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: The role of estrogen receptor beta ( ERÎ² ) in breast cancer is unclear . ERÎ² is considered to have a protective role in breast cancer development based on findings demonstrating that ERÎ² expression inhibits ERÎ±-mediated proliferation of breast cancer cells . We previously demonstrated that ERÎ² causes a ligand independent G2 cell cycle arrest in MCF-7 cells . To study the mechanisms of the ERÎ²-mediated G2 cell cycle arrest , we investigated its effects on the regulatory pathways responsible for the G2/M phase transition . We found that ERÎ² inhibits CDK1 activity , which is the critical determinant of the G2/M progression . CDK1 activity is modulated by both stimulatory and inhibitory factors . Cyclin B1 is the major activator of CDK1 . ERÎ² inhibited the cell cycle-dependent stimulation of cyclin B1 mRNA and protein . GADD45A and BTG2 are two major inhibitors of CDK1 , which have been implicated in breast tumor formation . Based on these findings , we explored if the expression pattern of GADD45A and BTG2 is affected by ERÎ² . We found that ERÎ² stimulates GADD45A and BTG2 mRNA levels . The induction of these two genes is caused by ERÎ² binding directly to these genes and recruiting c-jun and NCOA2 . Our findings demonstrated that unliganded ERÎ² causes a G2 cell cycle arrest by inactivating CDK1 through the repression of cyclin B1 and stimulation of GADD45A and BTG2 expression . These results provide evidence that drugs that stimulate the production of unliganded ERÎ² may be effective new therapies to prevent breast cancer .
    OUTPUT:

agent
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: The role of estrogen receptor beta ( ERÎ² ) in breast cancer is unclear . ERÎ² is considered to have a protective role in breast cancer development based on findings demonstrating that ERÎ² expression inhibits ERÎ±-mediated proliferation of breast cancer cells . We previously demonstrated that ERÎ² causes a ligand independent G2 cell cycle arrest in MCF-7 cells . To study the mechanisms of the ERÎ²-mediated G2 cell cycle arrest , we investigated its effects on the regulatory pathways responsible for the G2/M phase transition . We found that ERÎ² inhibits CDK1 activity , which is the critical determinant of the G2/M progression . CDK1 activity is modulated by both stimulatory and inhibitory factors . Cyclin B1 is the major activator of CDK1 . ERÎ² inhibited the cell cycle-dependent stimulation of cyclin B1 mRNA and protein . GADD45A and BTG2 are two major inhibitors of CDK1 , which have been implicated in breast tumor formation . Based on these findings , we explored if the expression pattern of GADD45A and BTG2 is affected by ERÎ² . We found that ERÎ² stimulates GADD45A and BTG2 mRNA levels . The induction of these two genes is caused by ERÎ² binding directly to these genes and recruiting c-jun and NCOA2 . Our findings demonstrated that unliganded ERÎ² causes a G2 cell cycle arrest by inactivating CDK1 through the repression of cyclin B1 and stimulation of GADD45A and BTG2 expression . These results provide evidence that drugs that stimulate the production of unliganded ERÎ² may be effective new therapies to prevent breast cancer .
    OUTPUT:
