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: TNF , an inflammatory cytokine that is enriched in the tumor microenvironment , promotes tumor growth and subverts innate immune responses to cancer cells . We previously reported that tumors implanted in TNF receptor-deficient ( Tnfr-/- ) mice are spontaneously rejected ; however , the molecular mechanisms underlying this rejection are unclear . Here we report that TNF signaling drives the peripheral accumulation of myeloid-derived suppressor cells ( MDSCs ) . MDSCs expand extensively during inflammation and tumor progression in mice and humans and can enhance tumor growth by repressing T cell-mediated antitumor responses . Peripheral accumulation of MDSCs was drastically impaired in Tnfr-/- mice . Signaling of TNFR-2 , but not TNFR-1 , promoted MDSC survival through upregulation of cellular FLICE-inhibitory protein ( c-FLIP ) and inhibition of caspase-8 activity . Loss of TNFRs impaired the induction of MDSCs from bone marrow cells , but this could be reversed by treatment with caspase inhibitors . These results demonstrate that TNFR-2 signaling promotes MDSC survival and accumulation and helps tumor cells evade the immune system .
    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.
    ###
    INPUT: TNF , an inflammatory cytokine that is enriched in the tumor microenvironment , promotes tumor growth and subverts innate immune responses to cancer cells . We previously reported that tumors implanted in TNF receptor-deficient ( Tnfr-/- ) mice are spontaneously rejected ; however , the molecular mechanisms underlying this rejection are unclear . Here we report that TNF signaling drives the peripheral accumulation of myeloid-derived suppressor cells ( MDSCs ) . MDSCs expand extensively during inflammation and tumor progression in mice and humans and can enhance tumor growth by repressing T cell-mediated antitumor responses . Peripheral accumulation of MDSCs was drastically impaired in Tnfr-/- mice . Signaling of TNFR-2 , but not TNFR-1 , promoted MDSC survival through upregulation of cellular FLICE-inhibitory protein ( c-FLIP ) and inhibition of caspase-8 activity . Loss of TNFRs impaired the induction of MDSCs from bone marrow cells , but this could be reversed by treatment with caspase inhibitors . These results demonstrate that TNFR-2 signaling promotes MDSC survival and accumulation and helps tumor cells evade the immune system .
    OUTPUT:
