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: Deregulation of D-type cyclin-dependent kinases ( CDK4 and 6 ) is widely observed in various human cancers , illustrating their importance in cell cycle control . Like other cyclin-dependent kinases ( CDKs ) , assembly with cyclins is the most critical step for activation of CDK4/6 . As previously reported elsewhere , we observed that the level of cyclinD1-CDK4 complex and its associated kinase activity were significantly low in asynchronously proliferating mouse embryo fibroblasts lacking both p21(Cip1) and p27(Kip1) ( p21/p27-null MEFs ) . These evidences imply that p21(Cip1) and p27(Kip1) CDK inhibitors are ' essential activators ' of cyclin D-kinases . We , however , discovered here that both the assembly and activation of cyclin D1-CDK4 complex occur when quiescent p21/p27-null MEFs were stimulated to re-enter the cell cycle . This mitogen-induced cyclin D1-kinase activity was blocked by overexpression of p16(INK4a) and resulted in the inhibition of S phase entry in p21/p27-null MEFs . Furthermore , ectopic expression of p34(SEI-1) , a mitogen-induced CDK4 binding protein , increased the levels of active cyclinD1-CDK4 complex in asynchronously proliferating p21/p27-null MEFs . Together , our results suggest that there are several independent ways to stimulate the assembly of cyclin D1-CDK4 kinases . Although p21(Cip1) and p27(Kip1) play a role in this process , our results demonstrate that additional mechanisms must occur in G0 to S phase transition .
    OUTPUT:

agent
evading growth suppressors;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: Deregulation of D-type cyclin-dependent kinases ( CDK4 and 6 ) is widely observed in various human cancers , illustrating their importance in cell cycle control . Like other cyclin-dependent kinases ( CDKs ) , assembly with cyclins is the most critical step for activation of CDK4/6 . As previously reported elsewhere , we observed that the level of cyclinD1-CDK4 complex and its associated kinase activity were significantly low in asynchronously proliferating mouse embryo fibroblasts lacking both p21(Cip1) and p27(Kip1) ( p21/p27-null MEFs ) . These evidences imply that p21(Cip1) and p27(Kip1) CDK inhibitors are ' essential activators ' of cyclin D-kinases . We , however , discovered here that both the assembly and activation of cyclin D1-CDK4 complex occur when quiescent p21/p27-null MEFs were stimulated to re-enter the cell cycle . This mitogen-induced cyclin D1-kinase activity was blocked by overexpression of p16(INK4a) and resulted in the inhibition of S phase entry in p21/p27-null MEFs . Furthermore , ectopic expression of p34(SEI-1) , a mitogen-induced CDK4 binding protein , increased the levels of active cyclinD1-CDK4 complex in asynchronously proliferating p21/p27-null MEFs . Together , our results suggest that there are several independent ways to stimulate the assembly of cyclin D1-CDK4 kinases . Although p21(Cip1) and p27(Kip1) play a role in this process , our results demonstrate that additional mechanisms must occur in G0 to S phase transition .
    OUTPUT:
