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: We examined the influence of the level of dietary protein or vitamin E ( VE ) on oxidative damage to DNA , lipids , and protein in the liver after total body irradiation ( TBI ) with X-rays at 1 or 4 Gy . Levels of 8-hydroxydeoxyguanosine , thiobarbituric acid-reactive substances , and protein carbonyls in the liver did not differ among the groups that did not receive TBI . However , oxidative damage to lipids and protein was increased by TBI only in the 1% protein group . DNA damage , lipid peroxidation , or protein oxidation in the liver was increased by TBI in a dose-dependent manner , and the damage was consistently higher in the 1% than in the 20% protein group . In the 1% protein group , a greater decrease in relative spleen weight by TBI was also observed . Concentrations of antioxidants ( vitamins C and E and glutathione ) in the liver were lower and the concentration of nonheme iron in the liver was higher in the 1% than in the 20% protein group . Mice fed a 1% protein diet became susceptible to TBI-induced oxidative damage , and decreases in antioxidant levels and an increase in iron level were involved in the mechanism of this susceptibility . These results suggest that dietary VE and protein can prevent oxidative damage to DNA , lipid , and protein in mice subjected to TBI . Consumption of a VE-free diet significantly increased 8-hydroxydeoxyguanosine levels in DNA from mice fed the 1% protein diet with TBI , but such changes were not detected in DNA from mice fed the 20% protein diet .
    OUTPUT:

agent
tumor promoting inflammation;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: We examined the influence of the level of dietary protein or vitamin E ( VE ) on oxidative damage to DNA , lipids , and protein in the liver after total body irradiation ( TBI ) with X-rays at 1 or 4 Gy . Levels of 8-hydroxydeoxyguanosine , thiobarbituric acid-reactive substances , and protein carbonyls in the liver did not differ among the groups that did not receive TBI . However , oxidative damage to lipids and protein was increased by TBI only in the 1% protein group . DNA damage , lipid peroxidation , or protein oxidation in the liver was increased by TBI in a dose-dependent manner , and the damage was consistently higher in the 1% than in the 20% protein group . In the 1% protein group , a greater decrease in relative spleen weight by TBI was also observed . Concentrations of antioxidants ( vitamins C and E and glutathione ) in the liver were lower and the concentration of nonheme iron in the liver was higher in the 1% than in the 20% protein group . Mice fed a 1% protein diet became susceptible to TBI-induced oxidative damage , and decreases in antioxidant levels and an increase in iron level were involved in the mechanism of this susceptibility . These results suggest that dietary VE and protein can prevent oxidative damage to DNA , lipid , and protein in mice subjected to TBI . Consumption of a VE-free diet significantly increased 8-hydroxydeoxyguanosine levels in DNA from mice fed the 1% protein diet with TBI , but such changes were not detected in DNA from mice fed the 20% protein diet .
    OUTPUT:
