genetic variants in APEX1 and XRCC1 may alter the risk of lung cancer in a special population in China

No significant effect on the risk for lung cancer was seen with the APEX1 polymorphism.

SNPs associated with prognosis of lung cancer was mapped to APEX1.

APE1/ref-1 is up-regulated in the tumor regions of non-small cell lung cancer

The APE1 -656T>G polymorphism has an influence on the APE1 promoter activity and is significantly associated with a reduced risk for lung cancer.

overexpression is associated with chemotherapy resistance in non-small cell lung cancer

Apurinic/apyrimidinic endonuclease gene polymorphism is associated with lung cancer

These data indicate that genetic variations in APE1/Ref-1 may modify susceptibility to lung cancer and provide new insights into an unexpected effect of APE1/Ref-1 on lung carcinogenesis.

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

Cytoplasmic Ape1 could enhance lung tumor malignancy through NF-kappaB activation.

The APE1 G allele was an increased risk factor for developing lung cancer among smokers.

found a statistically significant interaction between APEX1 Asp148Glu and the risk for lung cancer

Individuals homozygous for the variants APE1 -141GG showed a protective effect for lung cancer overall

Apurinic/apyrimidinic endonuclease 1/Ref-1 is unregulated in recurrent stage I lung adenocarcinoma.

These results suggest that the APE1 Asp/Asp genotype and the combination of the APE1 Asp/Asp and hOGG1-Cys variants are associated with increased risk of p53 mutation in non-small cell lung cancer.

OGG1 Ser326Cys show an increased lung cancer risk in Asians and non-smokers; APEX1 Asp148Glu polymorphism may be associated with decreased lung adenocarcinoma risk, and APEX1 Asp148Glu polymorphism show an increased lung cancer risk in Asians and smokers

XRCC1 Arg399Gln, PARP1 Va1762Ala and APE1 Asp148Glu SNPs in the base excision repair pathway may influence the prognosis of advanced non-small cell lung cancer patients following platinum-based chemotherapy.

results provide evidence that the non-synonymous polymorphism of APEX1 Asp(148)Glu may not be directly associated with lung cancer risk, nor enhance the effects of smoking habit on lung cancer development

Potential interactive contribution of RAGE and APE1 genes to the pathogenesis of lung cancer.

updated meta-analysis suggests that the APE1 Asp148Glu polymorphisms are not associated with lung cancer risk among Asians or Caucasians

meta-analysis shows that the polymorphism of APE1 Asp148Glu exerts risk effect on lung cancer development

This meta-analysis provides statistical evidence for a potential association between APE1 polymorphism and an increased risk of lung cancer in Asian population.

rs1130409 of APEX1 can be a predictor of RP grades >/=3 among patients with lung cancer.

Advanced non-small cell lung cancer patients with both APE1- and excision repair cross-complementing 1 -negative tumors had higher response rate to platinum-paclitaxel chemotherapy , longer progression-free survival and overall survival.

showed evidence on interaction between APEX1 148Glu variant and cigarette smoking in increasing lung cancer susceptibility among male Chinese

The results indicate that low APE1 activity is associated with lung cancer risk, consistent with the hypothesis that 'bad DNA repair', rather than 'bad luck', is involved in cancer etiology.

MCP- and CP-induced oxidative stress alters APE1-dependent BER-pathway and also mediates cell survival signalling mechanisms via APE1 regulation, thereby promoting lung cancer cell survival and proliferation.

APE1 stimulates EGFR-tyrosine kinase inhibitors resistance by activating Akt signaling through a redox-dependent mechanism in lung adenocarcinoma.

Increased lung cancer risk was revealed in workers-carriers of homozygous minor genotype of genes OGG1] Ser326Cys (OR - 4.67, p = 0.007), APE1 Asp148Glu (OR = 1.82, p = 0.063) and XRCC1 Gln399Arg (OR = 2.86, p = 0.026).

High APE1 expression is associated with cisplatin resistance of lung cancer cells by inducing Parkinmediated mitophagy.