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: Human fibroblasts undergo cellular senescence after a finite number of divisions , in response to the erosion of telomeres . In addition to being terminally arrested in the cell cycle , senescent fibroblasts express genes that are normally induced upon wounding , including genes that remodel the extracellular matrix . We have identified the novel zinc finger protein APA-1 , whose expression increased in senescent human fibroblasts independent of telomere shortening . Extended passage , telomerase-immortalized fibroblasts had increased levels of APA-1 as well as the cyclin-dependent kinase inhibitor p16 . In fibroblasts , APA-1 was modified by the ubiquitin-like protein SUMO-1 , which increased APA-1 half-life , possibly by blocking ubiquitin-mediated degradation . Overexpression of APA-1 did not cause cell cycle arrest ; but , it induced transcription of the extracellular matrix-remodeling genes MMP1 and PAI2 , which are associated with fibroblast senescence . MMP1 and PAI2 transcript levels also increased in telomerase-immortalized fibroblasts that had high levels of APA-1 , demonstrating that the matrix-remodeling phenotype of senescent fibroblasts was not induced by telomere attrition alone . APA-1 was able to transactivate and bind to the MMP1 promoter , suggesting that APA-1 is a transcription factor that regulates expression of matrix-remodeling genes during fibroblast senescence .
    OUTPUT:

agent
enabling replicative immortality;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.
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    INPUT: Human fibroblasts undergo cellular senescence after a finite number of divisions , in response to the erosion of telomeres . In addition to being terminally arrested in the cell cycle , senescent fibroblasts express genes that are normally induced upon wounding , including genes that remodel the extracellular matrix . We have identified the novel zinc finger protein APA-1 , whose expression increased in senescent human fibroblasts independent of telomere shortening . Extended passage , telomerase-immortalized fibroblasts had increased levels of APA-1 as well as the cyclin-dependent kinase inhibitor p16 . In fibroblasts , APA-1 was modified by the ubiquitin-like protein SUMO-1 , which increased APA-1 half-life , possibly by blocking ubiquitin-mediated degradation . Overexpression of APA-1 did not cause cell cycle arrest ; but , it induced transcription of the extracellular matrix-remodeling genes MMP1 and PAI2 , which are associated with fibroblast senescence . MMP1 and PAI2 transcript levels also increased in telomerase-immortalized fibroblasts that had high levels of APA-1 , demonstrating that the matrix-remodeling phenotype of senescent fibroblasts was not induced by telomere attrition alone . APA-1 was able to transactivate and bind to the MMP1 promoter , suggesting that APA-1 is a transcription factor that regulates expression of matrix-remodeling genes during fibroblast senescence .
    OUTPUT:
