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: It is thought that high linear energy transfer ( LET ) radiation induces more complex DNA damage than low-LET particles , specifically clustered DNA damage that causes cells to repair DNA double strand breaks ( DSB ) more slowly and leads to severe biological consequences . The present study aimed to investigate the role of exogenously added glutathione ( GSH ) on ( 12)C-beam ( 287keV/mum ) and ( 7)Li-beam ( 60keV/mum ) induced chromosome aberration ( CA ) formation , particularly on exchange aberration formation . In order to characterize the role of GSH in the joining of DNA DSBs , we induced DNA lesions with bleomycin ( Blem ) in conjunction with either high- or low-LET radiation ( X-rays ) since the chemistry of the free DNA ends created by Blem and X-rays is similar . CHO cells were exposed to reduced GSH at a concentration of 2mM for 3h before radiation . Treatment with Blem ( 20mug/ml ) was carried out for 2h before the cells were exposed to radiation . Our results show that the frequency of chromosomal aberration increases with increased LET . Heavy ion exposed cells show a higher frequency of CA over time than do X-irradiated cells . An analysis of the first post-irradiation mitosis of exposed CHO cells shows that high-LET radiation induces more breaks than exchange-type aberrations and exogenous GSH has no influence on high-LET radiation-induced DNA damage . The DNA lesions induced by low-LET radiation interact relatively strongly with Blem-induced lesions whereas interaction between Blem and high-LET radiations was poor . This could be attributed to differences in repair kinetics and qualitative differences in the DNA lesions induced by Blem and high-LET radiation .
    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: It is thought that high linear energy transfer ( LET ) radiation induces more complex DNA damage than low-LET particles , specifically clustered DNA damage that causes cells to repair DNA double strand breaks ( DSB ) more slowly and leads to severe biological consequences . The present study aimed to investigate the role of exogenously added glutathione ( GSH ) on ( 12)C-beam ( 287keV/mum ) and ( 7)Li-beam ( 60keV/mum ) induced chromosome aberration ( CA ) formation , particularly on exchange aberration formation . In order to characterize the role of GSH in the joining of DNA DSBs , we induced DNA lesions with bleomycin ( Blem ) in conjunction with either high- or low-LET radiation ( X-rays ) since the chemistry of the free DNA ends created by Blem and X-rays is similar . CHO cells were exposed to reduced GSH at a concentration of 2mM for 3h before radiation . Treatment with Blem ( 20mug/ml ) was carried out for 2h before the cells were exposed to radiation . Our results show that the frequency of chromosomal aberration increases with increased LET . Heavy ion exposed cells show a higher frequency of CA over time than do X-irradiated cells . An analysis of the first post-irradiation mitosis of exposed CHO cells shows that high-LET radiation induces more breaks than exchange-type aberrations and exogenous GSH has no influence on high-LET radiation-induced DNA damage . The DNA lesions induced by low-LET radiation interact relatively strongly with Blem-induced lesions whereas interaction between Blem and high-LET radiations was poor . This could be attributed to differences in repair kinetics and qualitative differences in the DNA lesions induced by Blem and high-LET radiation .
    OUTPUT:
