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: Previous studies have demonstrated that the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone ( NNK ) induced liver tumors in F344 rats but not in Syrian golden hamsters . The aim of this study was to determine whether there was a correlation between the persistence of O6-methylguanine ( O6-mGua ) adducts and the rate of recovery of O6-methylguanine-DNA methyltransferase ( O6-mGuaT ) after depletion in the liver and susceptibility to NNK in F344 rat and Syrian golden hamster injected s.c. with NNK ( 80 mg/kg ) . The levels of both 7-methylguanine and O6-mGua reached a maximum 24 h after NNK treatment . O6-mGua in NNK-treated rat liver was undetectable after 48 h . In the rat , the depletion of O6-mGuaT activity occurred within 4 h following NNK treatment . A subsequent rapid recovery of enzyme activity was observed 36 h after NNK exposure . In contrast , high levels of O6-mGua persisted in hamster liver DNA and no O6-mGuaT activity was detected up to 336 h after NNK injection . Thus , the persistence of O6-mGua in hamster liver is most likely related to a lack of recovery of the O6-mGuaT . These results suggested that factors other than O6-mGua may be determining NNK-induced hepatocarcinogenesis in rats . An aldehyde generated by alpha-hydroxylation of NNK , 4-oxo-4-(3-pyridyl)butanal , inhibited O6-mGuaT activity in rat hepatocytes , suggesting that this aldehyde contributes to the carcinogenicity of NNK by inhibiting this repair enzyme .
    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: Previous studies have demonstrated that the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone ( NNK ) induced liver tumors in F344 rats but not in Syrian golden hamsters . The aim of this study was to determine whether there was a correlation between the persistence of O6-methylguanine ( O6-mGua ) adducts and the rate of recovery of O6-methylguanine-DNA methyltransferase ( O6-mGuaT ) after depletion in the liver and susceptibility to NNK in F344 rat and Syrian golden hamster injected s.c. with NNK ( 80 mg/kg ) . The levels of both 7-methylguanine and O6-mGua reached a maximum 24 h after NNK treatment . O6-mGua in NNK-treated rat liver was undetectable after 48 h . In the rat , the depletion of O6-mGuaT activity occurred within 4 h following NNK treatment . A subsequent rapid recovery of enzyme activity was observed 36 h after NNK exposure . In contrast , high levels of O6-mGua persisted in hamster liver DNA and no O6-mGuaT activity was detected up to 336 h after NNK injection . Thus , the persistence of O6-mGua in hamster liver is most likely related to a lack of recovery of the O6-mGuaT . These results suggested that factors other than O6-mGua may be determining NNK-induced hepatocarcinogenesis in rats . An aldehyde generated by alpha-hydroxylation of NNK , 4-oxo-4-(3-pyridyl)butanal , inhibited O6-mGuaT activity in rat hepatocytes , suggesting that this aldehyde contributes to the carcinogenicity of NNK by inhibiting this repair enzyme .
    OUTPUT:
