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: Estrogen receptor ( ER ) and NF-ÎºB are transcription factors with profound effects on breast cancer cell proliferation and survival . While many studies demonstrate that ER and NF-ÎºB can repress each other , we previously identified a gene signature that is synergistically upregulated by these two factors in more aggressive luminal B breast tumors . Herein , we examine a novel mechanism of cross talk between ER and NF-ÎºB that results in the upregulation of the antiapoptotic gene BIRC3 ( also known as cIAP2 ) . We demonstrate that NF-ÎºB , acting through two response elements , is required for ER recruitment to an adjacent estrogen response element ( ERE ) in the BIRC3 promoter . This effect is accompanied by a major increase in NF-ÎºB-dependent histone acetylation around the ERE . Interestingly , CBP , a histone acetyltransferase previously implicated in repressive interactions between ER and NF-ÎºB , plays a permissive role by promoting histone acetylation and ER recruitment , as well as enhanced expression of BIRC3 . These findings suggest a new gene regulatory mechanism by which inflammation and NF-ÎºB activation can influence ER recruitment to inherently inactive ER binding sites . This fine-tuning mechanism may explain how two factors that generally repress each other's activity may work together on certain genes to promote breast cancer cell survival and tumor progression .
    OUTPUT:

agent
sustaining proliferative signaling;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: Estrogen receptor ( ER ) and NF-ÎºB are transcription factors with profound effects on breast cancer cell proliferation and survival . While many studies demonstrate that ER and NF-ÎºB can repress each other , we previously identified a gene signature that is synergistically upregulated by these two factors in more aggressive luminal B breast tumors . Herein , we examine a novel mechanism of cross talk between ER and NF-ÎºB that results in the upregulation of the antiapoptotic gene BIRC3 ( also known as cIAP2 ) . We demonstrate that NF-ÎºB , acting through two response elements , is required for ER recruitment to an adjacent estrogen response element ( ERE ) in the BIRC3 promoter . This effect is accompanied by a major increase in NF-ÎºB-dependent histone acetylation around the ERE . Interestingly , CBP , a histone acetyltransferase previously implicated in repressive interactions between ER and NF-ÎºB , plays a permissive role by promoting histone acetylation and ER recruitment , as well as enhanced expression of BIRC3 . These findings suggest a new gene regulatory mechanism by which inflammation and NF-ÎºB activation can influence ER recruitment to inherently inactive ER binding sites . This fine-tuning mechanism may explain how two factors that generally repress each other's activity may work together on certain genes to promote breast cancer cell survival and tumor progression .
    OUTPUT:
