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: We investigated the priming effect and mechanism of granulocyte colony-stimulating factor ( G-CSF ) in chemotherapy with low-dose Ara-C and VP-16 for acute myeloid leukemia . We analyzed cell proliferation , apoptosis , and cell cycle in vitro using leukemia cell lines 32Dcl3 , U937 , HL-60 , and Ba/F3 . Cell proliferation assays were performed using the Trypan Blue dye exclusion method . For detection of apoptosis , the Annexin V-binding capacity of treated cells was examined by flow cytometry . To evaluate the cell cycle , we used an FITC BrdU Flow kit and conducted analysis by flow cytometry . The combination of Ara-C and VP-16 significantly enhanced the observed effects compared with those of Ara-C or VP-16 alone . Concurrent administration of G-CSF further reduced the cell number and viability of 32Dcl3 and U937 cells , but not of HL-60 and Ba/F3 cells . Apoptotic cells were significantly increased in number by the addition of G-CSF to 32Dcl3 and U937 cells , while G-CSF had no significant effect on HL-60 and Ba/F3 cell lines . The addition of G-CSF significantly decreased the percentage of G0/G1-phase cells and significantly increased that of S-phase cells among 32Dcl3 and U937 cells . No significant effect was observed for HL-60 and Ba/F3 cells . An enhancement was confirmed for the combination of Ara-C , VP-16 , and G-CSF for 32Dcl3 and U937 cells but not for HL-60 and Ba/F3 cells . It was thought that this difference was a result of different responses to G-CSF . G-CSF potentiates Ara-C- and VP-16-induced cytotoxicities through apoptosis induction by mobilizing resting G0-G1-phase cells into S phase .
    OUTPUT:

agent
resisting cell death;sustaining proliferative signaling
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: We investigated the priming effect and mechanism of granulocyte colony-stimulating factor ( G-CSF ) in chemotherapy with low-dose Ara-C and VP-16 for acute myeloid leukemia . We analyzed cell proliferation , apoptosis , and cell cycle in vitro using leukemia cell lines 32Dcl3 , U937 , HL-60 , and Ba/F3 . Cell proliferation assays were performed using the Trypan Blue dye exclusion method . For detection of apoptosis , the Annexin V-binding capacity of treated cells was examined by flow cytometry . To evaluate the cell cycle , we used an FITC BrdU Flow kit and conducted analysis by flow cytometry . The combination of Ara-C and VP-16 significantly enhanced the observed effects compared with those of Ara-C or VP-16 alone . Concurrent administration of G-CSF further reduced the cell number and viability of 32Dcl3 and U937 cells , but not of HL-60 and Ba/F3 cells . Apoptotic cells were significantly increased in number by the addition of G-CSF to 32Dcl3 and U937 cells , while G-CSF had no significant effect on HL-60 and Ba/F3 cell lines . The addition of G-CSF significantly decreased the percentage of G0/G1-phase cells and significantly increased that of S-phase cells among 32Dcl3 and U937 cells . No significant effect was observed for HL-60 and Ba/F3 cells . An enhancement was confirmed for the combination of Ara-C , VP-16 , and G-CSF for 32Dcl3 and U937 cells but not for HL-60 and Ba/F3 cells . It was thought that this difference was a result of different responses to G-CSF . G-CSF potentiates Ara-C- and VP-16-induced cytotoxicities through apoptosis induction by mobilizing resting G0-G1-phase cells into S phase .
    OUTPUT:
