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: In spite of the fact that they occur at high rates , the clinical responses of BRAF(V600) mutant metastatic melanoma to BRAF inhibitors are usually short-lasting , with most cases progressing within less than 8 mo . Immunomodulatory strategies initiated after progression have recently been reported to be poorly efficient . By characterizing the immunological interactions between T cells and cancer cells in clinical material as well as the influence of the FDA-approved BRAF inhibitor vemurafenib on the immune system , we aimed at unraveling new strategies to expand the efficacy of adoptive T-cell transfer , which represents one of the most promising approaches currently in clinical development for the treatment of metastatic melanoma . Here we show that blocking the BRAF-MAPK pathway in BRAF signaling-addicted melanoma cells significantly increases the ability of T cells contained in clinical grade tumor-infiltrating lymphocytes to recognize autologous BRAF(V600) mutant melanoma cell lines in vitro . Antitumor reactivity was improved regardless of the class of antigen recognized by tumor-specific CD8(+) T cells . Microarray data suggests that improved tumor recognition is associated with modified expression of MHC Class I-associated proteins as well as of heat-shock proteins . In conclusion , our preclinical data suggest that an appropriately timed sequential treatment of BRAF(V600) mutant melanoma with vemurafenib and adoptive T-cell transfer might result in synergistic antineoplastic effects owing to an increased immunogenicity of cancer cells .
    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: In spite of the fact that they occur at high rates , the clinical responses of BRAF(V600) mutant metastatic melanoma to BRAF inhibitors are usually short-lasting , with most cases progressing within less than 8 mo . Immunomodulatory strategies initiated after progression have recently been reported to be poorly efficient . By characterizing the immunological interactions between T cells and cancer cells in clinical material as well as the influence of the FDA-approved BRAF inhibitor vemurafenib on the immune system , we aimed at unraveling new strategies to expand the efficacy of adoptive T-cell transfer , which represents one of the most promising approaches currently in clinical development for the treatment of metastatic melanoma . Here we show that blocking the BRAF-MAPK pathway in BRAF signaling-addicted melanoma cells significantly increases the ability of T cells contained in clinical grade tumor-infiltrating lymphocytes to recognize autologous BRAF(V600) mutant melanoma cell lines in vitro . Antitumor reactivity was improved regardless of the class of antigen recognized by tumor-specific CD8(+) T cells . Microarray data suggests that improved tumor recognition is associated with modified expression of MHC Class I-associated proteins as well as of heat-shock proteins . In conclusion , our preclinical data suggest that an appropriately timed sequential treatment of BRAF(V600) mutant melanoma with vemurafenib and adoptive T-cell transfer might result in synergistic antineoplastic effects owing to an increased immunogenicity of cancer cells .
    OUTPUT:
