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: Furan , a potent rodent liver carcinogen , is found in many cooked food items and thus represents a human cancer risk . Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays , combined with analysis of histopathological and gene expression changes . In addition , formamidopyrimidine DNA glycosylase ( Fpg ) and endonuclease III ( EndoIII)-sensitive DNA damage was monitored as a measure of oxidative DNA damage . Rats were treated by gavage on four consecutive days with 2 , 4 , and 8mg/kg bw furan , doses that were tumorigenic in 2-year cancer bioassays , and with two higher doses , 12 and 16mg/kg . Rats were killed 3h after the last dose , a time established as producing maximum levels of DNA damage in livers of furan-treated rats . Liver Comet assays indicated that both DNA strand breaks and oxidized purines and pyrimidines increased in a near-linear dose-responsive fashion , with statistically significant increases detected at cancer bioassay doses . No DNA damage was detected in bone marrow , a non-target tissue for cancer , and peripheral blood micronucleus assays were negative . Histopathological evaluation of liver from furan-exposed animals produced evidence of inflammation , single-cell necrosis , apoptosis , and cell proliferation . In addition , genes related to apoptosis , cell-cycle checkpoints , and DNA-repair were expressed at a slightly lower level in the furan-treated livers . Although a mixed mode of action involving direct DNA binding cannot be ruled out , the data suggest that furan induces cancer in rat livers mainly through a secondary genotoxic mechanism involving oxidative stress , accompanied by inflammation , cell proliferation , and toxicity .
    OUTPUT:

agent
genomic instability and mutation;resisting cell death;tumor promoting inflammation;evading growth suppressors
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: Furan , a potent rodent liver carcinogen , is found in many cooked food items and thus represents a human cancer risk . Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays , combined with analysis of histopathological and gene expression changes . In addition , formamidopyrimidine DNA glycosylase ( Fpg ) and endonuclease III ( EndoIII)-sensitive DNA damage was monitored as a measure of oxidative DNA damage . Rats were treated by gavage on four consecutive days with 2 , 4 , and 8mg/kg bw furan , doses that were tumorigenic in 2-year cancer bioassays , and with two higher doses , 12 and 16mg/kg . Rats were killed 3h after the last dose , a time established as producing maximum levels of DNA damage in livers of furan-treated rats . Liver Comet assays indicated that both DNA strand breaks and oxidized purines and pyrimidines increased in a near-linear dose-responsive fashion , with statistically significant increases detected at cancer bioassay doses . No DNA damage was detected in bone marrow , a non-target tissue for cancer , and peripheral blood micronucleus assays were negative . Histopathological evaluation of liver from furan-exposed animals produced evidence of inflammation , single-cell necrosis , apoptosis , and cell proliferation . In addition , genes related to apoptosis , cell-cycle checkpoints , and DNA-repair were expressed at a slightly lower level in the furan-treated livers . Although a mixed mode of action involving direct DNA binding cannot be ruled out , the data suggest that furan induces cancer in rat livers mainly through a secondary genotoxic mechanism involving oxidative stress , accompanied by inflammation , cell proliferation , and toxicity .
    OUTPUT:
