Published February 20, 2012 | Version v1
Journal article

Xenobiotic Metabolizing Gene Variants and Renal Cell Cancer: A Multicenter Study

  • 1. Department of Epidemiology, School of Public Health, University of California Los Angeles, Los Angeles, CA (United States)
  • 2. International Agency for Research on Cancer, Lyon (France)
  • 3. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (United States)
  • 4. Samuel Lunenfeld Research Institute of Mount Sinai Hospital, Toronto, ON (Canada)
  • 5. Department of Epidemiology, Institute of Occupational Medicine, Lodz (Poland)
  • 6. Cancer Research Centre, Institute of Carcinogenesis, Moscow (Russian Federation)
  • 7. Cancer Research Centre, Department of Epidemiology, Moscow (Russian Federation)
  • 8. Institute of Public Health, Bucharest (Romania)
  • 9. Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer Institute, Brno (Czech Republic)
  • 10. Department of Preventive Medicine, Faculty of Medicine, Palacky University, Olomouc (Czech Republic)
  • 11. First Faculty of Medicine, Institute of Hygiene and Epidemiology, Charles University in Prague, Prague, Czech Republic (Czech Republic)
  • 12. Tisch Cancer Institute, Mt. Sinai School of Medicine, New York, NY (United States)
  • 13. International Prevention Research Institute, Lyon (France)

Description

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.

Availability note (English)

Available from http://dx.doi.org/10.3389/fonc.2012.00016

Additional details

Identifiers

Publishing Information

Journal Title
Frontiers in Oncology
Journal Volume
2
Journal Page Range
[7 p.]
ISSN
2234-943X

INIS

Country of Publication
Switzerland
Country of Input or Organization
International Atomic Energy Agency (IAEA)
INIS RN
49035213
Subject category
S62: RADIOLOGY AND NUCLEAR MEDICINE;
Descriptors DEI
BIOLOGICAL PATHWAYS; EASTERN EUROPE; GENES; KIDNEYS; METABOLIC DISEASES; NEOPLASMS; OCCUPATIONAL EXPOSURE; XENOBIOTICS
Descriptors DEC
BODY; DISEASES; EUROPE; ORGANS

Optional Information

Copyright
Copyright (c) 2012 Heck, Moore, Lee, McKay, Hung, Karami, Gaborieau, Szeszenia-Dabrowska, Zaridze, Mukeriya, Mates, Foretova, Janout, Koll#Latin Small Letter A With Acute#rov#Latin Small Letter A With Acute#, Bencko, Rothman, Brennan, Chow and Boffetta.