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: Infection by Opisthorchis viverrini , a risk factor for cholangiocarcinoma ( CCA ) may act through chronic inflammation , oxidative stress and lipid peroxidation ( LPO)-related damage and growth stimuli. 1,N6-etheno-2'-deoxyadenosine ( epsilondA ) , and 3,N4-etheno-2'-deoxycytidine ( epsilondC ) , markers for LPO-derived DNA damage were highly increased in white blood cell and urine of O. viverrini-infected Thai patients . In order to investigate tissue specificity etheno adducts were measured in a cholangiocarcinogenesis model , in O. viverrini-infected hamsters that had received N-nitrosodimethylamine ( NDMA , 12.5 ppm in dw ) for 2 months. epsilondA- and epsilondC-levels were analyzed in paraffin-embedded liver sections by a novel immunohistochemical method , from 21 up to 180 days post-O. viverrini-infection . In inflamed areas of the liver , etheno adducts were localized in the nuclei of inflammatory cells and in the epithelial lining of the bile duct . Semi-quantitative image analysis showed higher adduct levels in the liver of O. viverrini-infected hamsters , treated with or w/o NDMA when compared with untreated controls . Levels were found highest in the liver of O. viverrini-infected plus NDMA-treated hamsters . Adducts increased in an age-dependent manner from O. viverrini-infection until CCA development . Increased adduct formation paralleled histopathological changes in plasma alkaline phosphatase ( ALP ) activity , bile duct hyperplasia , dysplasia , precancerous lesions , and CCA appearance . Also elevated expression of alkyladenine DNA glycosylase ( AAG ) , which excises 1,N6-ethenoadenine ( epsilonA ) was linked to higher adduct formation , suggesting imbalanced repair . Our results implicate accumulation of inflammation-related , promutagenic DNA damage in target tissue and possibly imbalanced repair in the onset of cholangiocarcinogenesis .
    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: Infection by Opisthorchis viverrini , a risk factor for cholangiocarcinoma ( CCA ) may act through chronic inflammation , oxidative stress and lipid peroxidation ( LPO)-related damage and growth stimuli. 1,N6-etheno-2'-deoxyadenosine ( epsilondA ) , and 3,N4-etheno-2'-deoxycytidine ( epsilondC ) , markers for LPO-derived DNA damage were highly increased in white blood cell and urine of O. viverrini-infected Thai patients . In order to investigate tissue specificity etheno adducts were measured in a cholangiocarcinogenesis model , in O. viverrini-infected hamsters that had received N-nitrosodimethylamine ( NDMA , 12.5 ppm in dw ) for 2 months. epsilondA- and epsilondC-levels were analyzed in paraffin-embedded liver sections by a novel immunohistochemical method , from 21 up to 180 days post-O. viverrini-infection . In inflamed areas of the liver , etheno adducts were localized in the nuclei of inflammatory cells and in the epithelial lining of the bile duct . Semi-quantitative image analysis showed higher adduct levels in the liver of O. viverrini-infected hamsters , treated with or w/o NDMA when compared with untreated controls . Levels were found highest in the liver of O. viverrini-infected plus NDMA-treated hamsters . Adducts increased in an age-dependent manner from O. viverrini-infection until CCA development . Increased adduct formation paralleled histopathological changes in plasma alkaline phosphatase ( ALP ) activity , bile duct hyperplasia , dysplasia , precancerous lesions , and CCA appearance . Also elevated expression of alkyladenine DNA glycosylase ( AAG ) , which excises 1,N6-ethenoadenine ( epsilonA ) was linked to higher adduct formation , suggesting imbalanced repair . Our results implicate accumulation of inflammation-related , promutagenic DNA damage in target tissue and possibly imbalanced repair in the onset of cholangiocarcinogenesis .
    OUTPUT:
