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: Senescence is a cellular response preventing tumorigenesis . The Ras oncogene is frequently activated or mutated in human cancers , but Ras activation is insufficient to transform primary cells . Ina search for cooperating oncogenes , we identify the lysine demethylase JMJD2A/KDM4A . We show that JMJD2A functions as a negative regulator of Ras-induced senescence and collaborates with oncogenic Ras to promote cellular transformation by negatively regulating the p53 pathway . We find CHD5 , a known tumor suppressor regulating p53 activity , as a target of JMJD2A . The expression of JMJD2A inhibits Ras-mediated CHD5 induction leading to a reduced activity of the p53 pathway . In addition , we show that JMJD2A is overexpressed inmouse and human lung cancers . Depletion of JMJD2A in the human lung cancer cell line A549 bearing an activated K-Ras allele triggers senescence . We propose that JMJD2A is an oncogene that represents a target for Ras-expressing tumors .
    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.
    ###
    INPUT: Senescence is a cellular response preventing tumorigenesis . The Ras oncogene is frequently activated or mutated in human cancers , but Ras activation is insufficient to transform primary cells . Ina search for cooperating oncogenes , we identify the lysine demethylase JMJD2A/KDM4A . We show that JMJD2A functions as a negative regulator of Ras-induced senescence and collaborates with oncogenic Ras to promote cellular transformation by negatively regulating the p53 pathway . We find CHD5 , a known tumor suppressor regulating p53 activity , as a target of JMJD2A . The expression of JMJD2A inhibits Ras-mediated CHD5 induction leading to a reduced activity of the p53 pathway . In addition , we show that JMJD2A is overexpressed inmouse and human lung cancers . Depletion of JMJD2A in the human lung cancer cell line A549 bearing an activated K-Ras allele triggers senescence . We propose that JMJD2A is an oncogene that represents a target for Ras-expressing tumors .
    OUTPUT:
