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: Androgen deprivation is currently a standard-of-care , first-line therapy for prostate cancer in the United States . Although this regimen effectively regresses androgen-dependent disease , relapse often occurs in an androgen-independent manner and is associated with poor prognosis . Such castration-resistant prostate cancer represents a major clinical challenge , and the mechanisms underlying castration resistance are not fully understood . Epithelial-mesenchymal transition ( EMT ) is a key developmental process and has also been implicated in cancer metastasis and therapeutic resistance in recent years . However , the factors contributing to EMT in human cancers remain unclear . Here , we show that both normal mouse prostate tissue and human LuCaP35 prostate tumor explants display an EMT as well as increased stem cell-like features following androgen deprivation . Importantly , we observed similar changes in mesenchymal features in prostate tumors from patients treated with androgen-deprivation therapy . In addition , we have delineated a feedback loop involving the androgen receptor and the Zeb1 transcription factor that seems to mediate this transition . In summary , we show for the first time that androgen deprivation induces EMT in both normal prostate and prostate cancer , revealing a potentially important consequence of a standard-of-care treatment for prostate cancer . This finding could have significant implications for second-line treatment strategies in this clinical setting .
    OUTPUT:

agent
activating invasion and metastasis;sustaining proliferative signaling
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: Androgen deprivation is currently a standard-of-care , first-line therapy for prostate cancer in the United States . Although this regimen effectively regresses androgen-dependent disease , relapse often occurs in an androgen-independent manner and is associated with poor prognosis . Such castration-resistant prostate cancer represents a major clinical challenge , and the mechanisms underlying castration resistance are not fully understood . Epithelial-mesenchymal transition ( EMT ) is a key developmental process and has also been implicated in cancer metastasis and therapeutic resistance in recent years . However , the factors contributing to EMT in human cancers remain unclear . Here , we show that both normal mouse prostate tissue and human LuCaP35 prostate tumor explants display an EMT as well as increased stem cell-like features following androgen deprivation . Importantly , we observed similar changes in mesenchymal features in prostate tumors from patients treated with androgen-deprivation therapy . In addition , we have delineated a feedback loop involving the androgen receptor and the Zeb1 transcription factor that seems to mediate this transition . In summary , we show for the first time that androgen deprivation induces EMT in both normal prostate and prostate cancer , revealing a potentially important consequence of a standard-of-care treatment for prostate cancer . This finding could have significant implications for second-line treatment strategies in this clinical setting .
    OUTPUT:
