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: Regulation of poly(ADP-ribose) ( PAR ) synthesis and turnover is critical to determining cell fate after genotoxic stress . Hyperactivation of PAR synthesis by poly(ADP-ribose) polymerase-1 ( PARP-1 ) occurs when cells deficient in DNA repair are exposed to genotoxic agents ; however , the function of this hyperactivation has not been adequately explained . Here , we examine PAR synthesis in mouse fibroblasts deficient in the base excision repair enzyme DNA polymerase β ( pol β ) . The extent and duration of PARP-1 activation was measured after exposure to either the DNA alkylating agent , methyl methanesulfonate ( MMS ) , or to low energy laser-induced DNA damage . There was strong DNA damage-induced hyperactivation of PARP-1 in pol β nullcells , but not in wild-type cells . In the case of MMS treatment , PAR synthesis did not lead to cell death in the pol β null cells , but instead resulted in increased PARylation of the nonhomologous end-joining ( NHEJ ) protein Ku70 and increased association of Ku70 with PARP-1 . Inhibition of the NHEJ factor DNA-PK , under conditions of MMS-induced PARP-1 hyperactivation , enhanced necrotic cell death . These data suggest that PARP-1 hyperactivation is a protective mechanism triggering the classical-NHEJ DNA repair pathway when the primary alkylated base damage repair pathway is compromised .
    OUTPUT:

agent
genomic instability and mutation;resisting cell death
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: Regulation of poly(ADP-ribose) ( PAR ) synthesis and turnover is critical to determining cell fate after genotoxic stress . Hyperactivation of PAR synthesis by poly(ADP-ribose) polymerase-1 ( PARP-1 ) occurs when cells deficient in DNA repair are exposed to genotoxic agents ; however , the function of this hyperactivation has not been adequately explained . Here , we examine PAR synthesis in mouse fibroblasts deficient in the base excision repair enzyme DNA polymerase β ( pol β ) . The extent and duration of PARP-1 activation was measured after exposure to either the DNA alkylating agent , methyl methanesulfonate ( MMS ) , or to low energy laser-induced DNA damage . There was strong DNA damage-induced hyperactivation of PARP-1 in pol β nullcells , but not in wild-type cells . In the case of MMS treatment , PAR synthesis did not lead to cell death in the pol β null cells , but instead resulted in increased PARylation of the nonhomologous end-joining ( NHEJ ) protein Ku70 and increased association of Ku70 with PARP-1 . Inhibition of the NHEJ factor DNA-PK , under conditions of MMS-induced PARP-1 hyperactivation , enhanced necrotic cell death . These data suggest that PARP-1 hyperactivation is a protective mechanism triggering the classical-NHEJ DNA repair pathway when the primary alkylated base damage repair pathway is compromised .
    OUTPUT:
