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: ATM(Tel1) and ATR(Rad3) checkpoint kinases phosphorylate the C-terminus of histone H2AX ( H2A in yeasts ) in chromatin flanking DNA damage , establishing a recruitment platform for checkpoint and repair proteins . Phospho-H2A/X ( gammaH2A/X)-binding proteins at double-strand breaks ( DSBs ) have been characterized , but those required for replication stress responses are unknown . Here , we present genetic , biochemical , small angle X-ray scattering ( SAXS ) , and X-ray structural studies of the Schizosaccharomyces pombe Brc1 , a 6-BRCT-domain protein that is structurally related to Saccharomyces cerevisiae Rtt107 and mammalian PTIP . Brc1 binds gammaH2A to form spontaneous and DNA damage-induced nuclear foci . Spontaneous Brc1 foci colocalize with ribosomal DNA repeats , a region prone to fork pausing and genomic instability , whereas DNA damage-induced Brc1 foci colocalize with DSB response factors. gammaH2A binding is critical for Brc1 function . The 1.45 A resolution crystal structure of Brc1-gammaH2A complex shows how variable BRCT insertion loops sculpt tandem-BRCT phosphoprotein-binding pockets to facilitate unique phosphoprotein-interaction specificities , and unveils an acidic DNA-mimicking Brc1 surface . From these results , Brc1 docking to gammaH2A emerges as a critical chromatin-specific response to replication-associated DNA damage .
    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.
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    INPUT: ATM(Tel1) and ATR(Rad3) checkpoint kinases phosphorylate the C-terminus of histone H2AX ( H2A in yeasts ) in chromatin flanking DNA damage , establishing a recruitment platform for checkpoint and repair proteins . Phospho-H2A/X ( gammaH2A/X)-binding proteins at double-strand breaks ( DSBs ) have been characterized , but those required for replication stress responses are unknown . Here , we present genetic , biochemical , small angle X-ray scattering ( SAXS ) , and X-ray structural studies of the Schizosaccharomyces pombe Brc1 , a 6-BRCT-domain protein that is structurally related to Saccharomyces cerevisiae Rtt107 and mammalian PTIP . Brc1 binds gammaH2A to form spontaneous and DNA damage-induced nuclear foci . Spontaneous Brc1 foci colocalize with ribosomal DNA repeats , a region prone to fork pausing and genomic instability , whereas DNA damage-induced Brc1 foci colocalize with DSB response factors. gammaH2A binding is critical for Brc1 function . The 1.45 A resolution crystal structure of Brc1-gammaH2A complex shows how variable BRCT insertion loops sculpt tandem-BRCT phosphoprotein-binding pockets to facilitate unique phosphoprotein-interaction specificities , and unveils an acidic DNA-mimicking Brc1 surface . From these results , Brc1 docking to gammaH2A emerges as a critical chromatin-specific response to replication-associated DNA damage .
    OUTPUT:
