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: Ovarian cancer , one of inflammation-associated cancers , is the fifth leading cause of cancer deaths among women . Inflammation in the tumor microenvironment is associated with peritoneal tumor dissemination and massive ascites , which contribute to high mortality in ovarian cancer . Tumor suppressor p53 is frequently deleted or mutated in aggressive and high-grade ovarian cancer , probably aggravating cancer progression and increasing mortality . We therefore investigated the influence of p53 on proinflammatory chemokines in ovarian cancer cells . A PCR array of the chemokine network revealed that ovarian cancer cells with low or mutated p53 expression expressed high levels of proinflammatory chemokines such as CXCL1 , 2 , 3 and 8 . Transient transfection of p53 into p53-null ovarian cancer cells downregulated proinflammatory chemokines induced by tumor necrosis factor-Î± ( TNF ) , a proinflammatory cytokine abundantly expressed in ovarian cancer . Furthermore , p53 restoration or stabilization blocked TNF-induced NF-ÎºB promoter activity and reduced TNF-activated IÎºB . Restoration of p53 increased ubiquitination of IÎºB , resulting from concurrently reduced proteasome activity followed by stability of IÎºB . A ubiquitination PCR array on restoration of p53 did not reveal any significant change in expression except for Mdm2 , indicating that the balance between p53 and Mdm2 is more important in regulating NF-ÎºB signaling rather than the direct effect of p53 on ubiquitin-related genes or IÎºB kinases . In addition , nutlin-3 , a specific inducer of p53 stabilization , inhibited proinflammatory chemokines by reducing TNF-activated IÎºB through p53 stabilization . Taken together , these results suggest that p53 inhibits proinflammatory chemokines in ovarian cancer cells by reducing proteasomal degradation of IÎºB . Thus , frequent loss or mutation of p53 may promote tumor progression by enhancing inflammation in the tumor microenvironment .
    OUTPUT:

agent
genomic instability and mutation;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.
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    INPUT: Ovarian cancer , one of inflammation-associated cancers , is the fifth leading cause of cancer deaths among women . Inflammation in the tumor microenvironment is associated with peritoneal tumor dissemination and massive ascites , which contribute to high mortality in ovarian cancer . Tumor suppressor p53 is frequently deleted or mutated in aggressive and high-grade ovarian cancer , probably aggravating cancer progression and increasing mortality . We therefore investigated the influence of p53 on proinflammatory chemokines in ovarian cancer cells . A PCR array of the chemokine network revealed that ovarian cancer cells with low or mutated p53 expression expressed high levels of proinflammatory chemokines such as CXCL1 , 2 , 3 and 8 . Transient transfection of p53 into p53-null ovarian cancer cells downregulated proinflammatory chemokines induced by tumor necrosis factor-Î± ( TNF ) , a proinflammatory cytokine abundantly expressed in ovarian cancer . Furthermore , p53 restoration or stabilization blocked TNF-induced NF-ÎºB promoter activity and reduced TNF-activated IÎºB . Restoration of p53 increased ubiquitination of IÎºB , resulting from concurrently reduced proteasome activity followed by stability of IÎºB . A ubiquitination PCR array on restoration of p53 did not reveal any significant change in expression except for Mdm2 , indicating that the balance between p53 and Mdm2 is more important in regulating NF-ÎºB signaling rather than the direct effect of p53 on ubiquitin-related genes or IÎºB kinases . In addition , nutlin-3 , a specific inducer of p53 stabilization , inhibited proinflammatory chemokines by reducing TNF-activated IÎºB through p53 stabilization . Taken together , these results suggest that p53 inhibits proinflammatory chemokines in ovarian cancer cells by reducing proteasomal degradation of IÎºB . Thus , frequent loss or mutation of p53 may promote tumor progression by enhancing inflammation in the tumor microenvironment .
    OUTPUT:
