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: Free radical-induced cellular stress contributes to cancer during chronic inflammation . Here , we investigated mechanisms of p53 activation by the free radical , NO . NO from donor drugs induced both ataxia-telangiectasia mutated ( ATM)- and ataxia-telangiectasia mutated and Rad3-related-dependent p53 posttranslational modifications , leading to an increase in p53 transcriptional targets and a G(2)M cell cycle checkpoint . Such modifications were also identified in cells cocultured with NO-releasing macrophages . In noncancerous colon tissues from patients with ulcerative colitis ( a cancer-prone chronic inflammatory disease ) , inducible NO synthase protein levels were positively correlated with p53 serine 15 phosphorylation levels . Immunostaining of HDM-2 and p21(WAF1) was consistent with transcriptionally active p53 . Our study highlights a pivotal role of NO in the induction of cellular stress and the activation of a p53 response pathway during chronic inflammation .
    OUTPUT:

agent
evading growth suppressors;genomic instability and mutation;tumor promoting inflammation
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: Free radical-induced cellular stress contributes to cancer during chronic inflammation . Here , we investigated mechanisms of p53 activation by the free radical , NO . NO from donor drugs induced both ataxia-telangiectasia mutated ( ATM)- and ataxia-telangiectasia mutated and Rad3-related-dependent p53 posttranslational modifications , leading to an increase in p53 transcriptional targets and a G(2)M cell cycle checkpoint . Such modifications were also identified in cells cocultured with NO-releasing macrophages . In noncancerous colon tissues from patients with ulcerative colitis ( a cancer-prone chronic inflammatory disease ) , inducible NO synthase protein levels were positively correlated with p53 serine 15 phosphorylation levels . Immunostaining of HDM-2 and p21(WAF1) was consistent with transcriptionally active p53 . Our study highlights a pivotal role of NO in the induction of cellular stress and the activation of a p53 response pathway during chronic inflammation .
    OUTPUT:
