Abstract
Lung cancer is a disease in which environmental factors play a major role, since 80 to 90% of cases of lung cancer in our countries may be attributable to tobacco [1]. However, the cumulative risk of lung cancer in a population of smokers remains largely lower than 1. There is no doubt that factors other than tobacco carcinogens are implied in its etiology and that some of them are probably genetic. Arguments for the role of genetic factors come from animal studies, family studies and studies on polymorphisms of enzymes implied in the metabolism of carcinogens, in particular the cytochrome P450 family.
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References
Hill C (1993) Mortalité liée au tabagisme. Rev Prat 43: 1209–1213.
Economou P, Samet JM, Lechner JF (1994) Familial and genetic factors in the pathogenesis of lung cancer. In: Samet JM (ed): Epidemiology of lung cancer Series: Lung biology in Health and Disease 74. Dekker M Inc, New York, pp 353–396.
Sellers TA, Bailey-Wilson JE, Elston RC, Wilson AF, Elston GZ, Ooi WL, Rothschild H (1990) Evidence for Mendelian inheritance in the pathogenesis of lung cancer. J Natl Cancer Inst 82: 1272–1279.
Pelkonen O, Nebert D (1982) Metabolism of polycyclic aromatic hydrocarbons: etiologic role in carcinogenesis. Pharmacological Rev 34: 189–222.
Butler MA, Guengerich FP, Kadlubar FF (1989) Metabolic activation of the carcinogens 4-aminobiphenyl and 4,4′-methylene-bis(2-chloroaniline) by human hepatic microsomes and purified rat hepatic cytochrome P-450 monooxygenases. Cancer Res 49: 25–31.
Shimada T, Iwasaki M, Martin MW, Guengerich FP (1989) Human liver microsomal cytochrome P-450 enzymes involved in the bioactivation of procarcinogens detected by umu gene response in Salmonella Typhimurium TA 1535/pSK1002. Cancer Res 49: 3218–3228.
McManus ME, Burgess WM, Veronese ME, Huggett A, Quattrochi LC, Tukey RH (1990) Metabolism of 2-acetylaminofluorene and benzo(a)pyrene and activation of food-derived heterocyclic amine mutagens by human cytochromes P-450. Cancer Res 1: 3367–3375.
Guengerich FP, Shimada T (1991) Oxidation of toxic and carcinogenic chemicals by human cytochrome P-450 enzymes. Chem Res Toxicol 4: 391–407.
Fujii-Kuriyama Y, Ema M, Mimura J, Matsushita N, Sogawa K (1995) Polymorphic forms of the Ah receptor and induction of the CYP1A1 gene. Pharmacogenetics 5: S149–S153.
Kouri RE, Nebert DW (1991) Genetic regulation of susceptibility to poly cyclic-hydrocarbon-induced tumors in the mouse. In: Hiatt HH, Watson JD, Winsten JA. Origins of human cancer. Cold Spring Harbor, New York, pp 811–835.
Nebert DW, Petersen DD, Puga A (1991) Human AH locus polymorphism and cancer: inducibility of CYP1A1 and other genes by combustion products and dioxin. Pharmacogenetics 1: 68–78.
Kellermann G, Luyten-Kellermann M, Shaw CR (1973) Genetic variation of aryl hydrocarbon hydroxylase in human lymphocytes. Am J Hum Genet 25: 327–331.
Kellermann G, Shaw CR, Luyten-Kellermann M (1973) Aryl hydrocarbon hydroxylase inducibility and bronchogenic carcinoma. N Engl J Med 289: 934–937.
Benhamou S, Bonaïti-Pellié C (1995) Susceptibilité au cancer bronchique: un exemple d’interaction génétique-environnement. Ann Biol Clin 53: 507–513.
Catteau A, Douriez E, Beaune P, Poisson N, Bonaïti-Pellié C, Laurent P (1995) Genetic polymorphism of induction of CYPlAl (EROD) activity. Pharmacogenetics 5: 110–119.
Itoh S, Kamataki T (1993) Human Ah receptor cDNA: Analysis for highly conserved sequences. Nucleic Acids Res 21: 3578.
Le Beau MM, Carver LA, Espinosa III R, Schmidt JV, Bradfield CA (1994) Chromosomal localization of the human AHR locus encoding the structural gene for the Ah receptor to 7p21-pl5. Cytogenet Cell Genet 66: 172–176.
Hildebrand CE, Gonzalez FJ, McBride OW, Nebert DW (1985) Assignment of the human 2,3,7,8-tetrachlorodibenzo-p-dioxin-inducible cytochrome P1-450 gene to chromosome 15. Nucleic Acids Res 13: 2009–2016.
Hayashi S, Watanabe J, Nakashi K, Kawajiri K (1991) Genetic linkage of lung cancer-associated Mspl polymorphism with amino acid replacement in the heme binding region of the human cytochrome P450IA1 gene. J Biochem 110: 407–411.
Kawajiri K, Nakashi K, Imai K, Yoshii A, Shinoda N, Watanabe J (1990) Identification of genetically high risk individuals to lung cancer by DNA polymorphisms of the cytochrome P4501A1 gene. FEBS Lett 263: 131–133.
Cosma G, Crofts F, Taioli E, Toniolo P, Garte S (1993) Relationship between genotype and function of the human CYP1A1 gene. J Toxicol Environ Health 40: 309–316.
Grant DM, Tang BK, Kalow W (1983) Variability in caffeine metabolism. Clin Pharmacol Ther 33:591–602.
Butler MA, Lang NP, Young JF, Caporaso NE, Vineis P, Hayes RB, Teitel CH, Massengill JP, Lawsen MF, Kadlubar FF (1992) Determination of CYP1A2 and NAT2 phenotypes in human populations by analysis of caffeine urinary metabolites. Pharmacogenetics 2: 116–127.
Bock KW, Schrenk D, Forster D, Griese E-U, Mörike K, Brockmeier D, Eichelbaum M (1994) The influence of environmental and genetic factors on CYP2D6, CYP1A2 and UDP-glucuronosyltransferases in man using sparteine, caffeine, and paracetamol as probes. Pharmacogenetics 4: 209–218.
Catteau A, Bechtel YC, Poisson N, Bechtel PR, Bonaïti-Pellié C (1995) A population and family study of CYP1A2 using caffeine urinary metabolites. Eur J Clin Pharmacol 47: 423–430.
Notarianni LJ, Oliver SE, Dobrocky P, Bennett PN, Silverman BW (1995) Caffeine as a metabolic probe: a comparison of the metabolic ratios used to assess CYP1A2 activity. Br J Clin Pharmacol 39: 65–69.
Price-Evans DAP, Maghoub A, Sloan TP, Idle JR, Smith RL (1980) A family and population study of the genetic polymorphism of debrisoquine oxidation in a white British population. J Med Genet 17: 102–105.
Gonzalez FJ, Skoda RC, Kimura S, Umeno M, Zanger UM, Nebert DW, Gelboin HV, Hardwick JP, Meyer UA (1988) Characterisation of the common genetic defect in humans deficient in debrisoquine metabolism. Nature 331: 442–446.
Broly F, Meyer UA (1993) Debrisoquine oxidation polymorphism: phenotypic consequences of a 3-base-pair deletion in exon 5 of the CYP2D6 gene. Pharmacogenetics 3: 123–130.
Crespi CL, Penman BW, Gelboin HV, Gonzalez FJA (1991) Tobacco smoke-derived nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, is activated by multiple human cytochrome P450s including the polymorphic human cytochrome P450 IID6. Carcinogenesis 12: 1197–1201.
Ayesh R, Idle JR, Ritchie JC, Crothers MJ, Hetzel MR (1984) Metabolic oxidation phenotypes as markers for susceptibility to lung cancer. Nature 312: 169–170.
Bouchardy C, Benhamou S, Dayer P (1996) The effect of tobacco on lung cancer risk depends on CYP2D6 activity. Cancer Res 56: 251–253.
Hayashi S-I, Watanabe J, Kawajiri K (1992) High susceptibility to lung cancer analyzed in terms of combined genotypes of P450IA1 and mu-class glutathione S-transferase genes. Jpn J Cancer Res 83: 866–870.
Nakachi K, Imai K, Hayashi S-I, Kawajiri K (1993) Polymorphisms of the CYP1A1 and glutathione S-transferase genes associated with susceptibility to lung cancer in relation to cigarette dose in a Japanese population. Cancer Res 53: 2994–2999.
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Benhamou, S., Bonaïti-Pellié, C. (1998). Cytochrome P450 Polymorphisms: Risk Factors for Lung Cancer?. In: Martinet, Y., Hirsch, F.R., Martinet, N., Vignaud, JM., Mulshine, J.L. (eds) Clinical and Biological Basis of Lung Cancer Prevention. Respiratory Pharmacology and Pharmacotherapy. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8924-7_17
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DOI: https://doi.org/10.1007/978-3-0348-8924-7_17
Publisher Name: Birkhäuser, Basel
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