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.
    ###
    INPUT: The aim of this study was to address whether there is a fundamental difference in regulation of histone gene expression in cells that have become quiescent but retain the ability to proliferate , compared with those cells that have differentiated . We compared multiple levels of regulation of histone gene expression during 3T3-L1 pre-adipocyte differentiation . Confluent cells induced to differentiate by treatment with insulin , dexamethasone , and isobutylmethylxanthine initially exhibited an increased proliferative response compared with cells given serum alone . This initial differentiation response was associated with a twofold increase in both histone gene transcription and cellular histone mRNA levels , as well as with enhanced sequence-specific binding of nuclear factors to the proximal cell-cycle-regulatory element of the H4 histone promoter . Transforming growth factor beta 1 , an inhibitor of 3T3-L1 differentiation , increased both the percentage of proliferating cells and the cellular levels of histone mRNA when given in addition to serum stimulation , but no enhancement of these parameters was observed upon addition of TGF beta 1 to the differentiation treatment . Interestingly , although TGF beta 1 enhanced binding of nuclear factors to the proximal cell cycle regulatory element of the histone promoter , these protein/DNA interactions were not associated with an increase in histone transcription . Our results are consistent with the down-regulation of histone gene expression at confluency being controlled primarily at the post-transcriptional level , in contrast to an increased involvement of transcriptional down-regulation at the onset of differentiation .
    OUTPUT:

agent
sustaining proliferative signaling
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 aim of this study was to address whether there is a fundamental difference in regulation of histone gene expression in cells that have become quiescent but retain the ability to proliferate , compared with those cells that have differentiated . We compared multiple levels of regulation of histone gene expression during 3T3-L1 pre-adipocyte differentiation . Confluent cells induced to differentiate by treatment with insulin , dexamethasone , and isobutylmethylxanthine initially exhibited an increased proliferative response compared with cells given serum alone . This initial differentiation response was associated with a twofold increase in both histone gene transcription and cellular histone mRNA levels , as well as with enhanced sequence-specific binding of nuclear factors to the proximal cell-cycle-regulatory element of the H4 histone promoter . Transforming growth factor beta 1 , an inhibitor of 3T3-L1 differentiation , increased both the percentage of proliferating cells and the cellular levels of histone mRNA when given in addition to serum stimulation , but no enhancement of these parameters was observed upon addition of TGF beta 1 to the differentiation treatment . Interestingly , although TGF beta 1 enhanced binding of nuclear factors to the proximal cell cycle regulatory element of the histone promoter , these protein/DNA interactions were not associated with an increase in histone transcription . Our results are consistent with the down-regulation of histone gene expression at confluency being controlled primarily at the post-transcriptional level , in contrast to an increased involvement of transcriptional down-regulation at the onset of differentiation .
    OUTPUT:
