A polymorphism in the APE1 gene promoter is associated with lung cancer risk

Cancer Epidemiology Biomarkers and Prevention

Volumn 18, Issue 1, 2009, Pages 223-229

  Lo, Yen Li ^a   Jou, Yuh Shan ^b   Hsiao, Chin Fu ^a   Chang, Gee Chen ^g   Tsai, Ying Huang ^c   Su, Wu Chou ^h   Chen, Kuan Yu ^d   Chen, Yuh Min ^e   Huang, Ming Shyan ⁱ   Chi, Yuan Hu ^a   Chen, Chien Jen ^f   Hsiung, Chao A ^a  

^a NATIONAL HEALTH RESEARCH INSTITUTES   (Taiwan)

^b INSTITUTE OF BIOMEDICAL SCIENCES   (Taiwan)

^c CHANG GUNG MEMORIAL HOSPITAL   (Taiwan)

^d NATIONAL TAIWAN UNIVERSITY HOSPITAL   (Taiwan)

^e TAIPEI VETERANS GENERAL HOSPITAL   (Taiwan)

^f GENOMICS RESEARCH CENTER   (Taiwan)

^g TAICHUNG VETERANS GENERAL HOSPITAL   (Taiwan)

^h NATIONAL CHENG KUNG UNIVERSITY   (Taiwan)

ⁱ KAOHSIUNG MEDICAL UNIVERSITY HOSPITAL   (Taiwan)

Author keywords

[No Author keywords available]

Indexed keywords

DNA (APURINIC OR APYRIMIDINIC SITE) LYASE;

ADULT; ALLELE; ARTICLE; CANCER RISK; CIGARETTE SMOKING; CONTROLLED STUDY; DNA POLYMORPHISM; FEMALE; GENE FREQUENCY; GENE INTERACTION; GENETIC ASSOCIATION; GENETIC VARIABILITY; GENOTYPE; HAPLOTYPE; HOMOZYGOTE; HUMAN; HUMAN CELL; IN VITRO STUDY; LUNG CANCER; MAJOR CLINICAL STUDY; MALE; PRIORITY JOURNAL; PROMOTER REGION; SINGLE NUCLEOTIDE POLYMORPHISM; TRANSCRIPTION INITIATION;

CASE-CONTROL STUDIES; CHI-SQUARE DISTRIBUTION; DNA-(APURINIC OR APYRIMIDINIC SITE) LYASE; FEMALE; GENOTYPE; HAPLOTYPES; HUMANS; LUNG NEOPLASMS; MALE; MIDDLE AGED; MONTE CARLO METHOD; POLYMORPHISM, SINGLE NUCLEOTIDE; PROMOTER REGIONS, GENETIC; RISK; SMOKING; TAIWAN;

EID: 58349113424     PISSN: 10559965     EISSN: None     Source Type: Journal    
DOI: 10.1158/1055-9965.EPI-08-0749     Document Type: Article

References (39)

1. Edwards BK, Brown ML, Wingo PA, et al. Annual report to the nation on the status of cancer, 1975-2002, featuring population-based trends in cancer treatment. J Natl Cancer Inst 2005;97:1407-27.
2. Hecht SS. Cigarette smoking and lung cancer: chemical mechanisms and approaches to prevention. Lancet Oncol 2002;3:461-9.
3. Mattson ME, Pollack ES, Cullen JW. What are the odds that smoking will kill you? Am J Public Health 1987;77:425-31.
4. Shields PG, Harris CC. Cancer risk and low-penetrance susceptibility genes in gene-environment interactions. J Clin Oncol 2000;18:2309-15.
5. Shields PG. Molecular epidemiology of smoking and lung cancer. Oncogene 2002;21:6870-6.
6. Caporaso N, Landi MT, Vineis P. Relevance of metabolic polymorphisms to human carcinogenesis: evaluation of epidemiologic evidence. Pharmacogenetics 1991;1:4-19.
7. Goode EL, Ulrich CM, Potter JD. Polymorphisms in DNA repair genes and associations with cancer risk. Cancer Epidemiol Biomarkers Prev 2002;11:1513-30.
8. Spitz MR, Wei Q, Dong Q, Amos CI, Wu X. Genetic susceptibility to lung cancer: the role of DNA damage and repair. Cancer Epidemiol Biomarkers Prev 2003;12:689-98.
9. Hoeijmakers JH. Genome maintenance mechanisms for preventing cancer. Nature 2001;411:366-74.
10. Fleck O, Nielsen O. DNA repair. J Cell Sci 2004;117:515-7.
11. Krokan HE, Nilsen H, Skorpen F, Otterlei M, Slupphaug G. Base excision repair of DNA in mammalian cells. FEBS Lett 2000;476:73-7.
12. Izumi T, Hazra TK, Boldogh I, et al. Requirement for human AP endonuclease 1 for repair of 3′-blocking damage at DNA single-strand breaks induced by reactive oxygen species. Carcinogenesis 2000;21:1329-34.
13. Fortini P, Pascucci B, Parlanti E, D'Errico M, Simonelli V, Dogliotti E. The base excision repair: mechanisms and its relevance for cancer susceptibility. Biochimie 2003;85:1053-71.
14. Tell G, Damante G, Caldwell D, Kelley MR. The intracellular localization of APE1/Ref-1: more than a passive phenomenon? Antioxid Redox Signal 2005;7:367-84.
15. Evans AR, Limp-Foster M, Kelley MR. Going APE over ref-1. Mutat Res 2000;461:83-108.
16. Jayaraman L, Murthy KG, Zhu C, Curran T, Xanthoudakis S, Prives C. Identification of redox/repair protein Ref-1 as a potent activator of p53. Genes Dev 1997;11:558-70.
17. Burdak-Rothkamm S, Rube CE, Nguyen TP, et al. Radiosensitivity of tumor cell lines after pretreatment with the EGFR tyrosine kinase inhibitor ZD1839 (Iressa). Strahlenther Onkol 2005;181:197-204.
18. Sham PC, Curtis D. Monte Carlo tests for associations between disease and alleles at highly polymorphic loci. Ann Hum Genet 1995;59:97-105.
19. Lewontin RC. The interaction of selection and linkage. II. Optimum models. Genetics 1964;50:757-82.
20. Stephens M, Smith NJ, Donnelly P. A new statistical method for haplotype reconstruction from population data. Am J Hum Genet 2001;68:978-89.
21. Wallenstein S, Hodge SE, Weston A. Logistic regression model for analyzing extended haplotype data. Genet Epidemiol 1998;15:173-81.
22. Lindahl T. Instability and decay of the primary structure of DNA. Nature 1993;362:709-15.
23. Hung RJ, Hall J, Brennan P, Boffetta P. Genetic polymorphisms in the base excision repair pathway and cancer risk: a HuGE review. Am J Epidemiol 2005;162:925-42.
24. David-Beabes GL, London SJ. Genetic polymorphism of XRCC1 and lung cancer risk among African-Americans and Caucasians. Lung Cancer 2001;34:333-9.
25. Hung RJ, Brennan P, Canzian F, et al. Large-scale investigation of base excision repair genetic polymorphisms and lung cancer risk in a multicenter study. J Natl Cancer Inst 2005;97:567-76.
26. Wang Y, Spitz MR, Zhu Y, Dong Q, Shete S, Wu X. From genotype to phenotype: correlating XRCC1 polymorphisms with mutagen sensitivity. DNA Repair (Amst) 2003;2:901-8.
27. van Zeeland AA, de Groot AJ, Hall J, Donato F. 8-Hydroxydeoxyguanosine in DNA from leukocytes of healthy adults: relationship with cigarette smoking, environmental tobacco smoke, alcohol and coffee consumption. Mutat Res 1999;439:249-57.
28. Besaratinia A, Van Schooten FJ, Schilderman PA, et al. A multibiomarker approach to study the effects of smoking on oxidative DNA damage and repair and antioxidative defense mechanisms. Carcinogenesis 2001;22:395-401.
29. Xi T, Jones IM, Mohrenweiser HW. Many amino acid substitution variants identified in DNA repair genes during human population screenings are predicted to impact protein function. Genomics 2004;83:970-9.
30. Hadi MZ, Coleman MA, Fidelis K, Mohrenweiser HW, Wilson DM III. Functional characterization of Ape1 variants identified in the human population. Nucleic Acids Res 2000;28:3871-9.
31. Kiyohara C, Takayama K, Nakanishi Y. Association of genetic polymorphisms in the base excision repair pathway with lung cancer risk: a meta-analysis. Lung Cancer 2006;54:267-83.
32. Ito H, Matsuo K, Hamajima N, et al. Gene-environment interactions between the smoking habit and polymorphisms in the DNA repair genes, APE1 Asp148Glu and XRCC1 Arg399Gln, in Japanese lung cancer risk. Carcinogenesis 2004;25:1395-401.
33. Shen M, Berndt SI, Rothman N, et al. Polymorphisms in the DNA base excision repair genes APEX1 and XRCC1 and lung cancer risk in Xuan Wei, China. Anticancer Res 2005;25:537-42.
34. Zienolddiny S, Campa D, Lind H, et al. Polymorphisms of DNA repair genes and risk of non-small cell lung cancer. Carcinogenesis 2006;27:560-7.
35. Misra RR, Ratnasinghe D, Tangrea JA, et al. Polymorphisms in the DNA repair genes XPD, XRCC1, XRCC3, and APE/ref-1, and the risk of lung cancer among male smokers in Finland. Cancer Lett 2003;191:171-8.
36. Ryk C, Kumar R, Thirumaran RK, Hou SM. Polymorphisms in the DNA repair genes XRCC1, APEX1, XRCC3 and NBS1, and the risk for lung cancer in never- and ever-smokers. Lung Cancer 2006;54:285-92.
37. Popanda O, Schattenberg T, Phong CT, et al. Specific combinations of DNA repair gene variants and increased risk for non-small cell lung cancer. Carcinogenesis 2004;25:2433-41.
38. Hu JJ, Smith TR, Miller MS, Mohrenweiser HW, Golden A, Case LD. Amino acid substitution variants of APE1 and XRCC1 genes associated with ionizing radiation sensitivity. Carcinogenesis 2001;22:917-22.
39. Yang HC, Lin CH, Hsu CL, et al. A comparison of major histocompatibility complex SNPs in Han Chinese residing in Taiwan and Caucasians. J Biomed Sci 2006;13:489-98.