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: Pegylated Interferon-Î±2b ( pIFN-Î± ) is an integral part of the drug regimen currently employed against melanoma . Interferon Regulatory Factor-1 ( IRF-1 ) plays an important role in the transcriptional regulation of the IFN response , cell cycle and apoptosis . We have studied pIFN-Î± induced responses when combined with the chemotherapy agent , vinblastine in tumor and endothelial cell lines and the connection to IRF-1 signaling . Levels of IRF-1/IRF-2 protein expression were found to be decreased in tumor versus normal tissues. pIFN-Î± induced IRF-1 signaling in human melanoma ( M14 ) and endothelial ( EA.hy926 ) cells and enhanced cell death when combined with vinblastine . Upon combined IFN-Î± and vinblastine treatment , p21 expression , PARP cleavage and activated Bak levels were increased in M14 cells . An increase in p21 and cyclin D1 expression occurred in EA.hy926 cells after 6 h of treatment with pIFN-Î± which dissipated by 24 h . This biphasic response , characteristic of cellular senescence , was more pronounced upon combined treatment . Exposure of the EA.hy926 cells to pIFN-Î± was associated with an enlarged , multinucleated , Î²-galactosidase-positive senescent phenotype . The overall therapeutic mechanism of IFN-Î± combined with chemotherapy may be due to both direct tumor cell death via IRF-1 signaling and by premature senescence of endothelial cells and subsequent effects on angiogenesis in the tumor microenvironment .
    OUTPUT:

agent
evading growth suppressors;resisting cell death;enabling replicative immortality;inducing angiogenesis
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: Pegylated Interferon-Î±2b ( pIFN-Î± ) is an integral part of the drug regimen currently employed against melanoma . Interferon Regulatory Factor-1 ( IRF-1 ) plays an important role in the transcriptional regulation of the IFN response , cell cycle and apoptosis . We have studied pIFN-Î± induced responses when combined with the chemotherapy agent , vinblastine in tumor and endothelial cell lines and the connection to IRF-1 signaling . Levels of IRF-1/IRF-2 protein expression were found to be decreased in tumor versus normal tissues. pIFN-Î± induced IRF-1 signaling in human melanoma ( M14 ) and endothelial ( EA.hy926 ) cells and enhanced cell death when combined with vinblastine . Upon combined IFN-Î± and vinblastine treatment , p21 expression , PARP cleavage and activated Bak levels were increased in M14 cells . An increase in p21 and cyclin D1 expression occurred in EA.hy926 cells after 6 h of treatment with pIFN-Î± which dissipated by 24 h . This biphasic response , characteristic of cellular senescence , was more pronounced upon combined treatment . Exposure of the EA.hy926 cells to pIFN-Î± was associated with an enlarged , multinucleated , Î²-galactosidase-positive senescent phenotype . The overall therapeutic mechanism of IFN-Î± combined with chemotherapy may be due to both direct tumor cell death via IRF-1 signaling and by premature senescence of endothelial cells and subsequent effects on angiogenesis in the tumor microenvironment .
    OUTPUT:
