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: The ability of p53 to alter , at the transcriptional level , the gene expression of downstream targets is critical for its role as a tumor suppressor . Most models of p53 activation postulate the stepwise recruitment by p53 of coactivators , histone acetyltransferases , and/or chromatin remodeling factors to a promoter region to facilitate the subsequent access of the general transcriptional machinery required for transcriptional induction . We demonstrate here , however , that the promoter regions for the p53 target genes , p21 , 14-3-3sigma , and KARP-1 , exist in a constitutively open conformation that is readily accessible to DNase I. This conformation was not altered by DNA damage or by whether p53 was present or absent in the cell . In contrast , p53 response elements , which resided outside the immediate promoter regions , existed within DNase I-resistant chromatin domains . Thus , p53 activation of downstream target genes occurs without p53 inducing chromatin alterations detectable by DNase I accessibility at either the promoter or the response element . As such , these data support models of p53 activation that do not require extensive chromatin alterations to support cognate gene expression .
    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: The ability of p53 to alter , at the transcriptional level , the gene expression of downstream targets is critical for its role as a tumor suppressor . Most models of p53 activation postulate the stepwise recruitment by p53 of coactivators , histone acetyltransferases , and/or chromatin remodeling factors to a promoter region to facilitate the subsequent access of the general transcriptional machinery required for transcriptional induction . We demonstrate here , however , that the promoter regions for the p53 target genes , p21 , 14-3-3sigma , and KARP-1 , exist in a constitutively open conformation that is readily accessible to DNase I. This conformation was not altered by DNA damage or by whether p53 was present or absent in the cell . In contrast , p53 response elements , which resided outside the immediate promoter regions , existed within DNase I-resistant chromatin domains . Thus , p53 activation of downstream target genes occurs without p53 inducing chromatin alterations detectable by DNase I accessibility at either the promoter or the response element . As such , these data support models of p53 activation that do not require extensive chromatin alterations to support cognate gene expression .
    OUTPUT:
