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: Ataxia-telangiectasia mutated ( ATM ) is a high molecular weight protein serine/threonine kinase that plays a central role in the maintenance of genomic integrity by activating cell cycle checkpoints and promoting repair of DNA double-strand breaks . Little is known about the regulatory mechanisms for ATM expression itself . MicroRNAs are naturally existing regulators that modulate gene expression in a sequence-specific manner . Here , we show that a human microRNA , miR-421 , suppresses ATM expression by targeting the 3'-untranslated region ( 3'UTR ) of ATM transcripts . Ectopic expression of miR-421 resulted in S-phase cell cycle checkpoint changes and an increased sensitivity to ionizing radiation , creating a cellular phenotype similar to that of cells derived from ataxia-telangiectasia ( A-T ) patients . Blocking the interaction between miR-421 and ATM 3'UTR with an antisense morpholino oligonucleotide rescued the defective phenotype caused by miR-421 overexpression , indicating that ATM mediates the effect of miR-421 on cell cycle checkpoint and radiosensitivity . Overexpression of the N-Myc transcription factor , an oncogene frequently amplified in neuroblastoma , induced miR-421 expression , which , in turn , down-regulated ATM expression , establishing a linear signaling pathway that may contribute to N-Myc-induced tumorigenesis in neuroblastoma . Taken together , our findings implicate a previously undescribed regulatory mechanism for ATM expression and ATM-dependent DNA damage response and provide several potential targets for treating neuroblastoma and perhaps A-T .
    OUTPUT:

agent
evading growth suppressors;genomic instability and mutation
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: Ataxia-telangiectasia mutated ( ATM ) is a high molecular weight protein serine/threonine kinase that plays a central role in the maintenance of genomic integrity by activating cell cycle checkpoints and promoting repair of DNA double-strand breaks . Little is known about the regulatory mechanisms for ATM expression itself . MicroRNAs are naturally existing regulators that modulate gene expression in a sequence-specific manner . Here , we show that a human microRNA , miR-421 , suppresses ATM expression by targeting the 3'-untranslated region ( 3'UTR ) of ATM transcripts . Ectopic expression of miR-421 resulted in S-phase cell cycle checkpoint changes and an increased sensitivity to ionizing radiation , creating a cellular phenotype similar to that of cells derived from ataxia-telangiectasia ( A-T ) patients . Blocking the interaction between miR-421 and ATM 3'UTR with an antisense morpholino oligonucleotide rescued the defective phenotype caused by miR-421 overexpression , indicating that ATM mediates the effect of miR-421 on cell cycle checkpoint and radiosensitivity . Overexpression of the N-Myc transcription factor , an oncogene frequently amplified in neuroblastoma , induced miR-421 expression , which , in turn , down-regulated ATM expression , establishing a linear signaling pathway that may contribute to N-Myc-induced tumorigenesis in neuroblastoma . Taken together , our findings implicate a previously undescribed regulatory mechanism for ATM expression and ATM-dependent DNA damage response and provide several potential targets for treating neuroblastoma and perhaps A-T .
    OUTPUT:
