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: Recent studies have demonstrated that n-3 polyunsaturated fatty acids such as eicosapentaenoic acid ( EPA ) are able to suppress cell proliferation and inhibit tumor growth . The objective of our study was to investigate the influence of a high dose EPA on the development of the tumor phenotype in ataxia-telangiectasia mutated ( Atm)-deficient mice , a genetic cancer model that is associated with increased levels of oxidative stress . We analyzed toxicity , proliferation , cell-cycle progression , and apoptosis of EPA in vitro and latency to tumorigenesis in vivo . Because of the impact of reactive oxygen species ( ROS ) on the tumor incidence in ataxia telangiectasia ( AT ) , we further analyzed the effect of EPA on the generation of ROS and oxidative DNA damage ( ODD ) . EPA effectively inhibited proliferation , altered cell-cycle progression , and induced apoptosis of tumor cells ( AT-4 ) . EPA showed no effect on the latency to tumorigenesis in Atm-deficient mice . EPA treatment was accompanied by a significant increase of ROS and ODD . Our results demonstrate the antiproliferative effect of EPA on tumor cells by alteration of cell-cycle progression and induction of apoptosis in vitro . On the other hand , EPA treatment of Atm-deficient mice led to the formation of ROS and accumulation of ODD that might have abrogated the anticarcinogenic effect caused by EPA .
    OUTPUT:

agent
evading growth suppressors;resisting cell death;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: Recent studies have demonstrated that n-3 polyunsaturated fatty acids such as eicosapentaenoic acid ( EPA ) are able to suppress cell proliferation and inhibit tumor growth . The objective of our study was to investigate the influence of a high dose EPA on the development of the tumor phenotype in ataxia-telangiectasia mutated ( Atm)-deficient mice , a genetic cancer model that is associated with increased levels of oxidative stress . We analyzed toxicity , proliferation , cell-cycle progression , and apoptosis of EPA in vitro and latency to tumorigenesis in vivo . Because of the impact of reactive oxygen species ( ROS ) on the tumor incidence in ataxia telangiectasia ( AT ) , we further analyzed the effect of EPA on the generation of ROS and oxidative DNA damage ( ODD ) . EPA effectively inhibited proliferation , altered cell-cycle progression , and induced apoptosis of tumor cells ( AT-4 ) . EPA showed no effect on the latency to tumorigenesis in Atm-deficient mice . EPA treatment was accompanied by a significant increase of ROS and ODD . Our results demonstrate the antiproliferative effect of EPA on tumor cells by alteration of cell-cycle progression and induction of apoptosis in vitro . On the other hand , EPA treatment of Atm-deficient mice led to the formation of ROS and accumulation of ODD that might have abrogated the anticarcinogenic effect caused by EPA .
    OUTPUT:
