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: BACKGROUND Oxidative stress and inflammation are important steps in the pathogenesis of atherosclerosis . We postulated that therapeutic concentrations of aspirin and pravastatin , especially in combination , may suppress oxidative stress and inflammation in endothelial cells , and this concept was examined in human coronary artery endothelial cells ( HCAECs ) . METHODS Human coronary artery endothelial cells were cultured and treated with oxidized-low density lipoprotein ( ox-LDL , 60 microg/ml for 24 hours ) alone , or pre-treated with aspirin ( 1 , 2 or 5 mmol/L ) , pravastatin ( 1 , 5 or 10 micromol/L ) or their combination ( 1 mmol/L aspirin and 5 micromol/L pravastatin ) , followed by ox-LDL treatment . After respective treatment , superoxide anion production , p38 mitogen activated protein kinase and transcription factor NF-kappaB activation , protein expression of lectin-like ox-LDL receptor-1 ( LOX-1 ) and adhesion molecules , and monocyte adhesion were measured . RESULTS Ox-LDL treatment greatly elicited its receptor LOX-1 expression , superoxide anion production and inflammatory response , which were minimally affected by low concentration of aspirin ( 1 mmol/L ) or pravastatin ( 5 micromol/L ) , but were markedly decreased by their combination . Activation of p38 mitogen activated protein kinase and NF-kappaB , the expression of intercellular adhesion molecule-1 and monocyte chemotactic protein-1 , which were only mildly affected by aspirin or pravastatin alone , were significantly attenuated by their combination . As a consequence , monocyte adhesion to endothelial cells was markedly attenuated by the combination of the two agents . Well-known anti-oxidants alpha-tocopherol and gamma-tocopherol had similar inhibitory effects on ox-LDL-mediated oxidative stress and LOX-1 expression as well as monocyte adhesion as did the combination of aspirin and pravastatin . CONCLUSIONS These studies point to a positive interaction between aspirin and pravastatin with regard to endothelial biology . Anti-oxidant and subsequent anti-inflammatory effect may be one of the potential underling mechanisms .
    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: BACKGROUND Oxidative stress and inflammation are important steps in the pathogenesis of atherosclerosis . We postulated that therapeutic concentrations of aspirin and pravastatin , especially in combination , may suppress oxidative stress and inflammation in endothelial cells , and this concept was examined in human coronary artery endothelial cells ( HCAECs ) . METHODS Human coronary artery endothelial cells were cultured and treated with oxidized-low density lipoprotein ( ox-LDL , 60 microg/ml for 24 hours ) alone , or pre-treated with aspirin ( 1 , 2 or 5 mmol/L ) , pravastatin ( 1 , 5 or 10 micromol/L ) or their combination ( 1 mmol/L aspirin and 5 micromol/L pravastatin ) , followed by ox-LDL treatment . After respective treatment , superoxide anion production , p38 mitogen activated protein kinase and transcription factor NF-kappaB activation , protein expression of lectin-like ox-LDL receptor-1 ( LOX-1 ) and adhesion molecules , and monocyte adhesion were measured . RESULTS Ox-LDL treatment greatly elicited its receptor LOX-1 expression , superoxide anion production and inflammatory response , which were minimally affected by low concentration of aspirin ( 1 mmol/L ) or pravastatin ( 5 micromol/L ) , but were markedly decreased by their combination . Activation of p38 mitogen activated protein kinase and NF-kappaB , the expression of intercellular adhesion molecule-1 and monocyte chemotactic protein-1 , which were only mildly affected by aspirin or pravastatin alone , were significantly attenuated by their combination . As a consequence , monocyte adhesion to endothelial cells was markedly attenuated by the combination of the two agents . Well-known anti-oxidants alpha-tocopherol and gamma-tocopherol had similar inhibitory effects on ox-LDL-mediated oxidative stress and LOX-1 expression as well as monocyte adhesion as did the combination of aspirin and pravastatin . CONCLUSIONS These studies point to a positive interaction between aspirin and pravastatin with regard to endothelial biology . Anti-oxidant and subsequent anti-inflammatory effect may be one of the potential underling mechanisms .
    OUTPUT:
