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: A better understanding of the underlying mechanisms of DNA repair after exposure to ionizing radiation represents a research priority aimed at improving the outcome of clinical radiotherapy . Because of the close association with DNA double strand break ( DSB ) repair , phosphorylation of the histone H2AX protein ( Î³H2AX ) , quantified by immunodetection , has recently been used as a method to study DSB induction and repair at low and clinically relevant radiation doses . However , the lack of consistency in literature points to the need to further validate the role of H2AX phosphorylation in DSB repair and the use of this technique to determine intrinsic radiosensitivity . In the present study we used human mammary epithelial MCF10A cells , characterized by a radiosensitive phenotype due to reduced levels of the Ku70 and Ku80 repair proteins , and investigated whether this repair-deficient cell line displays differences in the phosphorylation pattern of H2AX protein compared to repair-proficient MCF10A cells . This was established by measuring formation and disappearance of Î³H2AX foci after irradiating synchronized cell populations with ( 60)Co Î³-rays . Our results show statistically significant differences in the number of Î³H2AX foci between the repair-deficient and -proficient cell line , with a higher amount of Î³H2AX foci present at early times post-irradiation in the Ku-deficient cell line . However , the disappearance of those differences at later post-irradiation times questions the use of this assay to determine intrinsic radiosensitivity , especially in a clinical setting .
    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: A better understanding of the underlying mechanisms of DNA repair after exposure to ionizing radiation represents a research priority aimed at improving the outcome of clinical radiotherapy . Because of the close association with DNA double strand break ( DSB ) repair , phosphorylation of the histone H2AX protein ( Î³H2AX ) , quantified by immunodetection , has recently been used as a method to study DSB induction and repair at low and clinically relevant radiation doses . However , the lack of consistency in literature points to the need to further validate the role of H2AX phosphorylation in DSB repair and the use of this technique to determine intrinsic radiosensitivity . In the present study we used human mammary epithelial MCF10A cells , characterized by a radiosensitive phenotype due to reduced levels of the Ku70 and Ku80 repair proteins , and investigated whether this repair-deficient cell line displays differences in the phosphorylation pattern of H2AX protein compared to repair-proficient MCF10A cells . This was established by measuring formation and disappearance of Î³H2AX foci after irradiating synchronized cell populations with ( 60)Co Î³-rays . Our results show statistically significant differences in the number of Î³H2AX foci between the repair-deficient and -proficient cell line , with a higher amount of Î³H2AX foci present at early times post-irradiation in the Ku-deficient cell line . However , the disappearance of those differences at later post-irradiation times questions the use of this assay to determine intrinsic radiosensitivity , especially in a clinical setting .
    OUTPUT:
