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Xenobiotic‐Metabolizing gene polymorphisms and ovarian cancer risk
Author(s) -
Goode Ellen L.,
White Kristin L.,
Vierkant Robert A.,
Phelan Catherine M.,
Cunningham Julie M.,
Schildkraut Joellen M.,
Berchuck Andrew,
Larson Melissa C.,
Fridley Brooke L.,
Olson Janet E.,
Webb Penelope M.,
Chen Xiaoqing,
Beesley Jonathan,
ChenevixTrench Georgia,
Sellers Thomas A.
Publication year - 2011
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.20714
Subject(s) - biology , single nucleotide polymorphism , ovarian cancer , gstp1 , odds ratio , genotype , carcinogenesis , oncology , serous fluid , case control study , medicine , snp , cancer , genetics , bioinformatics , gene , biochemistry
Because selected xenobiotic‐metabolizing enzymes process pro‐carcinogens that could initiate ovarian carcinogenesis, we hypothesized that single nucleotide polymorphisms (SNPs) in the genes encoding xenobiotic‐metabolizing enzymes are associated with risk of ovarian cancer. Cases with invasive epithelial ovarian cancer ( N = 1,571 including 956 of serous sub‐type) and controls ( N = 2,046) from three studies were genotyped at 11 SNPs in EPHX1 , ADH4 , ADH1A , NQO2 , NAT2 , GSTP1 , CYP1A1 , and NQO1 , following an initial SNP screen in a subset of participants. Logistic regression analysis of genotypes obtained via Illumina GoldenGate and Sequenom iPlex technologies revealed the following age‐ and study‐adjusted associations: EPHX1 rs1051740 with increased serous ovarian cancer risk [per‐allele odds ratio (OR) 1.17, 95% confidence interval (95% CI) 1.04–1.32, P = 0.01), ADH4 r1042364 with decreased ovarian cancer risk (OR 0.90, 95% CI: 0.81–1.00, P = 0.05), and NQO1 rs291766 with increased ovarian cancer risk (OR 1.11, 95% CI: 1.00–1.23, P = 0.04). These findings are consistent with prior studies implicating these genes in carcinogenesis and suggest that this collection of variants is worthy of follow‐up in additional studies. © 2010 Wiley‐Liss, Inc.