Journal of Cancer Prevention

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pISSN 2288-3649

Literatures assessing the interaction between vitamin D and related genetic polymorphisms regarding the risk of colorectal neoplasia (n = 13)

Reference (year)Study designNo. of subjectOutcomeDietDiet-CRC associationGene polymorphismGene-CRC associationGene-diet interaction OR/RR (95% CI)
Kim et al.24 (2001)Case-control (clinic-based, USA)393/406Colorectal adenomaVitamin DNot significantVDR BsmI (rs1544410): BB/Bb/bbCompared to BsmI bb genotype, BB genotype: OR = 0.71 (0.46–1.11)Inverse association with colorectal adenoma risk among BsmI BB genotype in the presence of lowest vitamin D intake: OR = 0.24 (0.08–0.76), P = 0.094
Peters et al.26 (2001)Case-control (clinic-based, USA)239/228Colorectal adenomaVitamin DSerum 25(OH)D: OR = 0.74 (0.60–0.92)VDR FokI (rs10735810): FF/Ff/ffNo associationNo association
Boyapati et al.19 (2003)Case-control (clinic-based, USA)177/228Colorectal adenomaVitamin DNot determinedVDR BsmI (rs1544410): BB/Bb/bbNo associationVDR genotype Bb having high vitamin D intake: OR = 0.29 (0.09–0.95), P < 0.01
Peters et al.25 (2004)Nested case-control (population-based, USA)Genotype analysis: 763/774  Serum levels: 394/397Colorectal adenomaVitamin D: levels of 25(OH)D and 1,25(OH)2The average serum level of 25(OH)D in cases was lower than in controls: P = 0.06; Higher serum 25(OH)D levels: OR = 0.27 (0.11–0.69), P = 0.0002; Serum levels of 1,25(OH)2D: No associationVDR TaqI (rs731236): TT/Tt/ttNo associationNo association
Gong et al.17 (2005)Case-control (clinic-based, USA)171/220Colorectal adenomaVitamin DNot significant difference in dietary vitamin D intake between cases and controls (P = 0.16)VDR Tru9I G > A: UU/Uu/uuTru9I having at least ‘u’ allele : OR = 0.36 (0.13–0.97) for Sessile shape of adenoma; OR = 0.38 (0.17–0.88) for womenNo evidence suggesting an interaction with VDR Tru9I and dietary micronutients
Dong et al.22 (2009)Case-control (population-based, USA)1,600/1,949Colon cancerVitamin DHigher use of vitamin D supplements in controls; Not significant inverse associations for the highest vitamin D intakeCYP24A1 IVS4 + 1653C > T (rs4809958), IVS5 − 162T > C (rs6013905); CYP27B1CYP24A1 IVS4 + I653C > T GT: OR = 0.82 (0.71–0.96), P = 0.03; GG/GT: OR = 0.83 (0.72–0.96), P = 0.03; IVS5-162T > C CT: OR = 0.85 (0.72–0.96), P = 0.06; CC/CT: OR = 0.85 (0.73–0.99), P = 0.06No statistically significant interactions between genotypes in CYP24A1 and total vitamin D (P = 0.80)
Jenab et al.23 (2009)Nested case-control (population-based, European countries)1,248/1,248Colorectal, colon, and rectal cancerVitamin D: level of serum 25(OH)DNot determinedVDR BsmI (rs1544410), Fok1 (rs2228570); CASR G > T (rs1801725)Compared to wild-type bb, the BB genotype of VDR BsmI: RR = 0.76 (0.59–0.98), P = 0.10 with colorectum; RR = 0.69 (0.45–0.95), P = 0.05 with colon;VDR FokI or CASR: No associationNo association between VDR BsmI and CRC risk with interaction with serum 25(OH)D (P = 0.43); Stratified analysis: BsmI BB genotype at higher serum 25(OH)D: RR = 0.41 (0.24–0.69), P = 0.03
Poynter et al.27 (2010)Case-control (family-based, USA, Canada, Australia)585/837Colorectal cancerVitamin DSimilar vitamin D intake in cases and controlsVDR FokI (rs10735810); BsmI (rs154410), CDX2 (rs11568820), ApaI (rs7975232); GCNo associationNo association
Kupfer et al.20 (2011)Case-control (popoulation-based, USA/Spain)AA: 795/985 Caucasians: 1,324/990Colorectal cancerVitamin DNot determinedVDR gene (RFLPs: FokI, BsmI, ApaI, TaqI)VDR ApaI T allele additive model associated with AA CRC: OR = 1.15 (1.00–1.33), P = 0.05 None of other RFLP SNPs: No associationAssociation of intronic rs11574041 A allele with CRC by vitamin D intake (≥ 100 IU): OR = 0.30, P = 0.0009
Theodoratou et al.21 (2012)Case-control (population-based, Scotland)2,001/2,237Colorectal cancerVitamin DHighest quintiles of 25(OH)D associated with reducing CRC risk: OR = 0.47 (0.39–0.57), P < 0.0005CYP2R1 (rs10741657); GC (rs2282679), CYP24A1 (rs6013897)No associationCYP2R1 GA associated with a decreased CRC risk for those of low plasma 25(OH)D levels (< 10 ng/ml): OR = 0.74 (0.59–0.94), P = 0.01
Yamaji et al.28 (2012)Case-control (clinic-based, Japan)737/703Colorectal and colon adenomaVitamin DHighest levels of plasma 25(OH)D: OR = 0.64 (0.45–0.92), P = 0.09VDR FokI (rs2228570), TaqI (rs731236)No associationThe interaction between 25(OH)D levels and colorectal adenoma was modified by TaqI Tt/tt polymorphism: OR = 0.43 (0.23–0.79), P = 0.03
Atoum and Tchoporyan16 (2014)Case-control (clinic-based, Jordan)93/102Colorectal cancerVitamin DSignificantly lower vitamin D level among cases (P ≤ 0.05);Only 2.2% optimal vitamin D in cases compared to 23.5% among controls (P = 0.005)VDR TaqI (rs731236): TT/Tt/ttNo association found between TT, Tt, and tt among CRC patients and controlsLower mean vitamin D level (ng/ml) among cases vs. controls with TT (8.91 ± 4.31) vs. TT (21.3 ± 8.31), P = 0.01; Tt (9.15 ± 5.25) vs. Tt (19 ± 7.68), P = 0.04
Takeshige et al.18 (2015)Case-control (population based, Japan)685/778Colorectal, colon, and rectal cancerCalcium, vitamin DVitamin D intake associated with decreased risks for colon cancer (P = 0.004), and for reactal cancer (P = 0.06)VDR genes: FokI (rs2228570), BsmI (rs1544410), ApaI (rs7975232), TaqI (rs731236)ApaI AA/Aa: OR = 0.75 (0.56–0.99), P = 0.04 for rectal cancer:Among individuals with ApaI AA/Aa having high vitamin D: OR = 0.46 (0.28–0.74), P = 0.09 for risk of colon cancer; Among individuals with FokI Ff/ff having high vitamin D intake: OR = 0.53 (0.35–0.78), P = 0.09 for risk of colorectal cancer

CRC, colorectal cancer; RR, relative risk; VDR, vitamin D receptor; CYP24A1, cytochrome P450, family 24, subfamily A, polypeptide 1; CYP27B1, cytochrome P450, family 27, subfamily B, polypeptide 1; CASR, calcium-sensing receptor; CYP2R1, cytochrome P450, family 2, subfamily R, polypeptide 1; RFLP, restriction fragment length polymorphism.

Journal of Cancer Prevention -0001;20:97~105 https://doi.org/10.15430/JCP.2015.20.2.97
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