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: Ataxia telangiectasia ( AT ) cells , with their defective double-strand break ( DSB ) repair processes , exhibit high sensitivity to low-LET radiation such as X-rays irradiation and gamma beams . Since heavy ion beam treatment for cancer is becoming increasingly common in Japan and elsewhere , it is important to also determine their sensitivity to high-LET radiation . For this purpose we irradiated AT and normal human cells immortalized with the human telomerase gene using high- ( 24-60 keV/microm carbon and 200 keV/microm iron ions ) or low-LET ( X-rays ) radiation in non-proliferative conditions . In normal cells the RBE ( relative biological effectiveness ) of carbon and iron ions increased from 1.19 to 1.81 in proportion to LET . In contrast , their RBE in AT cells increased from 1.32 at 24 keV/microm to 1.59 at 40 keV/microm , and exhibited a plateau at over 40 keV/microm . In normal cells most gamma-H2AX foci induced by both carbon- and iron-ion beams had disappeared at 40 h . In AT cells , however , a significant number of gamma-H2AX foci were still observed at 40 h . The RBEs found in the AT cells after heavy-ion irradiation were consistent with the effects predicted from the presence of non-homologous end joining defects . The DSBs remaining after heavy-ion irradiation suggested defects in the AT cells ' DSB repair ability .
    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: Ataxia telangiectasia ( AT ) cells , with their defective double-strand break ( DSB ) repair processes , exhibit high sensitivity to low-LET radiation such as X-rays irradiation and gamma beams . Since heavy ion beam treatment for cancer is becoming increasingly common in Japan and elsewhere , it is important to also determine their sensitivity to high-LET radiation . For this purpose we irradiated AT and normal human cells immortalized with the human telomerase gene using high- ( 24-60 keV/microm carbon and 200 keV/microm iron ions ) or low-LET ( X-rays ) radiation in non-proliferative conditions . In normal cells the RBE ( relative biological effectiveness ) of carbon and iron ions increased from 1.19 to 1.81 in proportion to LET . In contrast , their RBE in AT cells increased from 1.32 at 24 keV/microm to 1.59 at 40 keV/microm , and exhibited a plateau at over 40 keV/microm . In normal cells most gamma-H2AX foci induced by both carbon- and iron-ion beams had disappeared at 40 h . In AT cells , however , a significant number of gamma-H2AX foci were still observed at 40 h . The RBEs found in the AT cells after heavy-ion irradiation were consistent with the effects predicted from the presence of non-homologous end joining defects . The DSBs remaining after heavy-ion irradiation suggested defects in the AT cells ' DSB repair ability .
    OUTPUT:
