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 have evaluated DNA damage ( DNA adduct formation ) after feeding benzo[a]pyrene ( BP ) to wild-type ( WT ) and cancer-susceptible Xpa(-/-)p53(+/-) mice deficient in nucleotide excision repair and haploinsufficient for the tumor suppressor p53 . DNA damage was evaluated by high-performance liquid chromatography/electrospray ionization tandem mass spectrometry ( HPLC/ES-MS/MS ) , which measures r7,t8,t9-trihydroxy-c-10-(N ( 2)-deoxyguanosyl)-7,8,9,10-tetrahydrobenzo[a]pyrene ( BPdG ) , and a chemiluminescence immunoassay ( CIA ) , using anti-r7,t8-dihydroxy-t-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene ( BPDE)-DNA antiserum , which measures both BPdG and the other stable BP-DNA adducts . When mice were fed 100 ppm BP for 28 days , BP-induced DNA damage measured in esophagus , liver and lung was typically higher in Xpa(-/-)p53(+/-) mice , compared with WT mice . This result is consistent with the previously observed tumor susceptibility of Xpa(-/-)p53(+/-) mice . BPdG , the major DNA adduct associated with tumorigenicity , was the primary DNA adduct formed in esophagus ( a target tissue in the mouse ) , whereas total BP-DNA adducts predominated in higher levels in the liver ( a non-target tissue in the mouse ) . In an attempt to lower BP-induced DNA damage , we fed the WT and Xpa(-/-)p53(+/-) mice 0.3% chlorophyllin ( CHL ) in the BP-containing diet for 28 days . The addition of CHL resulted in an increase of BP-DNA adducts in esophagus , liver and lung of WT mice , a lowering of BPdG in esophagi of WT mice and livers of Xpa(-/-)p53(+/-) mice and an increase of BPdG in livers of WT mice . Therefore , the addition of CHL to a BP-containing diet showed a lack of consistent chemoprotective effect , indicating that oral CHL administration may not reduce PAH-DNA adduct levels consistently in human organs .
    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: We have evaluated DNA damage ( DNA adduct formation ) after feeding benzo[a]pyrene ( BP ) to wild-type ( WT ) and cancer-susceptible Xpa(-/-)p53(+/-) mice deficient in nucleotide excision repair and haploinsufficient for the tumor suppressor p53 . DNA damage was evaluated by high-performance liquid chromatography/electrospray ionization tandem mass spectrometry ( HPLC/ES-MS/MS ) , which measures r7,t8,t9-trihydroxy-c-10-(N ( 2)-deoxyguanosyl)-7,8,9,10-tetrahydrobenzo[a]pyrene ( BPdG ) , and a chemiluminescence immunoassay ( CIA ) , using anti-r7,t8-dihydroxy-t-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene ( BPDE)-DNA antiserum , which measures both BPdG and the other stable BP-DNA adducts . When mice were fed 100 ppm BP for 28 days , BP-induced DNA damage measured in esophagus , liver and lung was typically higher in Xpa(-/-)p53(+/-) mice , compared with WT mice . This result is consistent with the previously observed tumor susceptibility of Xpa(-/-)p53(+/-) mice . BPdG , the major DNA adduct associated with tumorigenicity , was the primary DNA adduct formed in esophagus ( a target tissue in the mouse ) , whereas total BP-DNA adducts predominated in higher levels in the liver ( a non-target tissue in the mouse ) . In an attempt to lower BP-induced DNA damage , we fed the WT and Xpa(-/-)p53(+/-) mice 0.3% chlorophyllin ( CHL ) in the BP-containing diet for 28 days . The addition of CHL resulted in an increase of BP-DNA adducts in esophagus , liver and lung of WT mice , a lowering of BPdG in esophagi of WT mice and livers of Xpa(-/-)p53(+/-) mice and an increase of BPdG in livers of WT mice . Therefore , the addition of CHL to a BP-containing diet showed a lack of consistent chemoprotective effect , indicating that oral CHL administration may not reduce PAH-DNA adduct levels consistently in human organs .
    OUTPUT:
