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: Group VIB Phospholipase A(2) ( iPLA(2)Î³ ) is distributed in membranous organelles in which Î²-oxidation occurs , that is , mitochondria and peroxisomes , and is expressed by insulin-secreting pancreatic islet Î²-cells and INS-1 insulinoma cells , which can be injured by inflammatory cytokines , for example , IL-1Î² and IFN-Î³ , and by oxidants , for example , streptozotocin ( STZ ) or t-butyl-hydroperoxide ( TBHP ) , via processes pertinent to mechanisms of Î²-cell loss in types 1 and 2 diabetes mellitus . We find that incubating INS-1 cells with IL-1Î² and IFN-Î³ , with STZ , or with TBHP causes increased expression of iPLA(2)Î³ mRNA and protein . We prepared INS-1 knockdown ( KD ) cell lines with reduced iPLA(2)Î³ expression , and they proliferate more slowly than control INS-1 cells and undergo increased membrane peroxidation in response to cytokines or oxidants . Accumulation of oxidized phospholipid molecular species in STZ-treated INS-1 cells was demonstrated by LC/MS/MS scanning , and the levels in iPLA(2)Î³-KD cells exceeded those in control cells. iPLA(2)Î³-KD INS-1 cells also exhibited higher levels of apoptosis than control cells when incubated with STZ or with IL-1Î² and IFN-Î³ . These findings suggest that iPLA(2)Î³ promotes Î²-cell proliferation and that its expression is increased during inflammation or oxidative stress as a mechanism to mitigate membrane injury that may enhance Î²-cell survival .
    OUTPUT:

agent
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: Group VIB Phospholipase A(2) ( iPLA(2)Î³ ) is distributed in membranous organelles in which Î²-oxidation occurs , that is , mitochondria and peroxisomes , and is expressed by insulin-secreting pancreatic islet Î²-cells and INS-1 insulinoma cells , which can be injured by inflammatory cytokines , for example , IL-1Î² and IFN-Î³ , and by oxidants , for example , streptozotocin ( STZ ) or t-butyl-hydroperoxide ( TBHP ) , via processes pertinent to mechanisms of Î²-cell loss in types 1 and 2 diabetes mellitus . We find that incubating INS-1 cells with IL-1Î² and IFN-Î³ , with STZ , or with TBHP causes increased expression of iPLA(2)Î³ mRNA and protein . We prepared INS-1 knockdown ( KD ) cell lines with reduced iPLA(2)Î³ expression , and they proliferate more slowly than control INS-1 cells and undergo increased membrane peroxidation in response to cytokines or oxidants . Accumulation of oxidized phospholipid molecular species in STZ-treated INS-1 cells was demonstrated by LC/MS/MS scanning , and the levels in iPLA(2)Î³-KD cells exceeded those in control cells. iPLA(2)Î³-KD INS-1 cells also exhibited higher levels of apoptosis than control cells when incubated with STZ or with IL-1Î² and IFN-Î³ . These findings suggest that iPLA(2)Î³ promotes Î²-cell proliferation and that its expression is increased during inflammation or oxidative stress as a mechanism to mitigate membrane injury that may enhance Î²-cell survival .
    OUTPUT:
