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: In normal human cells , oncogene-induced senescence ( OIS ) depends on induction of DNA damage response . Oxidative stress and hyperreplication of genomic DNA have been proposed as major causes of DNA damage in OIS cells . Here , we report that down-regulation of deoxyribonucleoside pools is another endogenous source of DNA damage in normal human fibroblasts ( NHFs ) undergoing HRAS(G12V)-induced senescence . NHF-HRAS(G12V) cells underexpressed thymidylate synthase ( TS ) and ribonucleotide reductase ( RR ) , two enzymes required for the entire de novo deoxyribonucleotide biosynthesis , and possessed low dNTP levels . Chromatin at the promoters of the genes encoding TS and RR was enriched with retinoblastoma tumor suppressor protein and histone H3 tri-methylated at lysine 9 . Importantly , ectopic coexpression of TS and RR or addition of deoxyribonucleosides substantially suppressed DNA damage , senescence-associated phenotypes , and proliferation arrest in two types of NHF-expressing HRAS(G12V) . Reciprocally , short hairpin RNA-mediated suppression of TS and RR caused DNA damage and senescence in NHFs , although less efficiently than HRAS(G12V) . However , overexpression of TS and RR in quiescent NHFs did not overcome proliferation arrest , suggesting that unlike quiescence , OIS requires depletion of dNTP pools and activated DNA replication . Our data identify a previously unknown role of deoxyribonucleotides in regulation of OIS .
    OUTPUT:

agent
enabling replicative immortality;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: In normal human cells , oncogene-induced senescence ( OIS ) depends on induction of DNA damage response . Oxidative stress and hyperreplication of genomic DNA have been proposed as major causes of DNA damage in OIS cells . Here , we report that down-regulation of deoxyribonucleoside pools is another endogenous source of DNA damage in normal human fibroblasts ( NHFs ) undergoing HRAS(G12V)-induced senescence . NHF-HRAS(G12V) cells underexpressed thymidylate synthase ( TS ) and ribonucleotide reductase ( RR ) , two enzymes required for the entire de novo deoxyribonucleotide biosynthesis , and possessed low dNTP levels . Chromatin at the promoters of the genes encoding TS and RR was enriched with retinoblastoma tumor suppressor protein and histone H3 tri-methylated at lysine 9 . Importantly , ectopic coexpression of TS and RR or addition of deoxyribonucleosides substantially suppressed DNA damage , senescence-associated phenotypes , and proliferation arrest in two types of NHF-expressing HRAS(G12V) . Reciprocally , short hairpin RNA-mediated suppression of TS and RR caused DNA damage and senescence in NHFs , although less efficiently than HRAS(G12V) . However , overexpression of TS and RR in quiescent NHFs did not overcome proliferation arrest , suggesting that unlike quiescence , OIS requires depletion of dNTP pools and activated DNA replication . Our data identify a previously unknown role of deoxyribonucleotides in regulation of OIS .
    OUTPUT:
