scholarly journals Metabolomics identifies the intersection of phosphoethanolamine with menaquinone-triggered apoptosis in an in vitro model of leukemia

2015 ◽  
Vol 11 (9) ◽  
pp. 2406-2416 ◽  
Author(s):  
Suganthagunthalam Dhakshinamoorthy ◽  
Nha-Truc Dinh ◽  
Jeffrey Skolnick ◽  
Mark P. Styczynski

We characterize the anti-proliferative activity of menaquinone in a leukemia cell line and use metabolomics to link it to phosphoethanolamine.

1996 ◽  
Vol 24 (4) ◽  
pp. 581-587
Author(s):  
Cristiana Zanetti ◽  
Arrnalaura Stammati ◽  
Orazio Sapora ◽  
Flavia Zucco

The aim of this study was to investigate the endpoints related to cell death, either necrosis or apoptosis, induced by four chemicals in the promyelocytic leukemia cell line, HL-60. Cell morphology, DNA fragmentation, cytofluorimetric analysis and oxygen consumption were used to classify the type of cell death observed. In our analysis, we found that not all the selected parameters reproduced the differences observed in the cell death caused by the four chemicals tested. As cell death is a very complex phenomenon, several factors should be taken into account (cell type, exposure time and chemical concentration), if chemicals are to be classified according to differences in the mechanisms more directly involved in cell death.


Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1233-1244 ◽  
Author(s):  
SJ Collins

Abstract The HL-60 cell line, derived from a single patient with acute promyelocytic leukemia, provides a unique in vitro model system for studying the cellular and molecular events involved in the proliferation and differentiation of normal and leukemic cells of the granulocyte/monocyte/macrophage lineage.


Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1233-1244 ◽  
Author(s):  
SJ Collins

The HL-60 cell line, derived from a single patient with acute promyelocytic leukemia, provides a unique in vitro model system for studying the cellular and molecular events involved in the proliferation and differentiation of normal and leukemic cells of the granulocyte/monocyte/macrophage lineage.


Blood ◽  
2004 ◽  
Vol 103 (7) ◽  
pp. 2802-2805 ◽  
Author(s):  
Jan Cools ◽  
Hilmar Quentmeier ◽  
Brian J. P. Huntly ◽  
Peter Marynen ◽  
James D. Griffin ◽  
...  

Abstract We recently identified the chimeric kinase FIP1L1-platelet-derived growth factor receptor α (PDGFRα) as a cause of the hypereosinophilic syndrome and of chronic eosinophilic leukemia. To investigate the role of FIP1L1-PDGFRA in the pathogenesis of acute leukemia, we screened 87 leukemia cell lines for the presence of FIP1L1-PDGFRA. One cell line, EOL-1, expressed the FIP1L1-PDGFRA fusion. Three structurally divergent kinase inhibitors—imatinib (STI-571), PKC412, and SU5614—inhibited the growth of EOL-1 cells. These results indicate that the fusion of FIP1L1 to PDGFRA occurs rarely in leukemia cell lines, but they identify EOL-1 as an in vitro model for the study of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia and for the analysis of small molecule inhibitors of FIP1L1-PDGFRα. (Blood. 2004;103:2802-2805)


1979 ◽  
Vol 149 (4) ◽  
pp. 969-974 ◽  
Author(s):  
S J Collins ◽  
F W Ruscetti ◽  
R E Gallagher ◽  
R C Gallo

The HL-60 human promyelocytic leukemia cell line can be induced to terminally differentiate to mature myeloid cells sharing a number of functional characteristics with normal granulocytes including response to chemoattractants, development of complement receptors, phagocytosis, superoxide production, and nitroblue tetrazolium dye reduction. Hence the Me2SO-induced HL-60 cells provide a unique in vitro model for studying various important aspects of human myeloid cell differentiation.


1990 ◽  
Vol 81 (5) ◽  
pp. 449-453 ◽  
Author(s):  
Terutaka Sagawa ◽  
Takeshi Kodama ◽  
Akio Tominaga ◽  
Mariko Okada

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