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: Partial or whole-brain irradiation is often required to treat both primary and metastatic brain cancer . Radiation-induced normal tissue injury , including progressive cognitive impairment , however , can significantly affect the well-being of the approximately 200,000 patients who receive these treatments each year in the United States . Although the exact mechanisms underlying radiation-induced late effects remain unclear , oxidative stress and inflammation are thought to play a critical role . Microglia are key mediators of neuroinflammation . Peroxisomal proliferator-activated receptor ( PPAR ) Î´ has been shown to be a potent regulator of anti-inflammatory responses . Thus , we hypothesized that PPARÎ´ activation would modulate the radiation-induced inflammatory response in microglia . Incubating BV-2 murine microglial cells with the PPARÎ´ agonist L-165041 prevented the radiation-induced increase in : ( i ) intracellular reactive oxygen species generation , ( ii ) Cox-2 and MCP-1 expression , and ( iii ) IL-1Î² and TNF-Î± message levels . This occurred , in part , through PPARÎ´-mediated modulation of stress-activated kinases and proinflammatory transcription factors . PPARÎ´ inhibited NF-ÎºB via transrepression by physically interacting with the p65 subunit and prevented activation of the PKCÎ±/MEK1/2/ERK1/2/AP-1 pathway by inhibiting the radiation-induced increase in intracellular reactive oxygen species generation . These data support the hypothesis that PPARÎ´ activation can modulate radiation-induced oxidative stress and inflammatory responses in microglia .
    OUTPUT:

agent
tumor promoting inflammation
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: Partial or whole-brain irradiation is often required to treat both primary and metastatic brain cancer . Radiation-induced normal tissue injury , including progressive cognitive impairment , however , can significantly affect the well-being of the approximately 200,000 patients who receive these treatments each year in the United States . Although the exact mechanisms underlying radiation-induced late effects remain unclear , oxidative stress and inflammation are thought to play a critical role . Microglia are key mediators of neuroinflammation . Peroxisomal proliferator-activated receptor ( PPAR ) Î´ has been shown to be a potent regulator of anti-inflammatory responses . Thus , we hypothesized that PPARÎ´ activation would modulate the radiation-induced inflammatory response in microglia . Incubating BV-2 murine microglial cells with the PPARÎ´ agonist L-165041 prevented the radiation-induced increase in : ( i ) intracellular reactive oxygen species generation , ( ii ) Cox-2 and MCP-1 expression , and ( iii ) IL-1Î² and TNF-Î± message levels . This occurred , in part , through PPARÎ´-mediated modulation of stress-activated kinases and proinflammatory transcription factors . PPARÎ´ inhibited NF-ÎºB via transrepression by physically interacting with the p65 subunit and prevented activation of the PKCÎ±/MEK1/2/ERK1/2/AP-1 pathway by inhibiting the radiation-induced increase in intracellular reactive oxygen species generation . These data support the hypothesis that PPARÎ´ activation can modulate radiation-induced oxidative stress and inflammatory responses in microglia .
    OUTPUT:
