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: IFN-Î³ is a master regulator of the immune responses that occur in the transplanted kidney , acting both on the immune system and on the graft itself . The cellular responses to IFN-Î³ are complex , and emerging evidence suggests that IFN-Î³ may regulate autophagic functions . Conversely , autophagy modulates innate and adaptive immune functions in various contexts . In this study , we identify a novel mechanism by which IFN-Î³ activates autophagy in human kidney epithelial cells and provide new insights into how autophagy regulates immune functions in response to IFN-Î³ . Our results indicate that IFN-Î³ promotes tryptophan depletion , activates the eIF2Î± kinase general control nonderepressible-2 ( GCN2 ) , and leads to an increase in the autophagic flux . Further , tryptophan supplementation and RNA interference directed against GCN2 inhibited IFN-Î³-induced autophagy . This process is of functional relevance because autophagy regulates the secretion of inflammatory cytokines and growth factors by human kidney epithelial cells in response to IFN-Î³ . These findings assign to IFN-Î³ a novel function in the regulation of autophagy , which , in turn , modulates IFN-Î³-induced secretion of inflammatory cytokines .
    OUTPUT:

agent
resisting cell death;tumor promoting inflammation
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: IFN-Î³ is a master regulator of the immune responses that occur in the transplanted kidney , acting both on the immune system and on the graft itself . The cellular responses to IFN-Î³ are complex , and emerging evidence suggests that IFN-Î³ may regulate autophagic functions . Conversely , autophagy modulates innate and adaptive immune functions in various contexts . In this study , we identify a novel mechanism by which IFN-Î³ activates autophagy in human kidney epithelial cells and provide new insights into how autophagy regulates immune functions in response to IFN-Î³ . Our results indicate that IFN-Î³ promotes tryptophan depletion , activates the eIF2Î± kinase general control nonderepressible-2 ( GCN2 ) , and leads to an increase in the autophagic flux . Further , tryptophan supplementation and RNA interference directed against GCN2 inhibited IFN-Î³-induced autophagy . This process is of functional relevance because autophagy regulates the secretion of inflammatory cytokines and growth factors by human kidney epithelial cells in response to IFN-Î³ . These findings assign to IFN-Î³ a novel function in the regulation of autophagy , which , in turn , modulates IFN-Î³-induced secretion of inflammatory cytokines .
    OUTPUT:
