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 xeroderma pigmentosum group C ( XPC ) protein specifically involved in genome-wide damage recognition for nucleotide excision repair ( NER ) was purified as a tight complex with HR23B , one of the two mammalian homologs of RAD23 in budding yeast . This XPC-HR23B complex exhibits strong binding affinity for single-stranded DNA , as well as preferential binding to various types of damaged DNA . To examine the structure-function relationship of XPC , a series of truncated mutant proteins were generated and assayed for various binding activities . The two domains participating in binding to HR23B and damaged DNA , respectively , were mapped within the carboxy-terminal half of XPC , which also contains an evolutionary conserved amino acid sequence homologous to the yeast RAD4 protein . We established that the carboxy-terminal 125 amino acids are dispensable for both HR23B and damaged DNA binding , while interactions with transcription factor IIH ( TFIIH ) are significantly impaired by truncation of this domain . Furthermore , deletion of the extreme carboxy-terminal domain totally abolished XPC activity in the cell-free NER reaction . These results suggest that following initial damage recognition , the carboxy terminus of XPC may be essential for the recruitment of TFIIH , and that most truncation mutations identified in XP-C patients result in non-functional proteins .
    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: The xeroderma pigmentosum group C ( XPC ) protein specifically involved in genome-wide damage recognition for nucleotide excision repair ( NER ) was purified as a tight complex with HR23B , one of the two mammalian homologs of RAD23 in budding yeast . This XPC-HR23B complex exhibits strong binding affinity for single-stranded DNA , as well as preferential binding to various types of damaged DNA . To examine the structure-function relationship of XPC , a series of truncated mutant proteins were generated and assayed for various binding activities . The two domains participating in binding to HR23B and damaged DNA , respectively , were mapped within the carboxy-terminal half of XPC , which also contains an evolutionary conserved amino acid sequence homologous to the yeast RAD4 protein . We established that the carboxy-terminal 125 amino acids are dispensable for both HR23B and damaged DNA binding , while interactions with transcription factor IIH ( TFIIH ) are significantly impaired by truncation of this domain . Furthermore , deletion of the extreme carboxy-terminal domain totally abolished XPC activity in the cell-free NER reaction . These results suggest that following initial damage recognition , the carboxy terminus of XPC may be essential for the recruitment of TFIIH , and that most truncation mutations identified in XP-C patients result in non-functional proteins .
    OUTPUT:
