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Epidemiology and Prevention

Candidate Genetic Modifiers of Individual Susceptibility to Renal Cell Carcinoma

A Study of Polymorphic Human Xenobiotic-metabolizing Enzymes

Sandrine Longuemaux, Claudine Deloménie, Catherine Gallou, Arnaud Méjean, Monique Vincent-Viry, Raymonde Bouvier, Dominique Droz, Rajagopal Krishnamoorthy, Marie-Madeleine Galteau, Claudine Junien, Christophe Béroud and Jean-Marie Dupret
Sandrine Longuemaux
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Claudine Deloménie
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Catherine Gallou
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Arnaud Méjean
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Monique Vincent-Viry
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Raymonde Bouvier
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Dominique Droz
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Rajagopal Krishnamoorthy
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Marie-Madeleine Galteau
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Claudine Junien
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Christophe Béroud
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Jean-Marie Dupret
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DOI:  Published June 1999
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Abstract

The steady increase in sporadic renal cell carcinoma (RCC) observed in industrialized countries supports the notion that certain carcinogens present in the environment (tobacco smoke, drugs, pollutants, and dietary constituents) may affect the occurrence of RCC. Many of the enzymes dealing with such environmental factors are polymorphic and may, therefore, confer variable susceptibility to RCC.

This case-control study was designed to test for an association between genetic polymorphism of enzymes involved in xenobiotic metabolism and the risk of sporadic RCC. Genomic DNA was obtained from 173 patients with RCC and 211 controls of Caucasian origin. We used PCR-RFLP to investigate polymorphism for the most common alleles at two cytochrome-P450 mono-oxygenases (CYP1A1 and CYP2D6), one NAD[P]H:quinone oxidoreductase (NQO1), three glutathione S-transferases (GSTM1, GSTT1, and GSTP1), and one N-acetyltransferase (NAT2) loci.

The CYP1A1 (m) “variant” genotype, which contains at least one copy of the CYP1A1 variant alleles, was found to be associated with a 2.1-fold [95% confidence interval (CI), 1.1–3.9] increase in the risk of RCC. There was also a higher risk of RCC for subjects with the CYP1A1 (m) variant genotype combined with any of the following genotypes: GSTT1 (+) “active” [odds ratio (OR), 2.3; 95% CI, 1.2–4.5], GSTP1 (m) variant (OR, 2.4; 95% CI, 1.0–5.4), or NAT2 (−) “slow acetylator” (OR, 2.5; 95% CI, 1.1–5.5). A significant association was also found for the GSTM1 (−) “null” and GSTP1 (m) genotypes combined with either NAT2 (−) (OR, 2.6; 95% CI, 1.2–5.8) or CYP1A1 (m) (OR, 3.5; 95% CI, 1.1–11.2). The CYP2D6 (−) “poor metabolizer ” and the NQO1 (−) “defective” genotypes were not clearly associated with a higher risk of RCC.

Our data demonstrate for the first time a significant association between a group of pharmacogenetic polymorphisms and RCC risk. These positive findings suggest that interindividual variation in the metabolic pathways involved in the functionalization and detoxification of specific xenobiotics is an important susceptibility factor for RCC in Caucasians.

Footnotes

  • The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

  • ↵1 Presented at the International Society for the Study of Xenobiotics, 5th International Meeting, Cairns, Australia, October 25–29, 1998.

  • ↵2 To whom requests for reprints should be addressed, at INSERM U458, Hopital Robert Debre, 48 boulevard Serurier, 75019 Paris, France. Phone: 33-1-40-03-19-26; Fax: 33-1-40-03-19-03; E-mail: jmdupret{at}infobiogen.fr

  • Received December 17, 1998.
  • Accepted April 16, 1999.
  • ©1999 American Association for Cancer Research.
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June 1999
Volume 59, Issue 12
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Candidate Genetic Modifiers of Individual Susceptibility to Renal Cell Carcinoma
Sandrine Longuemaux, Claudine Deloménie, Catherine Gallou, Arnaud Méjean, Monique Vincent-Viry, Raymonde Bouvier, Dominique Droz, Rajagopal Krishnamoorthy, Marie-Madeleine Galteau, Claudine Junien, Christophe Béroud and Jean-Marie Dupret
Cancer Res June 15 1999 (59) (12) 2903-2908;

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Candidate Genetic Modifiers of Individual Susceptibility to Renal Cell Carcinoma
Sandrine Longuemaux, Claudine Deloménie, Catherine Gallou, Arnaud Méjean, Monique Vincent-Viry, Raymonde Bouvier, Dominique Droz, Rajagopal Krishnamoorthy, Marie-Madeleine Galteau, Claudine Junien, Christophe Béroud and Jean-Marie Dupret
Cancer Res June 15 1999 (59) (12) 2903-2908;
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