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: Centrosome overduplication or amplification has been observed in many human cancers and in premalignant tissue , but the mechanisms leading to such centrosome aberrations are not fully understood . We previously showed that abnormal mitotic cells with supernumerary centrosomes increase with replicative senescence in human fibroblasts , especially in a polyploid subpopulation . This study examines localization of p53 protein at centrosomes in mitotic cells , which is often observed in association with DNA damage response , to investigate a possible association between p53 localization and numerical centrosome aberrations induced by cellular senescence . Cultures at later passages or the 4th day after exposure to H(2)O(2) showed increased frequencies of mitotic cells with supernumerary centrosomes , especially in a polyploid subpopulation . Immunohistochemical analysis frequently showed p53-positive foci in mitotic cells , and some were localized at centrosomes . The number of p53-positive foci in mitotic cells and its localization to centrosomes increased with replicative and premature senescence . Supernumerary centrosomes showed higher frequencies of p53 localization compared to normally duplicated centrosomes . Centrosome-associated p53 protein was phosphorylated at Ser15 . These data suggest a possible association between localization of p53 protein and numerical centrosome aberrations in replicatively or prematurely senescent cells .
    OUTPUT:

agent
enabling replicative immortality
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: Centrosome overduplication or amplification has been observed in many human cancers and in premalignant tissue , but the mechanisms leading to such centrosome aberrations are not fully understood . We previously showed that abnormal mitotic cells with supernumerary centrosomes increase with replicative senescence in human fibroblasts , especially in a polyploid subpopulation . This study examines localization of p53 protein at centrosomes in mitotic cells , which is often observed in association with DNA damage response , to investigate a possible association between p53 localization and numerical centrosome aberrations induced by cellular senescence . Cultures at later passages or the 4th day after exposure to H(2)O(2) showed increased frequencies of mitotic cells with supernumerary centrosomes , especially in a polyploid subpopulation . Immunohistochemical analysis frequently showed p53-positive foci in mitotic cells , and some were localized at centrosomes . The number of p53-positive foci in mitotic cells and its localization to centrosomes increased with replicative and premature senescence . Supernumerary centrosomes showed higher frequencies of p53 localization compared to normally duplicated centrosomes . Centrosome-associated p53 protein was phosphorylated at Ser15 . These data suggest a possible association between localization of p53 protein and numerical centrosome aberrations in replicatively or prematurely senescent cells .
    OUTPUT:
