - Nutrients

SN - 2072-6643

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