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: Kaposi sarcoma is the most common neoplasm caused by Kaposi sarcoma-associated herpesvirus ( KSHV ) . It is prevalent among the elderly in the Mediterranean , inhabitants of sub-Saharan Africa , and immunocompromised individuals such as organ transplant recipients and AIDS patients . Current treatments for Kaposi sarcoma can inhibit tumor growth but are not able to eliminate KSHV from the host . When the host's immune system weakens , KSHV begins to replicate again , and active tumor growth ensues . New therapeutic approaches are needed . Cannabidiol ( CBD ) , a plant-derived cannabinoid , exhibits promising antitumor effects without inducing psychoactive side effects . CBD is emerging as a novel therapeutic for various disorders , including cancer . In this study , we investigated the effects of CBD both on the infection of endothelial cells ( ECs ) by KSHV and on the growth and apoptosis of KSHV-infected ECs , an in vitro model for the transformation of normal endothelium to Kaposi sarcoma . While CBD did not affect the efficiency with which KSHV infected ECs , it reduced proliferation and induced apoptosis in those infected by the virus . CBD inhibited the expression of KSHV viral G protein-coupled receptor ( vGPCR ) , its agonist , the chemokine growth-regulated protein Î± ( GRO-Î± ) , vascular endothelial growth factor receptor 3 ( VEGFR-3 ) , and the VEGFR-3 ligand , vascular endothelial growth factor C ( VEGF-C ) . This suggests a potential mechanism by which CBD exerts its effects on KSHV-infected endothelium and supports the further examination of CBD as a novel targeted agent for the treatment of Kaposi sarcoma .
    OUTPUT:

agent
resisting cell death;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.
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    INPUT: Kaposi sarcoma is the most common neoplasm caused by Kaposi sarcoma-associated herpesvirus ( KSHV ) . It is prevalent among the elderly in the Mediterranean , inhabitants of sub-Saharan Africa , and immunocompromised individuals such as organ transplant recipients and AIDS patients . Current treatments for Kaposi sarcoma can inhibit tumor growth but are not able to eliminate KSHV from the host . When the host's immune system weakens , KSHV begins to replicate again , and active tumor growth ensues . New therapeutic approaches are needed . Cannabidiol ( CBD ) , a plant-derived cannabinoid , exhibits promising antitumor effects without inducing psychoactive side effects . CBD is emerging as a novel therapeutic for various disorders , including cancer . In this study , we investigated the effects of CBD both on the infection of endothelial cells ( ECs ) by KSHV and on the growth and apoptosis of KSHV-infected ECs , an in vitro model for the transformation of normal endothelium to Kaposi sarcoma . While CBD did not affect the efficiency with which KSHV infected ECs , it reduced proliferation and induced apoptosis in those infected by the virus . CBD inhibited the expression of KSHV viral G protein-coupled receptor ( vGPCR ) , its agonist , the chemokine growth-regulated protein Î± ( GRO-Î± ) , vascular endothelial growth factor receptor 3 ( VEGFR-3 ) , and the VEGFR-3 ligand , vascular endothelial growth factor C ( VEGF-C ) . This suggests a potential mechanism by which CBD exerts its effects on KSHV-infected endothelium and supports the further examination of CBD as a novel targeted agent for the treatment of Kaposi sarcoma .
    OUTPUT:
