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: During mitotic exit , a small GTPase Tem1 needs to be activated . During most of the cell cycle , Tem1 activity is antagonized by a GTPase activating complex ( GAP ) composed of Bub2 and Bfa1 . Bfa1 protein has cell cycle regulated phosphorylation depending upon the Polo-like kinase Cdc5 . This phosphorylation dissociates Bfa1 from Tem1 and thus relieves the inhibition of Tem1 by the GAP complex . Bub2 and Bfa1 are also required to prevent mitotic exit when there is DNA damage , spindle damage or spindle misorientation at G(2)/M phase . While Cdc5 inhibits Bfa1/Bub2 , mutating the Cdc5 phosphorylation sites on Bfa1 does not have a strong activating effect on Bub2/Bfa1 , suggesting there must be additional regulation in this pathway . Here we report that Bub2 protein also has cell cycle regulated phosphorylation . This phosphorylation is partially dependent upon the Polo-like kinase Cdc5 and is consistent with negative regulation of the Bub2/Bfa1 GAP complex . Spindle damage or spindle misorientation prevents Bub2 phosphorylation . The spindle damage effect is dependent upon the spindle assembly checkpoint components Mad2 and Mps1 . Thus like Bfa1 , Bub2 protein is also controlled both during mitotic exit and in response to cell cycle checkpoints . Bub2 phosphorylation is likely to be controlled by a novel kinase .
    OUTPUT:

agent
sustaining proliferative signaling;evading growth suppressors
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: During mitotic exit , a small GTPase Tem1 needs to be activated . During most of the cell cycle , Tem1 activity is antagonized by a GTPase activating complex ( GAP ) composed of Bub2 and Bfa1 . Bfa1 protein has cell cycle regulated phosphorylation depending upon the Polo-like kinase Cdc5 . This phosphorylation dissociates Bfa1 from Tem1 and thus relieves the inhibition of Tem1 by the GAP complex . Bub2 and Bfa1 are also required to prevent mitotic exit when there is DNA damage , spindle damage or spindle misorientation at G(2)/M phase . While Cdc5 inhibits Bfa1/Bub2 , mutating the Cdc5 phosphorylation sites on Bfa1 does not have a strong activating effect on Bub2/Bfa1 , suggesting there must be additional regulation in this pathway . Here we report that Bub2 protein also has cell cycle regulated phosphorylation . This phosphorylation is partially dependent upon the Polo-like kinase Cdc5 and is consistent with negative regulation of the Bub2/Bfa1 GAP complex . Spindle damage or spindle misorientation prevents Bub2 phosphorylation . The spindle damage effect is dependent upon the spindle assembly checkpoint components Mad2 and Mps1 . Thus like Bfa1 , Bub2 protein is also controlled both during mitotic exit and in response to cell cycle checkpoints . Bub2 phosphorylation is likely to be controlled by a novel kinase .
    OUTPUT:
