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: The DNA damage response ( DDR ) cascade and ROS ( reactive oxygen species ) signaling are both involved in the induction of cell death after DNA damage , but a mechanistic link between these two pathways has not been clearly elucidated . This study demonstrates that ROS induction after treatment of cells with neocarzinostatin ( NCS ) , an ionizing radiation mimetic , is at least partly mediated by increasing histone H2AX . Increased levels of ROS and cell death induced by H2AX overexpression alone or DNA damage leading to H2AX accumulation are reduced by treating cells with the antioxidant N-Acetyl-L-Cysteine ( NAC ) , the NADP(H) oxidase ( Nox ) inhibitor DPI , expression of Rac1N17 , and knockdown of Nox1 , but not Nox4 , indicating that induction of ROS by H2AX is mediated through Nox1 and Rac1 GTPase . H2AX increases Nox1 activity partly by reducing the interaction between a Nox1 activator NOXA1 and its inhibitor 14-3-3zeta . These results point to a novel role of histone H2AX that regulates Nox1-mediated ROS generation after DNA damage .
    OUTPUT:

agent
genomic instability and mutation;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.
    ###
    INPUT: The DNA damage response ( DDR ) cascade and ROS ( reactive oxygen species ) signaling are both involved in the induction of cell death after DNA damage , but a mechanistic link between these two pathways has not been clearly elucidated . This study demonstrates that ROS induction after treatment of cells with neocarzinostatin ( NCS ) , an ionizing radiation mimetic , is at least partly mediated by increasing histone H2AX . Increased levels of ROS and cell death induced by H2AX overexpression alone or DNA damage leading to H2AX accumulation are reduced by treating cells with the antioxidant N-Acetyl-L-Cysteine ( NAC ) , the NADP(H) oxidase ( Nox ) inhibitor DPI , expression of Rac1N17 , and knockdown of Nox1 , but not Nox4 , indicating that induction of ROS by H2AX is mediated through Nox1 and Rac1 GTPase . H2AX increases Nox1 activity partly by reducing the interaction between a Nox1 activator NOXA1 and its inhibitor 14-3-3zeta . These results point to a novel role of histone H2AX that regulates Nox1-mediated ROS generation after DNA damage .
    OUTPUT:
