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: Tumor development requires angiogenesis and anti-angiogenic therapies have been introduced in the treatment of cancer . In this context , heparan sulfate proteoglycans ( HSPGs ) emerge as interesting targets , owing to their function as co-receptors of major , pro-angiogenic factors . Accordingly , previous studies have suggested anti-tumor effects of heparin , i.e. over-sulfated HS , and various heparin mimetics ; however , a significant drawback is their unspecific mechanism of action and potentially serious side-effects related to their anticoagulant properties . Here , we have explored the use of human ScFv anti-HS antibodies ( Î±HS ) as a more rational approach to target HSPG function in endothelial cells ( ECs). Î±HS were initially selected for their recognition of HS epitopes localized preferentially to the vasculature of patient glioblastoma tumors , i.e. highly angiogenic brain tumors . Unexpectedly , we found that these Î±HS exhibited potent pro-angiogenic effects in primary human ECs. Î±HS were shown to stimulate EC differentiation , which was associated with increased EC tube formation and proliferation . Moreover , Î±HS supported EC survival under hypoxia and starvation , i.e. conditions typical of the tumor microenvironment . Importantly , Î±HS-mediated proliferation was efficiently counter-acted by heparin and was absent in HSPG-deficient mutant cells , confirming HS-specific effects . On a mechanistic level , binding of Î±HS to HSPGs of ECs as well as glioblastoma cells was found to trigger p38 MAPK-dependent signaling resulting in increased proliferation . We conclude that several Î±HS that recognize HS epitopes abundant in the tumor vasculature may elicit a pro-angiogenic response , which has implications for the development of antibody-based targeting of HSPGs in cancer .
    OUTPUT:

agent
sustaining proliferative signaling;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: Tumor development requires angiogenesis and anti-angiogenic therapies have been introduced in the treatment of cancer . In this context , heparan sulfate proteoglycans ( HSPGs ) emerge as interesting targets , owing to their function as co-receptors of major , pro-angiogenic factors . Accordingly , previous studies have suggested anti-tumor effects of heparin , i.e. over-sulfated HS , and various heparin mimetics ; however , a significant drawback is their unspecific mechanism of action and potentially serious side-effects related to their anticoagulant properties . Here , we have explored the use of human ScFv anti-HS antibodies ( Î±HS ) as a more rational approach to target HSPG function in endothelial cells ( ECs). Î±HS were initially selected for their recognition of HS epitopes localized preferentially to the vasculature of patient glioblastoma tumors , i.e. highly angiogenic brain tumors . Unexpectedly , we found that these Î±HS exhibited potent pro-angiogenic effects in primary human ECs. Î±HS were shown to stimulate EC differentiation , which was associated with increased EC tube formation and proliferation . Moreover , Î±HS supported EC survival under hypoxia and starvation , i.e. conditions typical of the tumor microenvironment . Importantly , Î±HS-mediated proliferation was efficiently counter-acted by heparin and was absent in HSPG-deficient mutant cells , confirming HS-specific effects . On a mechanistic level , binding of Î±HS to HSPGs of ECs as well as glioblastoma cells was found to trigger p38 MAPK-dependent signaling resulting in increased proliferation . We conclude that several Î±HS that recognize HS epitopes abundant in the tumor vasculature may elicit a pro-angiogenic response , which has implications for the development of antibody-based targeting of HSPGs in cancer .
    OUTPUT:
