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: Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors . Although the full process depends on innate and adaptive immunity , it remains unclear whether innate immunity alone is capable of immunoediting . To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity , we compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-type , RAG2(-/-) , and RAG2(-/-)x Î³c(-/-) mice . We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity . This activity required natural killer ( NK ) cells and interferon Î³ ( IFN-Î³ ) , which mediated the induction of M1 macrophages . M1 macrophages could be elicited by administration of CD40 agonists , thereby restoring editing activity in RAG2(-/-)x Î³c(-/-) mice . Our results suggest that in the absence of adaptive immunity , NK cell production of IFN-Î³ induces M1 macrophages , which act as important effectors during cancer immunoediting .
    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.
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    INPUT: Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors . Although the full process depends on innate and adaptive immunity , it remains unclear whether innate immunity alone is capable of immunoediting . To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity , we compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-type , RAG2(-/-) , and RAG2(-/-)x Î³c(-/-) mice . We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity . This activity required natural killer ( NK ) cells and interferon Î³ ( IFN-Î³ ) , which mediated the induction of M1 macrophages . M1 macrophages could be elicited by administration of CD40 agonists , thereby restoring editing activity in RAG2(-/-)x Î³c(-/-) mice . Our results suggest that in the absence of adaptive immunity , NK cell production of IFN-Î³ induces M1 macrophages , which act as important effectors during cancer immunoediting .
    OUTPUT:
