human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: DNA repair enzymes play an important role in the development of various kinds of cancer . We here analyzed associations of XPD Lys751Gln , APEX1 Asp148Glu , XRCC1 Arg399Gln , and XRCC3 Thr241Met gene polymorphisms in DNA repair pathways in relation to the risk of lung cancer using PCR-RFLP . The study involved 104 lung cancer patients and 120 non-cancer controls divided into non-smokers and smokers . We found a statistically significant interaction between APEX1 Asp148Glu and the risk for lung cancer ( adjusted OR 2.78 , 95% CI 1.58-4.90 , p=0.0004 ) , of both adenocarcinoma ( adjusted OR 2.24 , 95%CI 1.18-4.25 , p=0.014 ) and squamous cell carcinoma ( adjusted OR 4.75 , 95%CI 1.79-12.6 , p=0.002 ) types . XRCC1 Arg399Gln showed a borderline significant association with adenocarcinoma ( adjusted OR 1.89 , 95%CI 1.00-3.57 , p=0.051 ) . The combined effect of smoking and presence of the APEX1 Asp148Glu demonstrated a significant association with risk of lung cancer ( adjusted OR 3.61 , 95% CI 1.74-7.50 , p=0.001 ) . The XPD Lys751Gln and XRCC3 Thr241Met genotypes displayed no statistically significant risk . Our findings suggest that the APEX1 Asp148Glu is associated with increased risk for primary lung cancer in Japanese individuals partaking in smoking .
    OUTPUT:

agent
genomic instability and mutation
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: DNA repair enzymes play an important role in the development of various kinds of cancer . We here analyzed associations of XPD Lys751Gln , APEX1 Asp148Glu , XRCC1 Arg399Gln , and XRCC3 Thr241Met gene polymorphisms in DNA repair pathways in relation to the risk of lung cancer using PCR-RFLP . The study involved 104 lung cancer patients and 120 non-cancer controls divided into non-smokers and smokers . We found a statistically significant interaction between APEX1 Asp148Glu and the risk for lung cancer ( adjusted OR 2.78 , 95% CI 1.58-4.90 , p=0.0004 ) , of both adenocarcinoma ( adjusted OR 2.24 , 95%CI 1.18-4.25 , p=0.014 ) and squamous cell carcinoma ( adjusted OR 4.75 , 95%CI 1.79-12.6 , p=0.002 ) types . XRCC1 Arg399Gln showed a borderline significant association with adenocarcinoma ( adjusted OR 1.89 , 95%CI 1.00-3.57 , p=0.051 ) . The combined effect of smoking and presence of the APEX1 Asp148Glu demonstrated a significant association with risk of lung cancer ( adjusted OR 3.61 , 95% CI 1.74-7.50 , p=0.001 ) . The XPD Lys751Gln and XRCC3 Thr241Met genotypes displayed no statistically significant risk . Our findings suggest that the APEX1 Asp148Glu is associated with increased risk for primary lung cancer in Japanese individuals partaking in smoking .
    OUTPUT:
