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: Ulcerative colitis ( UC ) is a major form of chronic inflammation that can frequently progress to colon cancer . Several studies have demonstrated massive infiltration of neutrophils and macrophages into the lamina propria and submucosa in the progression of UC-associated colon carcinogenesis . Macrophages contribute to the development of colitis-associated colon cancer ( CAC ) . However , the role of neutrophils is not well understood . To better understand the involvement of tumor-associated neutrophils ( TANs ) in the regulation of CAC , we used a mouse CAC model produced by administering azoxymethane ( AOM ) , followed by repeated dextran sulfate sodium ( DSS ) ingestion . This causes severe colonic inflammation and subsequent development of multiple tumors in mice colon . We observed that colorectal mucosal inflammation became increasingly severe with AOM and DSS treatment . Macrophages infiltrated the lamina propria and submucosa , together with a marked increase in neutrophil infiltration . The chemokine CXCL2 increased in the lamina propria and submucosal regions of the colons of the treated mice , together with the infiltration of neutrophils expressing CXCR2 , a specific receptor for CXCL2 . This process was followed by neoplastic transformation . After AOM and DSS treatment , the mice showed enhanced production of metalloproteinase ( MMP)-9 and neutrophil elastase ( NE ) , accompanied by excessive vessel generation and cell proliferation . Moreover , CXCL2 promoted neutrophil recruitment and induced neutrophils to express MMP-9 and NE in vitro . Furthermore , administration of neutrophil-neutralizing antibodies after the last DSS cycle markedly reduced the number and size of tumors and decreased the expression of CXCR2 , CXCL2 , MMP-9 , and NE . These observations indicate a crucial role for TANs in the initiation and progression of CAC and suggest that the CXCL2-CXCR2 axis might be useful in reducing the risk of UC-associated colon cancer .
    OUTPUT:

agent
tumor promoting inflammation;inducing angiogenesis
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: Ulcerative colitis ( UC ) is a major form of chronic inflammation that can frequently progress to colon cancer . Several studies have demonstrated massive infiltration of neutrophils and macrophages into the lamina propria and submucosa in the progression of UC-associated colon carcinogenesis . Macrophages contribute to the development of colitis-associated colon cancer ( CAC ) . However , the role of neutrophils is not well understood . To better understand the involvement of tumor-associated neutrophils ( TANs ) in the regulation of CAC , we used a mouse CAC model produced by administering azoxymethane ( AOM ) , followed by repeated dextran sulfate sodium ( DSS ) ingestion . This causes severe colonic inflammation and subsequent development of multiple tumors in mice colon . We observed that colorectal mucosal inflammation became increasingly severe with AOM and DSS treatment . Macrophages infiltrated the lamina propria and submucosa , together with a marked increase in neutrophil infiltration . The chemokine CXCL2 increased in the lamina propria and submucosal regions of the colons of the treated mice , together with the infiltration of neutrophils expressing CXCR2 , a specific receptor for CXCL2 . This process was followed by neoplastic transformation . After AOM and DSS treatment , the mice showed enhanced production of metalloproteinase ( MMP)-9 and neutrophil elastase ( NE ) , accompanied by excessive vessel generation and cell proliferation . Moreover , CXCL2 promoted neutrophil recruitment and induced neutrophils to express MMP-9 and NE in vitro . Furthermore , administration of neutrophil-neutralizing antibodies after the last DSS cycle markedly reduced the number and size of tumors and decreased the expression of CXCR2 , CXCL2 , MMP-9 , and NE . These observations indicate a crucial role for TANs in the initiation and progression of CAC and suggest that the CXCL2-CXCR2 axis might be useful in reducing the risk of UC-associated colon cancer .
    OUTPUT:
