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.
    ###
    INPUT: The therapeutic principle of allogeneic haematopoietic cell transplantation ( allo-HCT ) is based on an active donor immune system that eliminates host-derived tumour cells . We hypothesized that in addition to the alloantigen-driven anti-tumour response , disruption of the immunological microenvironment within the tumour is responsible for its elimination after allo-HCT . We observed that induction of graft-versus-host disease ( GvHD ) significantly reduced the abundance of luc(+) FoxP3(+) regulatory T ( Treg ) cells in the tumour tissue , which is indicative of impaired or over-ridden tumour recruitment signals towards Treg cells . Analysis of the intestines and liver revealed chemokines and purine nucleotides as candidates for attracting Treg to these sites of inflammation . Despite its expression on tissue-residing Treg cells , the chemokine receptor CCR3 was not critical for Treg-cell function following allo-HCT . Extracellular ATP can attract immune cells via P2Y2 . P2Y2 was found to be expressed on Treg cells , and we found a partial reduction of GvHD prevention when P2Y2(-/-) rather than P2Y2(+/+) Treg cells were given . Exogenous local inflammation reduced Treg-cell accumulation in the tumour , suggesting a potential clinical approach to prevent Treg-cell-mediated tumour escape . In conclusion , we demonstrate that GvHD-related inflammation reduced Treg-cell numbers at the tumour sites , which may in turn help to explain the observation that patients with GvHD have a lower risk of tumour relapse .
    OUTPUT:

agent
tumor promoting inflammation
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 therapeutic principle of allogeneic haematopoietic cell transplantation ( allo-HCT ) is based on an active donor immune system that eliminates host-derived tumour cells . We hypothesized that in addition to the alloantigen-driven anti-tumour response , disruption of the immunological microenvironment within the tumour is responsible for its elimination after allo-HCT . We observed that induction of graft-versus-host disease ( GvHD ) significantly reduced the abundance of luc(+) FoxP3(+) regulatory T ( Treg ) cells in the tumour tissue , which is indicative of impaired or over-ridden tumour recruitment signals towards Treg cells . Analysis of the intestines and liver revealed chemokines and purine nucleotides as candidates for attracting Treg to these sites of inflammation . Despite its expression on tissue-residing Treg cells , the chemokine receptor CCR3 was not critical for Treg-cell function following allo-HCT . Extracellular ATP can attract immune cells via P2Y2 . P2Y2 was found to be expressed on Treg cells , and we found a partial reduction of GvHD prevention when P2Y2(-/-) rather than P2Y2(+/+) Treg cells were given . Exogenous local inflammation reduced Treg-cell accumulation in the tumour , suggesting a potential clinical approach to prevent Treg-cell-mediated tumour escape . In conclusion , we demonstrate that GvHD-related inflammation reduced Treg-cell numbers at the tumour sites , which may in turn help to explain the observation that patients with GvHD have a lower risk of tumour relapse .
    OUTPUT:
