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 mammalian cells more than 90% of double-strand breaks are repaired by NHEJ . Impairment of this pathway is associated with cell cycle arrest , cell death , genomic instability and cancer . Human diseases such as Nijmegen breakage syndrome , due to mutations in the NBS1 gene , produce defects in resection of double-strand breaks . NBS1 hypomorphic mutant mice are viable , and cells from these mice are defective in S phase and G2/M checkpoints . NBS1 polymorphisms have been associated with increased risk of breast cancer . We previously demonstrated that estradiol protected estrogen receptor ( ER)-positive ( + ) breast cancer cell lines against double-strand breaks and cell death . We now demonstrate that protection from double-strand break damage in ER+ cells is mediated via regulation by c-myc , p53 , CBP and SRC1 coactivators in intron 1 of the NBS1 gene . We concluded that NBS1 is responsible for estradiol-mediated protection from double-strand breaks in ER+ breast cancer cells .
    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: In mammalian cells more than 90% of double-strand breaks are repaired by NHEJ . Impairment of this pathway is associated with cell cycle arrest , cell death , genomic instability and cancer . Human diseases such as Nijmegen breakage syndrome , due to mutations in the NBS1 gene , produce defects in resection of double-strand breaks . NBS1 hypomorphic mutant mice are viable , and cells from these mice are defective in S phase and G2/M checkpoints . NBS1 polymorphisms have been associated with increased risk of breast cancer . We previously demonstrated that estradiol protected estrogen receptor ( ER)-positive ( + ) breast cancer cell lines against double-strand breaks and cell death . We now demonstrate that protection from double-strand break damage in ER+ cells is mediated via regulation by c-myc , p53 , CBP and SRC1 coactivators in intron 1 of the NBS1 gene . We concluded that NBS1 is responsible for estradiol-mediated protection from double-strand breaks in ER+ breast cancer cells .
    OUTPUT:
