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: Genotoxic stress induces cell cycle arrest and DNA repair which may enable tumor cells to survive radiation therapy . Here , we defined the role of Ca(2+) signaling in the cell cycle control and survival of chronic myeloid leukemia ( CML ) cells subjected to ionizing radiation ( IR ) . To this end , K562 erythroid leukemia cells were irradiated ( 0-10 Gy ) . Tumor survival was analyzed by clonogenic survival assay and cell cycle progression via flow cytometry . Plasma membrane cation conductance was assessed by patch-clamp whole-cell recording and the cytosolic free Ca(2+) concentration ( [ Ca(2+)](i) ) was measured by fura-2 Ca(2+) imaging . Nuclear activity of Ca(2+)/calmodulin-dependent kinase II ( CaMKII ) was defined by Western blotting . In addition , the effect of IR ( 5 Gy ) on the cation conductance of primary CML cells was determined . The results indicated that IR ( 10 Gy ) induced a G(2)/M cell cycle arrest of K562 cells within 24 h post-irradiation ( p.i. ) and decreased the clonogenic survival to 0.5 % of that of the control cells . In K562 cells , G(2)/M cell cycle arrest was preceded by activation of TRPV5/6-like nonselective cation channels in the plasma membrane 1-5 h p.i. , resulting in an elevated Ca(2+) entry as evident from fura-2 Ca(2+) imaging . Similarly , IR stimulated a Ca(2+)-permeable nonselective cation conductance in primary CML cells within 2-4 h p.i. . Ca(2+) entry , into K562 cells was paralleled by an IR-induced activation of nuclear CaMKII . The IR-stimulated accumulation in G(2) phase was delayed upon buffering [ Ca(2+)](i) with the Ca(2+) chelator BAPTA-AM or inhibiting CaMKII with KN93 ( 1 nM ) . In addition , KN93 decreased the clonogenic survival of irradiated cells but not of control cells . In conclusion , the data suggest that IR-stimulated cation channel activation , Ca(2+) entry and CaMKII activity participate in control of cell cycle progression and survival of irradiated CML cells .
    OUTPUT:

agent
evading growth suppressors
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: Genotoxic stress induces cell cycle arrest and DNA repair which may enable tumor cells to survive radiation therapy . Here , we defined the role of Ca(2+) signaling in the cell cycle control and survival of chronic myeloid leukemia ( CML ) cells subjected to ionizing radiation ( IR ) . To this end , K562 erythroid leukemia cells were irradiated ( 0-10 Gy ) . Tumor survival was analyzed by clonogenic survival assay and cell cycle progression via flow cytometry . Plasma membrane cation conductance was assessed by patch-clamp whole-cell recording and the cytosolic free Ca(2+) concentration ( [ Ca(2+)](i) ) was measured by fura-2 Ca(2+) imaging . Nuclear activity of Ca(2+)/calmodulin-dependent kinase II ( CaMKII ) was defined by Western blotting . In addition , the effect of IR ( 5 Gy ) on the cation conductance of primary CML cells was determined . The results indicated that IR ( 10 Gy ) induced a G(2)/M cell cycle arrest of K562 cells within 24 h post-irradiation ( p.i. ) and decreased the clonogenic survival to 0.5 % of that of the control cells . In K562 cells , G(2)/M cell cycle arrest was preceded by activation of TRPV5/6-like nonselective cation channels in the plasma membrane 1-5 h p.i. , resulting in an elevated Ca(2+) entry as evident from fura-2 Ca(2+) imaging . Similarly , IR stimulated a Ca(2+)-permeable nonselective cation conductance in primary CML cells within 2-4 h p.i. . Ca(2+) entry , into K562 cells was paralleled by an IR-induced activation of nuclear CaMKII . The IR-stimulated accumulation in G(2) phase was delayed upon buffering [ Ca(2+)](i) with the Ca(2+) chelator BAPTA-AM or inhibiting CaMKII with KN93 ( 1 nM ) . In addition , KN93 decreased the clonogenic survival of irradiated cells but not of control cells . In conclusion , the data suggest that IR-stimulated cation channel activation , Ca(2+) entry and CaMKII activity participate in control of cell cycle progression and survival of irradiated CML cells .
    OUTPUT:
