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: Polycyclic aromatic hydrocarbons ( PAHs ) likely play a role in many cancers even in never-smokers . We tried to find a model to explain the relationship between variation in PAH-related DNA adduct levels among people with similar exposures , multiple genetic polymorphisms in genes related to metabolic and repair pathways , and nucleotide excision repair ( NER ) capacity . In 111 randomly selected female never-smokers from the Golestan Cohort Study in Iran , we evaluated 21 SNPs in 14 genes related to xenobiotic metabolism and 12 SNPs in eight DNA repair genes . NER capacity was evaluated by a modified comet assay , and aromatic DNA adduct levels were measured in blood by32P-postlabeling . Multivariable regression models were compared by Akaike's information criterion ( AIC ) . Aromatic DNA adduct levels ranged between 1.7 and 18.6 per 10(8) nucleotides ( mean : 5.8 ± 3.1 ) . DNA adduct level was significantly lower in homozygotes for NAT2 slow alleles and ERCC5 non-risk-allele genotype , and was higher in the MPO homozygote risk-allele genotype . The sum of risk alleles in these genes significantly correlated with the log-adduct level ( r = 0.4 , p &lt ; 0.001 ) . Compared with the environmental model , adding Phase I SNPs and NER capacity provided the best fit , and could explain 17% more of the variation in adduct levels . NER capacity was affected by polymorphisms in the MTHFR and ERCC1 genes . Female non-smokers in this population had PAH-related DNA adduct levels three to four times higher than smokers and occupationally-exposed groups in previous studies , with large inter-individual variation which could best be explained by a combination of Phase I genes and NER capacity .
    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.
    ###
    INPUT: Polycyclic aromatic hydrocarbons ( PAHs ) likely play a role in many cancers even in never-smokers . We tried to find a model to explain the relationship between variation in PAH-related DNA adduct levels among people with similar exposures , multiple genetic polymorphisms in genes related to metabolic and repair pathways , and nucleotide excision repair ( NER ) capacity . In 111 randomly selected female never-smokers from the Golestan Cohort Study in Iran , we evaluated 21 SNPs in 14 genes related to xenobiotic metabolism and 12 SNPs in eight DNA repair genes . NER capacity was evaluated by a modified comet assay , and aromatic DNA adduct levels were measured in blood by32P-postlabeling . Multivariable regression models were compared by Akaike's information criterion ( AIC ) . Aromatic DNA adduct levels ranged between 1.7 and 18.6 per 10(8) nucleotides ( mean : 5.8 ± 3.1 ) . DNA adduct level was significantly lower in homozygotes for NAT2 slow alleles and ERCC5 non-risk-allele genotype , and was higher in the MPO homozygote risk-allele genotype . The sum of risk alleles in these genes significantly correlated with the log-adduct level ( r = 0.4 , p &lt ; 0.001 ) . Compared with the environmental model , adding Phase I SNPs and NER capacity provided the best fit , and could explain 17% more of the variation in adduct levels . NER capacity was affected by polymorphisms in the MTHFR and ERCC1 genes . Female non-smokers in this population had PAH-related DNA adduct levels three to four times higher than smokers and occupationally-exposed groups in previous studies , with large inter-individual variation which could best be explained by a combination of Phase I genes and NER capacity .
    OUTPUT:
