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: It is commonly believed that neurons remain in G(0) phase of the cell cycle indefinitely . Cell-cycle re-entry , however , is known to contribute to neuronal apoptosis . Moreover , recent evidence demonstrates the expression of cell-cycle proteins in differentiated neurons under physiological conditions . The functional roles of such expression remain unclear . Since DNA repair is generally attenuated by differentiation in most cell types , the cell-cycle-associated events in postmitotic cells may reflect the need to re-enter the cell cycle to activate DNA repair . We show that cyclin-C-directed , pRb-dependent G(0) exit activates the non-homologous end joining pathway of DNA repair ( NHEJ ) in postmitotic neurons . Using RNA interference , we found that abrogation of cyclin-C-mediated exit from G(0) compromised DNA repair but did not initiate apoptosis . Forced G(1) entry combined with prevention of G(1) --&gt ; S progression triggered NHEJ activation even in the absence of DNA lesions , but did not induce apoptosis in contrast to unrestricted progression through G(1) --&gt ; S. We conclude that G(0) --&gt ; G(1) transition is functionally significant for NHEJ repair in postmitotic neurons . These findings reveal the importance of cell-cycle activation for controlling both DNA repair and apoptosis in postmitotic neurons , and underline the particular role of G(1) --&gt ; S progression in apoptotic signaling , providing new insights into the mechanisms of DNA damage response ( DDR ) in postmitotic neurons .
    OUTPUT:

agent
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: It is commonly believed that neurons remain in G(0) phase of the cell cycle indefinitely . Cell-cycle re-entry , however , is known to contribute to neuronal apoptosis . Moreover , recent evidence demonstrates the expression of cell-cycle proteins in differentiated neurons under physiological conditions . The functional roles of such expression remain unclear . Since DNA repair is generally attenuated by differentiation in most cell types , the cell-cycle-associated events in postmitotic cells may reflect the need to re-enter the cell cycle to activate DNA repair . We show that cyclin-C-directed , pRb-dependent G(0) exit activates the non-homologous end joining pathway of DNA repair ( NHEJ ) in postmitotic neurons . Using RNA interference , we found that abrogation of cyclin-C-mediated exit from G(0) compromised DNA repair but did not initiate apoptosis . Forced G(1) entry combined with prevention of G(1) --&gt ; S progression triggered NHEJ activation even in the absence of DNA lesions , but did not induce apoptosis in contrast to unrestricted progression through G(1) --&gt ; S. We conclude that G(0) --&gt ; G(1) transition is functionally significant for NHEJ repair in postmitotic neurons . These findings reveal the importance of cell-cycle activation for controlling both DNA repair and apoptosis in postmitotic neurons , and underline the particular role of G(1) --&gt ; S progression in apoptotic signaling , providing new insights into the mechanisms of DNA damage response ( DDR ) in postmitotic neurons .
    OUTPUT:
