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Xenobiotic metabolizing gene variants and renal cell cancer: A multicenter study

  • Julia E. Heck
  • , Lee E. Moore
  • , Yuan Chin A. Lee
  • , James D. McKay
  • , Rayjean J. Hung
  • , Sara Karami
  • , Valérie Gaborieau
  • , Neonila Szeszenia-Dabrowska
  • , David G. Zaridze
  • , Anush Mukeriya
  • , Dana Mates
  • , Lenka Foretova
  • , Vladimir Janout
  • , Helena Kollárová
  • , Vladimir Bencko
  • , Nathaniel Rothman
  • , Paul Brennan
  • , Wong Ho Chow
  • , Paolo Boffetta
  • International Agency for Research on Cancer
  • University of California at Los Angeles
  • National Institutes of Health
  • University of Toronto
  • Nofer Institute of Occupational Medicine
  • Blokhin Cancer Research Center
  • National Institute of Public Health
  • Masaryk Memorial Cancer Institute
  • Palacký University Olomouc
  • Charles University

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Background: The countries of Central and Eastern Europe have among the highest worldwide rates of renal cell cancer (RCC). Few studies have examined whether genetic variation in xenobiotic metabolic pathway genes may modify risk for this cancer. Methods: The Central and Eastern Europe Renal Cell Cancer study was a hospital-based case-control study conducted between 1998 and 2003 across seven centers in Central and Eastern Europe. Detailed data were collected from 874 cases and 2053 controls on demographics, work history, and occupational exposure to chemical agents. Genes [cytochrome P-450 family, N-acetyltransferases, NAD(P)H:quinone oxidoreductase I (NQO1), microsomal epoxide hydrolase (mEH), catechol-O-methyltransferase (COMT), uridine diphosphate-glucuronosyltransferase (UGT)] were selected for the present analysis based on their putative role in xenobiotic metabolism. Haplotypes were calculated using fastPhase. Odds ratios and 95% confidence intervals were estimated by unconditional logistic regression adjusted for country of residence, age, sex, smoking, alcohol intake, obesity, and hypertension. Results: We observed an increased risk of RCC with one SNP. After adjustment for multiple comparisons it did not remain significant. Neither NAT1 nor NAT2 slow acetylation was associated with disease. Conclusion: We observed no association between this pathway and renal cell cancer.

Original languageEnglish
Article number00016
JournalFrontiers in Oncology
Volume2
Issue numberFEB
DOIs
StatePublished - 2012

Keywords

  • COMT
  • CYP
  • Epidemiology
  • MEH
  • NAT1
  • NAT2
  • NQO1
  • Renal cell cancer

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