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: Cellular senescence is a permanent out-of-cycle state regulated by molecular circuits acting during the G1 phase of the cell cycle . Cdt1 is a central regulator of DNA replication licensing acting during the G1 phase and it is negatively controlled by Geminin . Here , we characterize the cell cycle expression pattern of Cdt1 and Geminin during successive passages of primary fibroblasts and compare it to tumour-derived cell lines . Cdt1 and Geminin are strictly expressed in distinct subpopulations of young fibroblasts , similarly to cancer cells , with Geminin accumulating shortly after the onset of S phase . Cdt1 and Geminin are down-regulated when primary human and mouse fibroblasts undergo replicative or stress-induced senescence . RNAi-mediated Geminin knock-down in human cells enhances the appearance of phenotypic and molecular features of senescence . Mouse embryonic fibroblasts heterozygous for Geminin exhibit accelerated senescence compared to control fibroblasts . In contrast , ectopic expression of Geminin in mouse embryonic fibroblasts delays the appearance of the senescent phenotype . Taken together , our data suggest that changes in Geminin expression levels affect the establishment of senescence pathways .
    OUTPUT:

agent
enabling replicative immortality
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: Cellular senescence is a permanent out-of-cycle state regulated by molecular circuits acting during the G1 phase of the cell cycle . Cdt1 is a central regulator of DNA replication licensing acting during the G1 phase and it is negatively controlled by Geminin . Here , we characterize the cell cycle expression pattern of Cdt1 and Geminin during successive passages of primary fibroblasts and compare it to tumour-derived cell lines . Cdt1 and Geminin are strictly expressed in distinct subpopulations of young fibroblasts , similarly to cancer cells , with Geminin accumulating shortly after the onset of S phase . Cdt1 and Geminin are down-regulated when primary human and mouse fibroblasts undergo replicative or stress-induced senescence . RNAi-mediated Geminin knock-down in human cells enhances the appearance of phenotypic and molecular features of senescence . Mouse embryonic fibroblasts heterozygous for Geminin exhibit accelerated senescence compared to control fibroblasts . In contrast , ectopic expression of Geminin in mouse embryonic fibroblasts delays the appearance of the senescent phenotype . Taken together , our data suggest that changes in Geminin expression levels affect the establishment of senescence pathways .
    OUTPUT:
