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: The secretion of immunosuppressive factors like transforming growth factor-beta ( TGF-beta ) by tumor cells has been recognized as one of the mechanisms involved in tumor immunological escape . This study aimed to examine whether dendritic cell ( DC ) immunization could reverse TGF-beta-induced immunosuppression by simulating the in vivo interaction among infused DCs , host T cells , and tumor-secreted TGF-beta in an in vitro study . We found that both immature and mature DCs were relatively resistant to TGF-beta . The addition of TGF-beta to naive human CD4+ T cells , which are required by genetically modified DC to elicit antitumor immunity , resulted in their hyporesponsiveness to DC stimulation in a dose-dependent manner . When activated by allogeneic DCs in the presence of TGF-beta , CD4+ T cells displayed a reduced capacity to proliferate . More importantly , activated CD4+ T cells induced by DC stimulation were very sensitive to TGF-beta , and this susceptibility was enhanced by their previous exposure to TGF-beta . The underlying mechanism was linked to TGF-beta-induced apoptosis of activated T cells . However , the presence of stimulation from DC or antibodies to CD3 plus CD28 could partly reverse the immunosuppressive effect of TGF-beta on activated CD4+ T cells . Taken together , our results indicate that the efficacy of DC immunization may be impaired by tumor-derived TGF-beta .
    OUTPUT:

agent
sustaining proliferative signaling;avoiding immune destruction;resisting cell death
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: The secretion of immunosuppressive factors like transforming growth factor-beta ( TGF-beta ) by tumor cells has been recognized as one of the mechanisms involved in tumor immunological escape . This study aimed to examine whether dendritic cell ( DC ) immunization could reverse TGF-beta-induced immunosuppression by simulating the in vivo interaction among infused DCs , host T cells , and tumor-secreted TGF-beta in an in vitro study . We found that both immature and mature DCs were relatively resistant to TGF-beta . The addition of TGF-beta to naive human CD4+ T cells , which are required by genetically modified DC to elicit antitumor immunity , resulted in their hyporesponsiveness to DC stimulation in a dose-dependent manner . When activated by allogeneic DCs in the presence of TGF-beta , CD4+ T cells displayed a reduced capacity to proliferate . More importantly , activated CD4+ T cells induced by DC stimulation were very sensitive to TGF-beta , and this susceptibility was enhanced by their previous exposure to TGF-beta . The underlying mechanism was linked to TGF-beta-induced apoptosis of activated T cells . However , the presence of stimulation from DC or antibodies to CD3 plus CD28 could partly reverse the immunosuppressive effect of TGF-beta on activated CD4+ T cells . Taken together , our results indicate that the efficacy of DC immunization may be impaired by tumor-derived TGF-beta .
    OUTPUT:
