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: BACKGROUND Prostate cancer is the second leading cause of cancer mortality among US men . Epidemiological evidence suggests that high vitamin D status protects men from prostate cancer and the active form of vitamin D , 1alpha,25 dihydroxyvitamin D3 ( 1,25(OH)2D ) has anti-cancer effects in cultured prostate cells . Still , the molecular mechanisms and the gene targets for vitamin D-mediated prostate cancer prevention are unknown . RESULTS We examined the effect of 1,25(OH)2D ( +/- 100 nM , 6 , 24 , 48 h ) on the transcript profile of proliferating RWPE1 cells , an immortalized , non-tumorigenic prostate epithelial cell line that is growth arrested by 1,25(OH)2D ( Affymetrix U133 Plus 2.0 , n = 4/treatment per time and dose ) . Our analysis revealed many transcript level changes at a 5% false detection rate : 6 h , 1571 ( 61% up ) , 24 h , 1816 ( 60% up ) , 48 h , 3566 ( 38% up). 288 transcripts were regulated similarly at all time points ( 182 up , 80 down ) and many of the promoters for these transcripts contained putative vitamin D response elements . Functional analysis by pathway or Gene Set Analysis revealed early suppression of WNT , Notch , NF-kB , and IGF1 signaling . Transcripts related to inflammation were suppressed at 6 h ( e.g . IL-1 pathway ) and suppression of proinflammatory pathways continued at later time points ( e.g . IL-17 and IL-6 pathways ) . There was also evidence for induction of anti-angiogenic pathways and induction of transcripts for protection from oxidative stress or maintenance of cell redox homeostasis at 6 h . CONCLUSIONS Our data reveal of large number of potential new , direct vitamin D target genes relevant to prostate cancer prevention . In addition , our data suggests that rather than having a single strong regulatory effect , vitamin D orchestrates a pattern of changes within prostate epithelial cells that limit or slow carcinogenesis .
    OUTPUT:

agent
tumor promoting inflammation;inducing angiogenesis
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: BACKGROUND Prostate cancer is the second leading cause of cancer mortality among US men . Epidemiological evidence suggests that high vitamin D status protects men from prostate cancer and the active form of vitamin D , 1alpha,25 dihydroxyvitamin D3 ( 1,25(OH)2D ) has anti-cancer effects in cultured prostate cells . Still , the molecular mechanisms and the gene targets for vitamin D-mediated prostate cancer prevention are unknown . RESULTS We examined the effect of 1,25(OH)2D ( +/- 100 nM , 6 , 24 , 48 h ) on the transcript profile of proliferating RWPE1 cells , an immortalized , non-tumorigenic prostate epithelial cell line that is growth arrested by 1,25(OH)2D ( Affymetrix U133 Plus 2.0 , n = 4/treatment per time and dose ) . Our analysis revealed many transcript level changes at a 5% false detection rate : 6 h , 1571 ( 61% up ) , 24 h , 1816 ( 60% up ) , 48 h , 3566 ( 38% up). 288 transcripts were regulated similarly at all time points ( 182 up , 80 down ) and many of the promoters for these transcripts contained putative vitamin D response elements . Functional analysis by pathway or Gene Set Analysis revealed early suppression of WNT , Notch , NF-kB , and IGF1 signaling . Transcripts related to inflammation were suppressed at 6 h ( e.g . IL-1 pathway ) and suppression of proinflammatory pathways continued at later time points ( e.g . IL-17 and IL-6 pathways ) . There was also evidence for induction of anti-angiogenic pathways and induction of transcripts for protection from oxidative stress or maintenance of cell redox homeostasis at 6 h . CONCLUSIONS Our data reveal of large number of potential new , direct vitamin D target genes relevant to prostate cancer prevention . In addition , our data suggests that rather than having a single strong regulatory effect , vitamin D orchestrates a pattern of changes within prostate epithelial cells that limit or slow carcinogenesis .
    OUTPUT:
