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: The ATM/ATR DNA damage checkpoint functions in the maintenance of genetic stability and some missense variants of the ATM gene have been shown to confer a moderate increased risk of prostate cancer . However , whether inactivation of this checkpoint contributes directly to prostate specific cancer predisposition is still unknown . Here , we show that exposure of non-malignant prostate epithelial cells ( HPr-1AR ) to androgen led to activation of the ATM/ATR DNA damage response and induction of cellular senescence . Notably , knockdown of the ATM gene expression in HPr-1AR cells can promote androgen-induced TMPRSS2 : ERG rearrangement , a prostate-specific chromosome translocation frequently found in prostate cancer cells . Intriguingly , unlike the non-malignant prostate epithelial cells , the ATM/ATR DNA damage checkpoint appears to be defective in prostate cancer cells , since androgen treatment only induced a partial activation of the DNA damage response . This mechanism appears to preserve androgen induced autophosphorylation of ATM and phosphorylation of H2AX , lesion processing and repair pathway yet restrain ATM/CHK1/CHK2 and p53 signaling pathway . Our findings demonstrate that ATM/ATR inactivation is a crucial step in promoting androgen-induced genomic instability and prostate carcinogenesis .
    OUTPUT:

agent
enabling replicative immortality;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: The ATM/ATR DNA damage checkpoint functions in the maintenance of genetic stability and some missense variants of the ATM gene have been shown to confer a moderate increased risk of prostate cancer . However , whether inactivation of this checkpoint contributes directly to prostate specific cancer predisposition is still unknown . Here , we show that exposure of non-malignant prostate epithelial cells ( HPr-1AR ) to androgen led to activation of the ATM/ATR DNA damage response and induction of cellular senescence . Notably , knockdown of the ATM gene expression in HPr-1AR cells can promote androgen-induced TMPRSS2 : ERG rearrangement , a prostate-specific chromosome translocation frequently found in prostate cancer cells . Intriguingly , unlike the non-malignant prostate epithelial cells , the ATM/ATR DNA damage checkpoint appears to be defective in prostate cancer cells , since androgen treatment only induced a partial activation of the DNA damage response . This mechanism appears to preserve androgen induced autophosphorylation of ATM and phosphorylation of H2AX , lesion processing and repair pathway yet restrain ATM/CHK1/CHK2 and p53 signaling pathway . Our findings demonstrate that ATM/ATR inactivation is a crucial step in promoting androgen-induced genomic instability and prostate carcinogenesis .
    OUTPUT:
