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: BACKGROUND Alcohol consumption promotes hepatocellular carcinoma ( HCC ) . The responsible mechanisms are not well understood . Hepatocarcinogenesis increases with age and is enhanced by factors that impose a demand for liver regeneration . Because alcohol is hepatotoxic , habitual alcohol ingestion evokes a recurrent demand for hepatic regeneration . The alcohol-preferring ( P ) rat model mimics the level of alcohol consumption by humans who habitually abuse alcohol . Previously , we showed that habitual heavy alcohol ingestion amplified age-related hepatocarcinogenesis in P rats , with over 80% of alcohol-consuming P rats developing HCCs after 18months of alcohol exposure , compared with only 5% of water-drinking controls . METHODS Herein , we used quantitative real-time PCR and quantitative immunocytochemistry to compare liver tissues from alcohol-consuming P rats and water-fed P rat controls after 6 , 12 , or 18months of drinking . We aimed to identify potential mechanisms that might underlie the differences in liver cancer formation and hypothesized that chronic alcohol ingestion would activate Hedgehog ( HH ) , a regenerative signaling pathway that is overactivated in HCC . RESULTS Chronic alcohol ingestion amplified age-related degenerative changes in hepatocytes , but did not cause appreciable liver inflammation or fibrosis even after 18months of heavy drinking . HH signaling was also enhanced by alcohol exposure , as evidenced by increased levels of mRNAs encoding HH ligands , HH-regulated transcription factors , and HH target genes . Immunocytochemistry confirmed increased alcohol-related accumulation of HH ligand-producing cells and HH-responsive target cells . HH-related regenerative responses were also induced in alcohol-exposed rats . Three of these processes ( i.e. , deregulated progenitor expansion , the reverse Warburg effect , and epithelial-to-mesenchymal transitions ) are known to promote cancer growth in other tissues . CONCLUSIONS Alcohol-related changes in Hedgehog signaling and resultant deregulation of liver cell replacement might promote hepatocarcinogenesis .
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agent
tumor promoting inflammation;activating invasion and metastasis;cellular energetics
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: BACKGROUND Alcohol consumption promotes hepatocellular carcinoma ( HCC ) . The responsible mechanisms are not well understood . Hepatocarcinogenesis increases with age and is enhanced by factors that impose a demand for liver regeneration . Because alcohol is hepatotoxic , habitual alcohol ingestion evokes a recurrent demand for hepatic regeneration . The alcohol-preferring ( P ) rat model mimics the level of alcohol consumption by humans who habitually abuse alcohol . Previously , we showed that habitual heavy alcohol ingestion amplified age-related hepatocarcinogenesis in P rats , with over 80% of alcohol-consuming P rats developing HCCs after 18months of alcohol exposure , compared with only 5% of water-drinking controls . METHODS Herein , we used quantitative real-time PCR and quantitative immunocytochemistry to compare liver tissues from alcohol-consuming P rats and water-fed P rat controls after 6 , 12 , or 18months of drinking . We aimed to identify potential mechanisms that might underlie the differences in liver cancer formation and hypothesized that chronic alcohol ingestion would activate Hedgehog ( HH ) , a regenerative signaling pathway that is overactivated in HCC . RESULTS Chronic alcohol ingestion amplified age-related degenerative changes in hepatocytes , but did not cause appreciable liver inflammation or fibrosis even after 18months of heavy drinking . HH signaling was also enhanced by alcohol exposure , as evidenced by increased levels of mRNAs encoding HH ligands , HH-regulated transcription factors , and HH target genes . Immunocytochemistry confirmed increased alcohol-related accumulation of HH ligand-producing cells and HH-responsive target cells . HH-related regenerative responses were also induced in alcohol-exposed rats . Three of these processes ( i.e. , deregulated progenitor expansion , the reverse Warburg effect , and epithelial-to-mesenchymal transitions ) are known to promote cancer growth in other tissues . CONCLUSIONS Alcohol-related changes in Hedgehog signaling and resultant deregulation of liver cell replacement might promote hepatocarcinogenesis .
    OUTPUT:
