Increased risk of acute myeloid leukaemia due to polymorphisms in detoxification and DNA repair enzymes

Annals of Oncology

Volumn 18, Issue 9, 2007, Pages 1523-1528

  Voso, M Teresa ^a   Fabiani, E ^a   D'Alo', F ^a   Guidi, F ^a   Di Ruscio, A ^a   Sica, S ^a   Pagano, L ^a   Greco, M ^a   Hohaus, S ^a   Leone, G ^a  

^a CATHOLIC UNIVERSITY   (Italy)

Author keywords

Acute myeloid leukaemia; Detoxification; DNA repair; Polymorphisms

Indexed keywords

CYTOCHROME P450 3A4; POLYDEOXYRIBONUCLEOTIDE SYNTHASE; RAD51 PROTEIN; XENOBIOTIC AGENT;

ACUTE GRANULOCYTIC LEUKEMIA; ADOLESCENT; ADULT; AGED; AMINO ACID SUBSTITUTION; ARTICLE; CANCER RISK; CASE CONTROL STUDY; CONTROLLED STUDY; DNA REPAIR; DNA STRAND BREAKAGE; DRUG DETOXIFICATION; ENZYME POLYMORPHISM; FEMALE; GENETIC POLYMORPHISM; GENETIC RISK; GENETIC VARIABILITY; HETEROZYGOTE; HIGH RISK POPULATION; HUMAN; HUMAN CELL; LEUKEMOGENESIS; MAJOR CLINICAL STUDY; MALE; MONONUCLEAR CELL; PRIORITY JOURNAL;

ADULT; AGED; AGED, 80 AND OVER; CASE-CONTROL STUDIES; CYTOCHROME P-450 ENZYME SYSTEM; DNA REPAIR ENZYMES; DNA-BINDING PROTEINS; FEMALE; GENE FREQUENCY; GLUTATHIONE TRANSFERASE; HUMANS; ISOENZYMES; LEUKEMIA, MYELOID, ACUTE; MALE; METABOLIC DETOXICATION, PHASE I; METABOLIC DETOXICATION, PHASE II; MIDDLE AGED; NAD(P)H DEHYDROGENASE (QUINONE); POLYMORPHISM, GENETIC; RAD51 RECOMBINASE; RISK FACTORS;

EID: 34548399471     PISSN: 09237534     EISSN: 15698041     Source Type: Journal    
DOI: 10.1093/annonc/mdm191     Document Type: Article

References (31)

1. Aminimani B, Ning B, Deitz AC et al. Increased transcriptional activity of the CYP3A4*1B promoter variant. Environ Mol Mutagen 2003; 42: 299-305.
2. Felix CA, Walker AH, Lange BJ et al. Association of CYP3A4 genotype with treatment-related leukaemia. Proc Natl Acad Sci USA 1998; 95: 13176-13181.
3. D'Alò F, Voso MT, Guidi F et al. Polymorphisms of CYP1A1 and glutathione S-transferase and susceptibility to adult acute myeloid leukaemia. Haematologica 2004; 89: 664-670.
4. Voso MT, D'Alo F, Putzulu R et al. Negative prognostic value of glutathione S-transferase (GSTM1 and GSTT1) deletions in adult acute myeloid leukaemia. Blood 2002; 100: 2703-2707.
5. Coles BF, Morel F, Rauch C et al. Effect of polymorphism in the human glutathione S-transferase A1 promoter on hepatic GSTA1 and GSTA2 expression. Pharmacogenetics 2001; 11: 663-669.
6. Ali-Osman F, Akande O, Antoun G et al. Molecular cloning, characterization and expression in Escherichia coli of full-length cDNAs of three human glutathione S-transferase Pi gene variants: evidence for differential catalytic activity of the encoded proteins. J Biol Chem 1997; 272: 10004-10012.
7. Sundberg K, Johansson, AS, Stenberg G et al. Differences in the catalytic efficiencies of allelic variants of glutathione transferase P1-1 towards carcinogenic diol epoxides of polycyclic aromatic hydrocarbons. Carcinogenesis 1998; 19: 433-436.
8. Allan JM, Wild CP, Rollinson S et al. Polymorphism in glutathione S-transferase P1 is associated with susceptibility to chemotherapy-induced leukaemia. Proc Natl Acad Sci USA 2001; 98: 11592-11597.
9. Traver RD, Siegel D, Beall HD et al. Characterization of a polymorphism in NAD(P)H: Quinone oxidoreductase (DT-diaphorase). Br J Cancer 1997; 75: 69-75.
10. Siegel D, McGuinness SM, Winski SL, Ross D. Genotype-phenotype relationships in studies of a polymorphism in NAD(P)H:qUinone oxidoreductase 1. Pharmacogenetics 1999; 9: 113-121.
11. Fern L, Pallis M, Ian Carter G et al. Clonal haemopoiesis may occur after conventional chemotherapy and is associated with accelerated telomere shortening and defects in the NQO1 pathway; possible mechanisms leading to an increased risk of t-AML/MDS. Br J Haematol 2004; 126: 63-71.
12. Larson RA, Wang Y, Banerjee M et al. Prevalence of the inactivating 609C-T polymorphism in the NAD(P)H:qUinone oxidoreductase (NQO1) gene in patients with primary and therapy-related myeloid leukaemia. Blood 1999; 94: 803-807.
13. Kennedy RD, D'Andrea AD. DNA repair pathways in clinical practice: lessons from pediatric cancer susceptibility syndromes. J Clin Oncol 2006; 24: 3799-3808.
14. Vispe S, Cazaux C, Lesca C, Defais M. Overexpression of Rad51 protein stimulates homologous recombination and increases resistance of mammalian cells to ionizing radiation. Nucleic Acids Res 1998; 26: 2859-2864.
15. Kim PM, Allen C, Wagener BM et al. Overexpression of human RAD51 and RAD52 reduces double-strand break-induced homologous recombination in mammalian cells. Nucleic Acids Res 2001; 29: 4352-4360.
16. Richardson C, Stark JM, Ommundsen M, Jasin M. Rad51 overexpression promotes alternative double-strand break repair pathways and genome instability. Oncogene 2004; 23: 546-553.
17. Seedhouse C, Faulkner R, Ashraf N et al. Polymorphisms in genes involved in homologous recombination repair interact to increase the risk of developing acute myeloid leukaemia. Clin Cancer Res 2004; 10: 2675-2680.
18. Harris NL, Jaffe ES, Diebold J et al. The World Health Organization classification of hematological malignancies report of the Clinical Advisory Committee Meeting, Airlie House, Virginia November 1997. Mod Pathol. 2000; 13: 193-207.
19. Hohaus S, Di Ruscio A, Di Febo A et al. Glutathione S-transferase P1 genotype and prognosis in Hodgkin's lymphoma. Clin Cancer Res 2005; 11: 2175-2179.
20. Naoe T, Takeyama K, Yokozawa T et al. Analysis of genetic polymorphism in NQO1, GST-M1, GST-T1, and CYP3A4 in 469 Japanese patients with therapy-related leukemia/myelodysplastic syndrome and de novo acute myeloid leukaemia. Clin Cancer Res 2000; 6: 4091-4095.
21. Sanyal S, Festa F, Sakano S et al. Polymorphisms in DNA repair and metabolic gene in bladder cancer. Carcinogenesis 2004; 25: 729-734.
22. Pierce AJ, Johnson RD, Thompson LH, Jasin M. XRCC3 promotes homology-directed repair of DNA damage in mammalian cells. Genes Dev 1999; 13: 2633-2638.
23. Liu N, Lamerdin JE, Tebbs RS et al. XRCC2 and XRCC3, new human Rad51-family members, promote chromosome stability and protect against DNA cross-links and other damages. Mol Cell 1998; 1: 783-793.
24. Shen MR, Jones IM, Mohrenweiser H. Nonconservative amino acid substitution variants exist at polymorphic frequency in DNA repair genes in healthy humans, Cancer Res 1998; 58: 604-608.
25. Winsey SL, Haldar NA, Marsh HP et al. A variant within the DNA repair gene XRCC3 is associated with the development of melanoma skin cancer. Cancer Res 2000; 60: 5612-5616.
26. Matullo G, Guarrera S, Carturan S et al. DNA repair gene polymorphisms, bulky DNA adducts in white blood cells and bladder cancer in a case-control study. Int J Cancer 2001; 92: 562-567.
27. Wang T, Arifoglu P, Ronai Z, Tew KD. Glutathione S-transferase P1-1 (GSTP1-1) inhibits c-Jun N-terminal kinase (JNK1) signaling through interaction with the C terminus. J Biol Chem 2001; 276: 20999-21003.
28. Wu Y, Fan Y, Xue B et al. Human glutathione S-transferase P1-1 interacts with TRAF2 and regulates TRAF2-ASK1 signals. Oncogene 2006; 25: 5787-5800.
29. Dirven HA, Van Ommen B, Van Bladeren PJ. Glutathione conjugation of alkylating cytostatic drugs with a nitrogen mustard group and the role of glutathione S-transferases. Chem Res Toxicol 1996; 9: 351-360.
30. Seedhouse C, Bainton R, Lewis M, Harding A, Russell N, Das-Gupta E. The genotype distribution of the XRCC1 gene indicates a role for base excision repair in the development of therapy-related acute myeloblastic leukaemia. Blood 2002; 100: 3761-3766.
31. Smith AG, Worrillow LJ, Allan JM. A common genetic variant in XPD associates with risk of 5q- and 7q-deleted acute myeloid leukaemia. Blood 2007; 109: 1233-1236.