title: Genetic polymorphisms in ATM, ERCC1, APE1 and iASPP genes and lung cancer risk in a population of southeast China.
abstract: Polymorphisms in DNA repair and apoptosis genes are suspected to alter the individual susceptibility to develop lung cancer. We investigated the relationship between polymorphisms in ATM (A60G), ERCC1 (Asn118Asn), APE1 (Asn148Glu) and iASPP (A67T) and the risk of developing lung cancer. A case-control study was conducted with 315 patients with lung cancer and 315 cancer-free controls, matched on age and sex. Genotypes were detected using the ABI 7500 real-time PCR system. The T/T homozygote in ERCC1 (Asn118Asn) was correlated with a strong statistically significant increased risk of developing lung cancer (adjusted OR=2.44; 95% CI=1.13-5.28; P=0.023), especially lung adenocarcinoma (adjusted OR=3.18) and small cell lung cancer (adjusted OR=6.08). For iASPP (A67T), smokers with at least one T allele (A/T+T/T) were more likely to develop lung cancer (95% CI, 1.07-2.84, P=0.026). Subjects carrying the G allele in APE1 (Asn148Glu) had a decreased risk of lung cancer (P<0.05), which showing a protective effect. Our results suggest that polymorphism Asn118Asn in ERCC1, A67T in iASPP and Asn148Glu in APE1 may associated with early onset of lung cancer as well as some specific subtype of lung cancer. Detection of these biomarkers may be helpful for screening this high-risk population for primary preventing.
authors.affiliation: Department of Radiation Oncology, Zhejiang Cancer Hospital, 38 Banshan Road, Hangzhou, 310022, China.
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Deng
authors.forename: Liming
authors.initials: L
authors.lastname: Sheng
authors.forename: Dan
authors.initials: D
authors.lastname: Su
authors.forename: Lizhen
authors.initials: L
authors.lastname: Zhang
authors.forename: Peng
authors.initials: P
authors.lastname: Liu
authors.forename: Ke
authors.initials: K
authors.lastname: Lu
authors.forename: Shenglin
authors.initials: S
authors.lastname: Ma
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D064007:Ataxia Telangiectasia Mutated Proteins; D014408:Biomarkers, Tumor / Q000235:genetics; D016022:Case-Control Studies; D018797:Cell Cycle Proteins / Q000235:genetics*; D002681:China; D004260:DNA Repair / Q000235:genetics; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000235:genetics*; D004720:Endonucleases / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics*; D008175:Lung Neoplasms / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*; D060888:Real-Time Polymerase Chain Reaction; D012097:Repressor Proteins / Q000235:genetics*; D012307:Risk Factors; D055752:Small Cell Lung Carcinoma / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000235:genetics*
chemical_list: D014408:Biomarkers, Tumor; D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; C119612:PPP1R13L protein, human; D012097:Repressor Proteins; D025521:Tumor Suppressor Proteins; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases; C071447:ERCC1 protein, human; D004720:Endonucleases; C085108:APEX1 protein, human; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase