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: Imiquimod is a synthetic compound with antitumor properties ; a 5% cream formulation is successfully used to treat skin tumors . The antitumor effect of imiquimod is multifactorial , although its ability to modulate immune responses by triggering TLR7/8 is thought to be key . Among the immune cells suggested to be involved are plasmacytoid DCs ( pDCs ) . However , a direct contribution of pDCs to tumor killing in vivo and the mechanism of their recruitment to imiquimod-treated sites have never been demonstrated . Using a mouse model of melanoma , we have now demonstrated that pDCs can directly clear tumors without the need for the adaptive immune system . Topical imiquimod treatment led to TLR7-dependent and IFN-Î±/Î² receptor 1-dependent ( IFNAR1-dependent ) upregulation of expression of the chemokine CCL2 in mast cells . This was essential to induce skin inflammation and for the recruitment of pDCs to the skin . The recruited pDCs were CD8Î±+ and induced tumor regression in a TLR7/MyD88- and IFNAR1-dependent manner . Lack of TLR7 and IFNAR1 or depletion of pDCs or CD8Î±+ cells from tumor-bearing mice completely abolished the effect of imiquimod . TLR7 was essential for imiquimod-stimulated pDCs to produce IFN-Î±/Î² , which led to TRAIL and granzyme B secretion by pDCs via IFNAR1 signaling . Blocking these cytolytic molecules impaired pDC-mediated tumor killing . Our results demonstrate that imiquimod treatment leads to CCL2-dependent recruitment of pDCs and their transformation into a subset of killer DCs able to directly eliminate tumor cells .
    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: Imiquimod is a synthetic compound with antitumor properties ; a 5% cream formulation is successfully used to treat skin tumors . The antitumor effect of imiquimod is multifactorial , although its ability to modulate immune responses by triggering TLR7/8 is thought to be key . Among the immune cells suggested to be involved are plasmacytoid DCs ( pDCs ) . However , a direct contribution of pDCs to tumor killing in vivo and the mechanism of their recruitment to imiquimod-treated sites have never been demonstrated . Using a mouse model of melanoma , we have now demonstrated that pDCs can directly clear tumors without the need for the adaptive immune system . Topical imiquimod treatment led to TLR7-dependent and IFN-Î±/Î² receptor 1-dependent ( IFNAR1-dependent ) upregulation of expression of the chemokine CCL2 in mast cells . This was essential to induce skin inflammation and for the recruitment of pDCs to the skin . The recruited pDCs were CD8Î±+ and induced tumor regression in a TLR7/MyD88- and IFNAR1-dependent manner . Lack of TLR7 and IFNAR1 or depletion of pDCs or CD8Î±+ cells from tumor-bearing mice completely abolished the effect of imiquimod . TLR7 was essential for imiquimod-stimulated pDCs to produce IFN-Î±/Î² , which led to TRAIL and granzyme B secretion by pDCs via IFNAR1 signaling . Blocking these cytolytic molecules impaired pDC-mediated tumor killing . Our results demonstrate that imiquimod treatment leads to CCL2-dependent recruitment of pDCs and their transformation into a subset of killer DCs able to directly eliminate tumor cells .
    OUTPUT:
