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: We investigated the effects of valproic acid ( VPA ) , a histone deacetylase inhibitor , in combination with hydralazine , a DNA methylation inhibitor , on the expression of cell-surface Fas and MHC-class I-related chain molecules A and B ( MICA and B ) , the ligands of NKG2D which is an activating receptor of NK cells , and on production of their soluble forms in HOS , U-2 OS and SaOS-2 human osteosarcoma cell lines . We also examined the susceptibility of these cells to Fas- and NK cell-mediated cell death . VPA did not increase the expression of Fas on the surface of osteosarcoma cells , while hydralazine did , and the combination of VPA with hydralazine increased the expression of cell-surface Fas . In contrast , the combination of VPA with hydralazine did not increase the production of soluble Fas by osteosarcoma cells . Both VPA and hydralazine increased the expression of cell-surface MICA and B in osteosarcoma cells , and their combination induced a greater increase in their expression . VPA inhibited the production of both soluble MICA and MICB by osteosarcoma cells while hydralazine produced no effect . Both VPA and hydralazine enhanced the susceptibility of osteosarcoma cells to Fas- and NK cell-mediated cell death and the combination of VPA with hydralazine further enhanced the effects . The present results suggest that combined administration of VPA and hydrazine is valuable for enhancing the therapeutic effects of immunotherapy for osteosarcomas .
    OUTPUT:

agent
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.
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    INPUT: We investigated the effects of valproic acid ( VPA ) , a histone deacetylase inhibitor , in combination with hydralazine , a DNA methylation inhibitor , on the expression of cell-surface Fas and MHC-class I-related chain molecules A and B ( MICA and B ) , the ligands of NKG2D which is an activating receptor of NK cells , and on production of their soluble forms in HOS , U-2 OS and SaOS-2 human osteosarcoma cell lines . We also examined the susceptibility of these cells to Fas- and NK cell-mediated cell death . VPA did not increase the expression of Fas on the surface of osteosarcoma cells , while hydralazine did , and the combination of VPA with hydralazine increased the expression of cell-surface Fas . In contrast , the combination of VPA with hydralazine did not increase the production of soluble Fas by osteosarcoma cells . Both VPA and hydralazine increased the expression of cell-surface MICA and B in osteosarcoma cells , and their combination induced a greater increase in their expression . VPA inhibited the production of both soluble MICA and MICB by osteosarcoma cells while hydralazine produced no effect . Both VPA and hydralazine enhanced the susceptibility of osteosarcoma cells to Fas- and NK cell-mediated cell death and the combination of VPA with hydralazine further enhanced the effects . The present results suggest that combined administration of VPA and hydrazine is valuable for enhancing the therapeutic effects of immunotherapy for osteosarcomas .
    OUTPUT:
