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: OBJECTIVES : Cigarette smoking is a major risk factor for pancreatic cancer ( PaCa ) . However , the mechanisms of smoking-induced PaCa remain unknown . Here we investigated the effect of smoking compounds on cell death pathways in pancreatic ductal cells , precursors of PaCa . METHODS : Human pancreatic ductal cells ( HPDE6-c7 ) were cultured with cigarette smoke extract ( CSE ) or smoking compound 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone ( NNK ) . Apoptosis and autophagy were assessed by DNA fragmentation and immunofluorescence , respectively . RESULTS : Exposure to CSE or NNK decreased DNA fragmentation and up-regulated BclXL . Akt kinase was activated by smoking compounds through reactive oxygen species-dependent mechanism . Specifically , Akt activation was prevented by inhibition of nicotinamide adenine dinucleotide oxidase . Molecular or pharmacologic inhibitions of Akt prevented the antiapoptotic effect of smoking compounds . Smoking compounds stimulated rapid ( 1 hour ) and transient activation of 5'-adenosine monophosphate-activated protein kinase and formation of autophagic vacuoles , indicating stimulation of autophagy . Repeated exposure to CSE/NNK ( 48 hours or longer ) abolished the early activation of autophagic markers . Inhibition of Akt prevented the antiautophagic effect of long exposure to smoking compounds , indicating that smoking-induced late activation of Akt prevents autophagy . CONCLUSIONS : Long exposure of pancreatic ductal cells to smoking compounds inhibited apoptosis and autophagy . The results revealed a central role for Akt kinase in mediating key procarcinogenic effects of smoking compounds .
    OUTPUT:

agent
tumor promoting inflammation;resisting cell death
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: OBJECTIVES : Cigarette smoking is a major risk factor for pancreatic cancer ( PaCa ) . However , the mechanisms of smoking-induced PaCa remain unknown . Here we investigated the effect of smoking compounds on cell death pathways in pancreatic ductal cells , precursors of PaCa . METHODS : Human pancreatic ductal cells ( HPDE6-c7 ) were cultured with cigarette smoke extract ( CSE ) or smoking compound 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone ( NNK ) . Apoptosis and autophagy were assessed by DNA fragmentation and immunofluorescence , respectively . RESULTS : Exposure to CSE or NNK decreased DNA fragmentation and up-regulated BclXL . Akt kinase was activated by smoking compounds through reactive oxygen species-dependent mechanism . Specifically , Akt activation was prevented by inhibition of nicotinamide adenine dinucleotide oxidase . Molecular or pharmacologic inhibitions of Akt prevented the antiapoptotic effect of smoking compounds . Smoking compounds stimulated rapid ( 1 hour ) and transient activation of 5'-adenosine monophosphate-activated protein kinase and formation of autophagic vacuoles , indicating stimulation of autophagy . Repeated exposure to CSE/NNK ( 48 hours or longer ) abolished the early activation of autophagic markers . Inhibition of Akt prevented the antiautophagic effect of long exposure to smoking compounds , indicating that smoking-induced late activation of Akt prevents autophagy . CONCLUSIONS : Long exposure of pancreatic ductal cells to smoking compounds inhibited apoptosis and autophagy . The results revealed a central role for Akt kinase in mediating key procarcinogenic effects of smoking compounds .
    OUTPUT:
