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: Most hepatocellular carcinomas ( HCC ) develop in the context of severe liver fibrosis and cirrhosis caused by chronic liver inflammation , which also results in accumulation of reactive oxygen species ( ROS ) . In this study , we examined whether the stress-activated protein kinase p38Î± ( Mapk14 ) controls ROS metabolism and development of fibrosis and cancer in mice given thioacetamide to induce chronic liver injury . Liver-specific p38Î± ablation was found to enhance ROS accumulation , which appears to be exerted through the reduced expression of antioxidant protein HSP25 ( Hspb1 ) , a mouse homolog of HSP27 . Its reexpression in p38Î±-deficient liver prevents ROS accumulation and thioacetamide-induced fibrosis. p38Î± deficiency increased expression of SOX2 , a marker for cancer stem cells and the liver oncoproteins c-Jun ( Jun ) and Gankyrin ( Psmd10 ) and led to enhanced thioacetamide-induced hepatocarcinogenesis . The upregulation of SOX2 and c-Jun was prevented by administration of the antioxidant butylated hydroxyanisole . Intriguingly , the risk of human HCC recurrence is positively correlated with ROS accumulation in liver . Thus , p38Î± and its target HSP25/HSP27 appear to play a conserved and critical hepatoprotective function by curtailing ROS accumulation in liver parenchymal cells engaged in oxidative metabolism of exogenous chemicals . Augmented oxidative stress of liver parenchymal cells may explain the close relationship between liver fibrosis and hepatocarcinogenesis .
    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.
    ###
    INPUT: Most hepatocellular carcinomas ( HCC ) develop in the context of severe liver fibrosis and cirrhosis caused by chronic liver inflammation , which also results in accumulation of reactive oxygen species ( ROS ) . In this study , we examined whether the stress-activated protein kinase p38Î± ( Mapk14 ) controls ROS metabolism and development of fibrosis and cancer in mice given thioacetamide to induce chronic liver injury . Liver-specific p38Î± ablation was found to enhance ROS accumulation , which appears to be exerted through the reduced expression of antioxidant protein HSP25 ( Hspb1 ) , a mouse homolog of HSP27 . Its reexpression in p38Î±-deficient liver prevents ROS accumulation and thioacetamide-induced fibrosis. p38Î± deficiency increased expression of SOX2 , a marker for cancer stem cells and the liver oncoproteins c-Jun ( Jun ) and Gankyrin ( Psmd10 ) and led to enhanced thioacetamide-induced hepatocarcinogenesis . The upregulation of SOX2 and c-Jun was prevented by administration of the antioxidant butylated hydroxyanisole . Intriguingly , the risk of human HCC recurrence is positively correlated with ROS accumulation in liver . Thus , p38Î± and its target HSP25/HSP27 appear to play a conserved and critical hepatoprotective function by curtailing ROS accumulation in liver parenchymal cells engaged in oxidative metabolism of exogenous chemicals . Augmented oxidative stress of liver parenchymal cells may explain the close relationship between liver fibrosis and hepatocarcinogenesis .
    OUTPUT:
