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: XRCC4 , in association with DNA ligase IV , is thought to play a critical role in the ligation of two DNA ends in DNA double-strand break ( DSB ) repair through non-homologous end-joining ( NHEJ ) pathway . In the present study , we captured radiation-induced chromatin-recruitment of XRCC4 by biochemical fractionation using detergent Nonidet P-40 . A subpopulation of XRCC4 changed into a form that is resistant to the extraction with 0.5% Nonidet P-40-containing buffer after irradiation . This form of XRCC4 was liberated by micrococcal nuclease treatment , indicating that it had been tethered to chromatin DNA . This chromatin-recruitment of XRCC4 could be seen immediately ( &lt ; 0.1 hr ) after irradiation and remained up to 4 hr after 20 Gy irradiation . It was seen even after irradiation of small doses , i.e. , 2 Gy , but the residence of XRCC4 on chromatin was very transient after 2 Gy irradiation , returning to near normal level in 0.2-0.5 hr after irradiation . The chromatin-bound XRCC4 represented only approximately 1% of total XRCC4 molecules even after 20 Gy irradiation and the quantitative analysis using purified protein as the reference suggested that only a few XRCC4-DNA ligase IV complexes were recruited to each DNA end . We further show that the chromatin-recruitment of XRCC4 was not attenuated by wortmannin , an inhibitor of DNA-PK , or siRNA-mediated knockdown of the DNA-PK catalytic subunit ( DNA-PKcs ) , indicating that this process does not require DNA-PKcs . These results would provide us with useful experimental tools and important insights to understand the DNA repair process through NHEJ pathway .
    OUTPUT:

agent
genomic instability and mutation
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: XRCC4 , in association with DNA ligase IV , is thought to play a critical role in the ligation of two DNA ends in DNA double-strand break ( DSB ) repair through non-homologous end-joining ( NHEJ ) pathway . In the present study , we captured radiation-induced chromatin-recruitment of XRCC4 by biochemical fractionation using detergent Nonidet P-40 . A subpopulation of XRCC4 changed into a form that is resistant to the extraction with 0.5% Nonidet P-40-containing buffer after irradiation . This form of XRCC4 was liberated by micrococcal nuclease treatment , indicating that it had been tethered to chromatin DNA . This chromatin-recruitment of XRCC4 could be seen immediately ( &lt ; 0.1 hr ) after irradiation and remained up to 4 hr after 20 Gy irradiation . It was seen even after irradiation of small doses , i.e. , 2 Gy , but the residence of XRCC4 on chromatin was very transient after 2 Gy irradiation , returning to near normal level in 0.2-0.5 hr after irradiation . The chromatin-bound XRCC4 represented only approximately 1% of total XRCC4 molecules even after 20 Gy irradiation and the quantitative analysis using purified protein as the reference suggested that only a few XRCC4-DNA ligase IV complexes were recruited to each DNA end . We further show that the chromatin-recruitment of XRCC4 was not attenuated by wortmannin , an inhibitor of DNA-PK , or siRNA-mediated knockdown of the DNA-PK catalytic subunit ( DNA-PKcs ) , indicating that this process does not require DNA-PKcs . These results would provide us with useful experimental tools and important insights to understand the DNA repair process through NHEJ pathway .
    OUTPUT:
