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: Arsenic trioxide ( ATO ) is a novel agent to treat acute promyelocytic leukemia ( APL ) . ATO can degrade chimeric PML-RAR proteins and induce apoptosis in various cancer cells . However , its effects on primary hematopoietic CD34+ have not been examined . In this study , we compared the effects of ATO on HL60 leukemic cells and primary umbilical cord blood ( UCB ) CD34+ cells . HL60 cells and UCB CD34+ cells were cultured with different concentrations of ATO for up to three weeks and examined for changes of cell cycle . We found that ATO ( &lt ; or = 5 microM ) caused prolongation of G1/S and G2/M phase in a dose-dependent manner . The percentage of cells in G2/M increased significantly ( from 8.6 to 53.8% ) . High-dose ATO ( &gt ; or = 25 microM ) caused non-specific cell death in HL60 cells without any changes in cell cycle . In contrast to HL60 cells , UCB CD34+ cells were more resistant to high-dose ATO and most ATO-resistant CD34+ cells remained in G0/G1 phase . Primary cells that were resistant to ATO were rich in CD34+ cells . We further show that the ATO resistance was not related to the expression of P-glycoprotein ( MDR-1 ) . Our results suggest that the resistance to ATO in primitive UCB CD34+ cells is most likely related to its cell-cycle status . These results could be useful to design treatments for non-APL malignancies and to enrich hematopoietic stem cells in clinically applicable settings .
    OUTPUT:

agent
sustaining proliferative signaling;resisting cell death
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: Arsenic trioxide ( ATO ) is a novel agent to treat acute promyelocytic leukemia ( APL ) . ATO can degrade chimeric PML-RAR proteins and induce apoptosis in various cancer cells . However , its effects on primary hematopoietic CD34+ have not been examined . In this study , we compared the effects of ATO on HL60 leukemic cells and primary umbilical cord blood ( UCB ) CD34+ cells . HL60 cells and UCB CD34+ cells were cultured with different concentrations of ATO for up to three weeks and examined for changes of cell cycle . We found that ATO ( &lt ; or = 5 microM ) caused prolongation of G1/S and G2/M phase in a dose-dependent manner . The percentage of cells in G2/M increased significantly ( from 8.6 to 53.8% ) . High-dose ATO ( &gt ; or = 25 microM ) caused non-specific cell death in HL60 cells without any changes in cell cycle . In contrast to HL60 cells , UCB CD34+ cells were more resistant to high-dose ATO and most ATO-resistant CD34+ cells remained in G0/G1 phase . Primary cells that were resistant to ATO were rich in CD34+ cells . We further show that the ATO resistance was not related to the expression of P-glycoprotein ( MDR-1 ) . Our results suggest that the resistance to ATO in primitive UCB CD34+ cells is most likely related to its cell-cycle status . These results could be useful to design treatments for non-APL malignancies and to enrich hematopoietic stem cells in clinically applicable settings .
    OUTPUT:
