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: Although tumor-associated macrophages ( TAMs ) are involved in tumor growth and metastasis , the mechanisms controlling their pro-tumoral activities remain largely unknown . The transcription factor c-MYC has been recently shown to regulate in vitro human macrophage polarization and be expressed in macrophages infiltrating human tumors . In this study , we exploited the predominant expression of LysM in myeloid cells to generate c-Myc(fl/fl) LysM(cre/+) mice , which lack c-Myc in macrophages , to investigate the role of macrophage c-MYC expression in cancer . Under steady-state conditions , immune system parameters in c-Myc(fl/fl) LysM(cre/+) mice appeared normal , including the abundance of different subsets of bone marrow hematopoietic stem cells , precursors and circulating cells , macrophage density , and immune organ structure . In a model of melanoma , however , TAMs lacking c-Myc displayed a delay in maturation and showed an attenuation of pro-tumoral functions ( e.g. , reduced expression of VEGF , MMP9 , and HIF1Î± ) that was associated with impaired tissue remodeling and angiogenesis and limited tumor growth in c-Myc(fl/fl) LysM(cre/+) mice . Macrophage c-Myc deletion also diminished fibrosarcoma growth . These data identify c-Myc as a positive regulator of the pro-tumoral program of TAMs and suggest c-Myc inactivation as an attractive target for anti-cancer therapy .
    OUTPUT:

agent
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: Although tumor-associated macrophages ( TAMs ) are involved in tumor growth and metastasis , the mechanisms controlling their pro-tumoral activities remain largely unknown . The transcription factor c-MYC has been recently shown to regulate in vitro human macrophage polarization and be expressed in macrophages infiltrating human tumors . In this study , we exploited the predominant expression of LysM in myeloid cells to generate c-Myc(fl/fl) LysM(cre/+) mice , which lack c-Myc in macrophages , to investigate the role of macrophage c-MYC expression in cancer . Under steady-state conditions , immune system parameters in c-Myc(fl/fl) LysM(cre/+) mice appeared normal , including the abundance of different subsets of bone marrow hematopoietic stem cells , precursors and circulating cells , macrophage density , and immune organ structure . In a model of melanoma , however , TAMs lacking c-Myc displayed a delay in maturation and showed an attenuation of pro-tumoral functions ( e.g. , reduced expression of VEGF , MMP9 , and HIF1Î± ) that was associated with impaired tissue remodeling and angiogenesis and limited tumor growth in c-Myc(fl/fl) LysM(cre/+) mice . Macrophage c-Myc deletion also diminished fibrosarcoma growth . These data identify c-Myc as a positive regulator of the pro-tumoral program of TAMs and suggest c-Myc inactivation as an attractive target for anti-cancer therapy .
    OUTPUT:
