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.
    ###
    INPUT: Cigarette smoking is implicated in numerous diseases , including emphysema and lung cancer . The clinical expression of lung disease in smokers is not well explained by currently defined variations in gene expression or simple differences in smoking exposure . Alveolar macrophages play a critical role in the inflammation and remodeling of the lung parenchyma in smoking-related lung disease . Significant gene expression changes in alveolar macrophages from smokers have been identified . However , the mechanism for these changes remains unknown . One potential mechanism for smoking-altered gene expression is via changes in cytosine methylation in DNA regions proximal to gene-coding sequences . In this study , alveolar macrophage DNA from heavy smokers and never smokers was isolated and methylation status at 25,000 loci determined . We found differential methylation in genes from immune-system and inflammatory pathways . Analysis of matching gene expression data demonstrated a parallel enrichment for changes in immune-system and inflammatory pathways . A significant number of genes with smoking-altered mRNA expression had inverse changes in methylation status . One gene highlighted by this data was the FLT1 , and further studies found particular up-regulation of a splice variant encoding a soluble inhibitory form of the receptor . In conclusion , chronic cigarette smoke exposure altered DNA methylation in specific gene promoter regions in human alveolar macrophages .
    OUTPUT:

agent
tumor promoting inflammation
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: Cigarette smoking is implicated in numerous diseases , including emphysema and lung cancer . The clinical expression of lung disease in smokers is not well explained by currently defined variations in gene expression or simple differences in smoking exposure . Alveolar macrophages play a critical role in the inflammation and remodeling of the lung parenchyma in smoking-related lung disease . Significant gene expression changes in alveolar macrophages from smokers have been identified . However , the mechanism for these changes remains unknown . One potential mechanism for smoking-altered gene expression is via changes in cytosine methylation in DNA regions proximal to gene-coding sequences . In this study , alveolar macrophage DNA from heavy smokers and never smokers was isolated and methylation status at 25,000 loci determined . We found differential methylation in genes from immune-system and inflammatory pathways . Analysis of matching gene expression data demonstrated a parallel enrichment for changes in immune-system and inflammatory pathways . A significant number of genes with smoking-altered mRNA expression had inverse changes in methylation status . One gene highlighted by this data was the FLT1 , and further studies found particular up-regulation of a splice variant encoding a soluble inhibitory form of the receptor . In conclusion , chronic cigarette smoke exposure altered DNA methylation in specific gene promoter regions in human alveolar macrophages .
    OUTPUT:
