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: The recent approval of a prostate cancer vaccine has renewed hope for anticancer immunotherapies . However , the immunosuppressive tumor microenvironment may limit the effectiveness of current immunotherapies . Antiangiogenic agents have the potential to modulate the tumor microenvironment and improve immunotherapy , but they often are used at high doses in the clinic to prune tumor vessels and paradoxically may compromise various therapies . Here , we demonstrate that targeting tumor vasculature with lower vascular-normalizing doses , but not high antivascular/antiangiogenic doses , of an anti-VEGF receptor 2 ( VEGFR2 ) antibody results in a more homogeneous distribution of functional tumor vessels . Furthermore , lower doses are superior to the high doses in polarizing tumor-associated macrophages from an immune inhibitory M2-like phenotype toward an immune stimulatory M1-like phenotype and in facilitating CD4(+) and CD8(+) T-cell tumor infiltration . Based on this mechanism , scheduling lower-dose anti-VEGFR2 therapy with T-cell activation induced by a whole cancer cell vaccine therapy enhanced anticancer efficacy in a CD8(+) T-cell-dependent manner in both immune-tolerant and immunogenic murine breast cancer models . These findings indicate that vascular-normalizing lower doses of anti-VEGFR2 antibody can reprogram the tumor microenvironment away from immunosuppression toward potentiation of cancer vaccine therapies . Given that the combinations of high doses of bevacizumab with chemotherapy have not improved overall survival of breast cancer patients , our study suggests a strategy to use antiangiogenic agents in breast cancer more effectively with active immunotherapy and potentially other anticancer therapies .
    OUTPUT:

agent
inducing angiogenesis;avoiding immune destruction
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: The recent approval of a prostate cancer vaccine has renewed hope for anticancer immunotherapies . However , the immunosuppressive tumor microenvironment may limit the effectiveness of current immunotherapies . Antiangiogenic agents have the potential to modulate the tumor microenvironment and improve immunotherapy , but they often are used at high doses in the clinic to prune tumor vessels and paradoxically may compromise various therapies . Here , we demonstrate that targeting tumor vasculature with lower vascular-normalizing doses , but not high antivascular/antiangiogenic doses , of an anti-VEGF receptor 2 ( VEGFR2 ) antibody results in a more homogeneous distribution of functional tumor vessels . Furthermore , lower doses are superior to the high doses in polarizing tumor-associated macrophages from an immune inhibitory M2-like phenotype toward an immune stimulatory M1-like phenotype and in facilitating CD4(+) and CD8(+) T-cell tumor infiltration . Based on this mechanism , scheduling lower-dose anti-VEGFR2 therapy with T-cell activation induced by a whole cancer cell vaccine therapy enhanced anticancer efficacy in a CD8(+) T-cell-dependent manner in both immune-tolerant and immunogenic murine breast cancer models . These findings indicate that vascular-normalizing lower doses of anti-VEGFR2 antibody can reprogram the tumor microenvironment away from immunosuppression toward potentiation of cancer vaccine therapies . Given that the combinations of high doses of bevacizumab with chemotherapy have not improved overall survival of breast cancer patients , our study suggests a strategy to use antiangiogenic agents in breast cancer more effectively with active immunotherapy and potentially other anticancer therapies .
    OUTPUT:
