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: Macrophages are the prominent components of solid tumors and have complex dual functions in their interaction with cancer cells . Strong evidence suggests that TAM is a part of inflammatory circuits that promote tumor progression . B7-homologue 3 ( B7-H3 ) , a recently identified homologue of B7.1/2 ( CD80/86 ) , has been described to exert co-stimulatory and immune regulatory functions . Here , we showed that a fraction of macrophages in tumor stroma expressed surface B7-H3 molecule . Normal macrophages , which did not express B7-H3 , would be induced expressing B7-H3 molecule when culturing with tumor cell . Although a lung cancer cell line constitutively expressed B7-H3 mRNA and protein in plasma , primary tumor cell isolated from the transplanted lung carcinoma model expressed B7-H3 on the surface . Interestingly , in transplanted lung carcinoma model , the expression of membrane-bound B7-H3 in tumor cells was increased as prolonging of tumor transformation . In support , IL-10 released from TAM could stimulate cancer cell expression of membrane bound B7-H3 . Furthermore , Lung cancer and TAM-related B7-H3 was identified as a strong inhibitor of T-cell effect and influenced the outcome of T cell immune response . In conclusion , TAM-tumor cell interaction-induced membrane-bound B7-H3 represents a novel immune escape mechanism which links the pro-inflammatory response to immune tolerance in the tumor milieu .
    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: Macrophages are the prominent components of solid tumors and have complex dual functions in their interaction with cancer cells . Strong evidence suggests that TAM is a part of inflammatory circuits that promote tumor progression . B7-homologue 3 ( B7-H3 ) , a recently identified homologue of B7.1/2 ( CD80/86 ) , has been described to exert co-stimulatory and immune regulatory functions . Here , we showed that a fraction of macrophages in tumor stroma expressed surface B7-H3 molecule . Normal macrophages , which did not express B7-H3 , would be induced expressing B7-H3 molecule when culturing with tumor cell . Although a lung cancer cell line constitutively expressed B7-H3 mRNA and protein in plasma , primary tumor cell isolated from the transplanted lung carcinoma model expressed B7-H3 on the surface . Interestingly , in transplanted lung carcinoma model , the expression of membrane-bound B7-H3 in tumor cells was increased as prolonging of tumor transformation . In support , IL-10 released from TAM could stimulate cancer cell expression of membrane bound B7-H3 . Furthermore , Lung cancer and TAM-related B7-H3 was identified as a strong inhibitor of T-cell effect and influenced the outcome of T cell immune response . In conclusion , TAM-tumor cell interaction-induced membrane-bound B7-H3 represents a novel immune escape mechanism which links the pro-inflammatory response to immune tolerance in the tumor milieu .
    OUTPUT:
