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: Peptide growth factors have been implicated in progression of prostate cancer ( PCa ) to the androgen-independent state ; however , much of the evidence linking diffusible mitogens and survival factors to this process remains circumstantial . Heparin-binding epidermal growth factor-like growth factor ( HB-EGF ) , a prostate stroma-derived factor , promotes survival , proliferation , and neuroendocrine differentiation of androgen-dependent LNCaP PCa cells in vitro . To test whether sustained exposure to HB-EGF can confer an androgen-independent phenotype , we generated stable populations of LNCaP cells that express constitutively a secreted form of HB-EGF ( LNCaP/sHB ) . LNCaP/sHB cells proliferated more rapidly under androgen-depleted conditions in vitro and formed larger tumors with higher frequency in intact and castrated severe combined immunodeficient mice , in comparison to control cells . LNCaP/sHB tumors also expressed higher levels of the neuroendocrine marker , neuron-specific enolase , compared with control tumors . In castrates , increased neuron-specific enolase expression in LNCaP/sHB tumors was associated with reduced androgen receptor ( AR ) levels . In vitro , AR protein levels were reduced in LNCaP/sHB cells , and in transient transfection assays using an androgen-responsive promoter ( mouse mammary tumor virus-long terminal repeat ) , LNCaP/sHB cells showed reduced sensitivity to dihydrotestosterone compared with controls . This is the first demonstration that continuous exposure of AR-positive PCa cells to a single growth factor can promote an androgen-independent phenotype in vivo . These findings also emphasize the potential role of pathways other than the AR axis in acquisition of androgen independence .
    OUTPUT:

agent
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: Peptide growth factors have been implicated in progression of prostate cancer ( PCa ) to the androgen-independent state ; however , much of the evidence linking diffusible mitogens and survival factors to this process remains circumstantial . Heparin-binding epidermal growth factor-like growth factor ( HB-EGF ) , a prostate stroma-derived factor , promotes survival , proliferation , and neuroendocrine differentiation of androgen-dependent LNCaP PCa cells in vitro . To test whether sustained exposure to HB-EGF can confer an androgen-independent phenotype , we generated stable populations of LNCaP cells that express constitutively a secreted form of HB-EGF ( LNCaP/sHB ) . LNCaP/sHB cells proliferated more rapidly under androgen-depleted conditions in vitro and formed larger tumors with higher frequency in intact and castrated severe combined immunodeficient mice , in comparison to control cells . LNCaP/sHB tumors also expressed higher levels of the neuroendocrine marker , neuron-specific enolase , compared with control tumors . In castrates , increased neuron-specific enolase expression in LNCaP/sHB tumors was associated with reduced androgen receptor ( AR ) levels . In vitro , AR protein levels were reduced in LNCaP/sHB cells , and in transient transfection assays using an androgen-responsive promoter ( mouse mammary tumor virus-long terminal repeat ) , LNCaP/sHB cells showed reduced sensitivity to dihydrotestosterone compared with controls . This is the first demonstration that continuous exposure of AR-positive PCa cells to a single growth factor can promote an androgen-independent phenotype in vivo . These findings also emphasize the potential role of pathways other than the AR axis in acquisition of androgen independence .
    OUTPUT:
