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: Abstract Different cyclooxygenase ( COX)-2 inhibitors were known to cause different cell cycle changes . We investigated whether this different effect on cell cycle change was due to concentration-dependent effect . We investigated the effects of celecoxib , a COX-2 selective inhibitor , on cell cycle regulation in irradiated cancer cells that express high or low levels of COX-2 . Four stably COX-2 knocked-down or overexpressed cell lines were treated with various concentrations of celecoxib with or without radiation . Celecoxib differentially modulated the cell cycle according to the concentrations applied . G(1) arrest was induced at lower concentrations , whereas G(2)/M arrest was induced at higher concentrations in each cell line tested . Radiation-induced G(2)/M arrest was enhanced at lower concentrations but reduced at higher concentrations . The cutoff values to divide lower and higher concentrations were cell-type specific . Celecoxib treatment activated Cdc25C and inhibited p21 expression in both unirradiated and irradiated cells , regardless of COX-2 expression . Apoptosis was induced in irradiated cells 48 hours after treatment with celecoxib dependent of COX-2 . These results imply that celecoxib deactivates the G(2) checkpoint via both Cdc25C- and p21-dependent pathways in irradiated cells , which subsequently die by secondary apoptosis . Cell cycle modulating effects in irradiated cells resulting from treatment with celecoxib may have clinical importance with regard to the potential application of celecoxib in cancer patients undergoing radiotherapy .
    OUTPUT:

agent
evading growth suppressors;sustaining proliferative signaling;resisting cell death
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: Abstract Different cyclooxygenase ( COX)-2 inhibitors were known to cause different cell cycle changes . We investigated whether this different effect on cell cycle change was due to concentration-dependent effect . We investigated the effects of celecoxib , a COX-2 selective inhibitor , on cell cycle regulation in irradiated cancer cells that express high or low levels of COX-2 . Four stably COX-2 knocked-down or overexpressed cell lines were treated with various concentrations of celecoxib with or without radiation . Celecoxib differentially modulated the cell cycle according to the concentrations applied . G(1) arrest was induced at lower concentrations , whereas G(2)/M arrest was induced at higher concentrations in each cell line tested . Radiation-induced G(2)/M arrest was enhanced at lower concentrations but reduced at higher concentrations . The cutoff values to divide lower and higher concentrations were cell-type specific . Celecoxib treatment activated Cdc25C and inhibited p21 expression in both unirradiated and irradiated cells , regardless of COX-2 expression . Apoptosis was induced in irradiated cells 48 hours after treatment with celecoxib dependent of COX-2 . These results imply that celecoxib deactivates the G(2) checkpoint via both Cdc25C- and p21-dependent pathways in irradiated cells , which subsequently die by secondary apoptosis . Cell cycle modulating effects in irradiated cells resulting from treatment with celecoxib may have clinical importance with regard to the potential application of celecoxib in cancer patients undergoing radiotherapy .
    OUTPUT:
