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: Helicobacter hepaticus-infected Rag2(-/-) mice emulate many aspects of human inflammatory bowel disease , including the development of colitis and colon cancer . To elucidate mechanisms of inflammation-induced carcinogenesis , we undertook a comprehensive analysis of histopathology , molecular damage , and gene expression changes during disease progression in these mice . Infected mice developed severe colitis and hepatitis by 10wk post-infection , progressing into colon carcinoma by 20wk post-infection , with pronounced pathology in the cecum and proximal colon marked by infiltration of neutrophils and macrophages . Transcriptional profiling revealed decreased expression of DNA repair and oxidative stress response genes in colon , but not in liver . Mass spectrometric analysis revealed higher levels of DNA and RNA damage products in liver compared to colon and infection-induced increases in 5-chlorocytosine in DNA and RNA and hypoxanthine in DNA . Paradoxically , infection was associated with decreased levels of DNA etheno adducts . Levels of nucleic acid damage from the same chemical class were strongly correlated in both liver and colon . The results support a model of inflammation-mediated carcinogenesis involving infiltration of phagocytes and generation of reactive species that cause local molecular damage leading to cell dysfunction , mutation , and cell death . There are strong correlations among histopathology , phagocyte infiltration , and damage chemistry that suggest a major role for neutrophils in inflammation-associated cancer progression . Further , paradoxical changes in nucleic acid damage were observed in tissue- and chemistry-specific patterns . The results also reveal features of cell stress response that point to microbial pathophysiology and mechanisms of cell senescence as important mechanistic links to cancer .
    OUTPUT:

agent
tumor promoting inflammation;genomic instability and mutation;resisting cell death
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: Helicobacter hepaticus-infected Rag2(-/-) mice emulate many aspects of human inflammatory bowel disease , including the development of colitis and colon cancer . To elucidate mechanisms of inflammation-induced carcinogenesis , we undertook a comprehensive analysis of histopathology , molecular damage , and gene expression changes during disease progression in these mice . Infected mice developed severe colitis and hepatitis by 10wk post-infection , progressing into colon carcinoma by 20wk post-infection , with pronounced pathology in the cecum and proximal colon marked by infiltration of neutrophils and macrophages . Transcriptional profiling revealed decreased expression of DNA repair and oxidative stress response genes in colon , but not in liver . Mass spectrometric analysis revealed higher levels of DNA and RNA damage products in liver compared to colon and infection-induced increases in 5-chlorocytosine in DNA and RNA and hypoxanthine in DNA . Paradoxically , infection was associated with decreased levels of DNA etheno adducts . Levels of nucleic acid damage from the same chemical class were strongly correlated in both liver and colon . The results support a model of inflammation-mediated carcinogenesis involving infiltration of phagocytes and generation of reactive species that cause local molecular damage leading to cell dysfunction , mutation , and cell death . There are strong correlations among histopathology , phagocyte infiltration , and damage chemistry that suggest a major role for neutrophils in inflammation-associated cancer progression . Further , paradoxical changes in nucleic acid damage were observed in tissue- and chemistry-specific patterns . The results also reveal features of cell stress response that point to microbial pathophysiology and mechanisms of cell senescence as important mechanistic links to cancer .
    OUTPUT:
