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 green fluorescent protein ( GFP ) is the most commonly used reporter protein for monitoring gene expression and protein localization in a variety of living and fixed cells , including not only prokaryotes , but also eukaryotes , e.g. , yeasts , mammals , plants and fish . In general , it is thought that GFP is nontoxic to cells , although there are some reports on the side effect of GFP . Further , details of the molecular mechanism concerning the side effect of GFP remain unclear . Here we show that Ku80 , but not XRCC4 , plays an important role in the mechanism of the resistance to cytotoxicity induced by enhanced GFP ( EGFP ) . EGFP inhibited both cell proliferation and colony formation , and induced cell death in Ku80-deficient hamster cells , i.e. , xrs-6 cells . In addition , Ku80 attenuated EGFP-induced cytotoxicity in the xrs-6 cells . No EGFP-induced cytotoxicity was observed in the NHEJ core protein XRCC4-deficient hamster cells , i.e. , XR-1 cells . Furthermore , EGFP markedly enhanced X-ray-induced cytotoxicity in the xrs-6 cells . These results suggest that Ku80 plays a key role in the novel NHEJ-independent defense mechanism against EGFP-induced cytotoxicity . Caution should be taken in considering of the potential influence by the stress response mechanism , namely , the Ku80-dependent elimination mechanism of EGFP-induced cytotoxicity , being activated , even when using EGFP-expressing cells in which Ku80 functions normally .
    OUTPUT:

agent
genomic instability and mutation
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 green fluorescent protein ( GFP ) is the most commonly used reporter protein for monitoring gene expression and protein localization in a variety of living and fixed cells , including not only prokaryotes , but also eukaryotes , e.g. , yeasts , mammals , plants and fish . In general , it is thought that GFP is nontoxic to cells , although there are some reports on the side effect of GFP . Further , details of the molecular mechanism concerning the side effect of GFP remain unclear . Here we show that Ku80 , but not XRCC4 , plays an important role in the mechanism of the resistance to cytotoxicity induced by enhanced GFP ( EGFP ) . EGFP inhibited both cell proliferation and colony formation , and induced cell death in Ku80-deficient hamster cells , i.e. , xrs-6 cells . In addition , Ku80 attenuated EGFP-induced cytotoxicity in the xrs-6 cells . No EGFP-induced cytotoxicity was observed in the NHEJ core protein XRCC4-deficient hamster cells , i.e. , XR-1 cells . Furthermore , EGFP markedly enhanced X-ray-induced cytotoxicity in the xrs-6 cells . These results suggest that Ku80 plays a key role in the novel NHEJ-independent defense mechanism against EGFP-induced cytotoxicity . Caution should be taken in considering of the potential influence by the stress response mechanism , namely , the Ku80-dependent elimination mechanism of EGFP-induced cytotoxicity , being activated , even when using EGFP-expressing cells in which Ku80 functions normally .
    OUTPUT:
