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: Reciprocity of inflammation , oxidative stress and neovascularization is emerging as an important mechanism underlying numerous processes from tissue healing and remodelling to cancer progression . Whereas the mechanism of hypoxia-driven angiogenesis is well understood , the link between inflammation-induced oxidation and de novo blood vessel growth remains obscure . Here we show that the end products of lipid oxidation , Ï-(2-carboxyethyl)pyrrole ( CEP ) and other related pyrroles , are generated during inflammation and wound healing and accumulate at high levels in ageing tissues in mice and in highly vascularized tumours in both murine and human melanoma . The molecular patterns of carboxyalkylpyrroles are recognized by Toll-like receptor 2 ( TLR2 ) , but not TLR4 or scavenger receptors on endothelial cells , leading to an angiogenic response that is independent of vascular endothelial growth factor . CEP promoted angiogenesis in hindlimb ischaemia and wound healing models through MyD88-dependent TLR2 signalling . Neutralization of endogenous carboxyalkylpyrroles impaired wound healing and tissue revascularization and diminished tumour angiogenesis . Both TLR2 and MyD88 are required for CEP-induced stimulation of Rac1 and endothelial migration . Taken together , these findings establish a new function of TLR2 as a sensor of oxidation-associated molecular patterns , providing a key link connecting inflammation , oxidative stress , innate immunity and angiogenesis .
    OUTPUT:

agent
tumor promoting inflammation;inducing angiogenesis
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: Reciprocity of inflammation , oxidative stress and neovascularization is emerging as an important mechanism underlying numerous processes from tissue healing and remodelling to cancer progression . Whereas the mechanism of hypoxia-driven angiogenesis is well understood , the link between inflammation-induced oxidation and de novo blood vessel growth remains obscure . Here we show that the end products of lipid oxidation , Ï-(2-carboxyethyl)pyrrole ( CEP ) and other related pyrroles , are generated during inflammation and wound healing and accumulate at high levels in ageing tissues in mice and in highly vascularized tumours in both murine and human melanoma . The molecular patterns of carboxyalkylpyrroles are recognized by Toll-like receptor 2 ( TLR2 ) , but not TLR4 or scavenger receptors on endothelial cells , leading to an angiogenic response that is independent of vascular endothelial growth factor . CEP promoted angiogenesis in hindlimb ischaemia and wound healing models through MyD88-dependent TLR2 signalling . Neutralization of endogenous carboxyalkylpyrroles impaired wound healing and tissue revascularization and diminished tumour angiogenesis . Both TLR2 and MyD88 are required for CEP-induced stimulation of Rac1 and endothelial migration . Taken together , these findings establish a new function of TLR2 as a sensor of oxidation-associated molecular patterns , providing a key link connecting inflammation , oxidative stress , innate immunity and angiogenesis .
    OUTPUT:
