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: Binding of erythropoietin ( EPO ) to its receptor ( EPOR ) on erythroid cells induces the activation of numerous signal transduction pathways , including the mitogen-activated protein kinase Jun-N-terminal kinase ( JNK ) . In an effort to understand the regulation of EPO-induced proliferation and JNK activation , we have examined the role of potential autocrine factors in the proliferation of the murine erythroleukemia cell line HCD57 . We report here that treatment of these cells with EPO induced the expression and secretion of tumor necrosis factor alpha ( TNF-alpha ) . EPO-dependent proliferation was reduced by the addition of neutralizing antibodies to TNF-alpha , and exogenously added TNF-alpha induced proliferation of HCD57 cells . EPO also could induce TNF-alpha expression in BAF3 and DA3 myeloid cells ectopically expressing EPOR . Addition of TNF-alpha activated JNK in HCD57 cells , and the activity of JNK was partially inhibited by addition of a TNF-alpha neutralizing antibody . Primary human and murine erythroid progenitors expressed TNF-alpha in either an EPO-dependent or constitutive manner . However , TNF-alpha had an inhibitory effect on both immature primary human and murine cells , suggestive that the proliferative effects of TNF-alpha may be limited to erythroleukemic cells . This study suggests a novel role for autocrine TNF-alpha expression in the proliferation of erythroleukemia cells that is distinct from the effect of TNF-alpha in normal erythropoiesis .
    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.
    ###
    INPUT: Binding of erythropoietin ( EPO ) to its receptor ( EPOR ) on erythroid cells induces the activation of numerous signal transduction pathways , including the mitogen-activated protein kinase Jun-N-terminal kinase ( JNK ) . In an effort to understand the regulation of EPO-induced proliferation and JNK activation , we have examined the role of potential autocrine factors in the proliferation of the murine erythroleukemia cell line HCD57 . We report here that treatment of these cells with EPO induced the expression and secretion of tumor necrosis factor alpha ( TNF-alpha ) . EPO-dependent proliferation was reduced by the addition of neutralizing antibodies to TNF-alpha , and exogenously added TNF-alpha induced proliferation of HCD57 cells . EPO also could induce TNF-alpha expression in BAF3 and DA3 myeloid cells ectopically expressing EPOR . Addition of TNF-alpha activated JNK in HCD57 cells , and the activity of JNK was partially inhibited by addition of a TNF-alpha neutralizing antibody . Primary human and murine erythroid progenitors expressed TNF-alpha in either an EPO-dependent or constitutive manner . However , TNF-alpha had an inhibitory effect on both immature primary human and murine cells , suggestive that the proliferative effects of TNF-alpha may be limited to erythroleukemic cells . This study suggests a novel role for autocrine TNF-alpha expression in the proliferation of erythroleukemia cells that is distinct from the effect of TNF-alpha in normal erythropoiesis .
    OUTPUT:
