Effect of cyclosporin A on daunorubicin accumulation in multidrug-resistant P388 leukemia cells measured by real-time flow cytometry

1989 ◽  
Vol 23 (5) ◽  
pp. 296-300 ◽  
Author(s):  
Kees Nooter ◽  
Robert Oostrum ◽  
Richard Jonker ◽  
Herman van Dekken ◽  
Willem Stokdijk ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cyclosporin A ◽  
Real Time ◽  
Multidrug Resistant ◽  
Leukemia Cells ◽  
P388 Leukemia ◽  
Time Flow

scholarly journals Near Real-Time Flow Cytometry Monitoring of Bacterial and Viral Removal Efficiencies during Water Reclamation Processes

Water ◽  
2016 ◽  
Vol 8 (10) ◽  
pp. 464 ◽  
Author(s):  
Xiao Huang ◽  
Zheng Zhao ◽  
Dana Hernandez ◽  
Sunny Jiang
Keyword(s):  
Flow Cytometry ◽  
Real Time ◽  
Water Reclamation ◽  
Time Flow ◽  
Removal Efficiencies

APX3330 inhibition of the redox function of ape-1/ref-1 (Ref-1) in promyelocytic leukemia cells enhances retinoic acid (ATRA) induced myeloid differentiation and limits cell proliferation as an approach to the prevention of the retinoic acid syndrome (RAS)

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e14613-e14613
Author(s):  
K. A. Robertson ◽  
E. S. Colvin ◽  
M. R. Kelley ◽  
M. L. Fishel
Keyword(s):  
Flow Cytometry ◽  
Retinoic Acid ◽  
Cell Growth ◽  
Real Time ◽  
Real Time Pcr ◽  
Mapk Pathway ◽  
Promyelocytic Leukemia ◽  
Leukemia Cells ◽  
Myeloid Differentiation ◽  
Granulocytic Differentiation

e14613 Background: ATRA + chemotherapy has improved the treatment of promyelocytic leukemia(APL). However, 25% of ATRA treated APL patients experience toxicities that comprise the RAS (life-threatening respiratory distress, edema, renal failure, hypotension, coagulopathy and rising blast count). One approach to prevent RAS is to limit blast proliferation and enhance myeloid differentiation. Ref-1 is a DNA repair protein that functions in redox regulation of cellular proteins, such as Fos, Jun, p53, and NFkB. HL60 myeloid leukemia cells are promyeloblasts that respond to ATRA with granulocytic differentiation/growth arrest. Prior studies suggest Ref-1 redox control is integral to ATRA-induced differentiation. To define the role of the redox function of Ref-1, we used the Ref-1 specific drug, APX3330, to block Ref-1 redox function and examined the response of HL60 cells to ATRA. Methods: Cell growth assessed using trypan blue. Differentiation was evaluated by morphology and expression of CD11b by flow cytometry. Apoptosis was assayed by annexin-PI staining on flow cytometry and cell cycle analysis assayed with propidium iodide flow cytometry. To assess activation of the MAPK pathway, BLR-1 expression was determined by real time PCR. Results: 1) APX3330 blockade of Ref-1 redox function resulted in limited cell growth yet a profound increase in differentiation and a moderate increase in apoptosis. 2) dose dependent studies with ATRA showed a similar degree of differentiation in cells treated with 10 μM ATRA to cells treated with APX3330 + 0.01 μM ATRA; allowing HL60 cells + APX3330 to give a similar response to a 1000 fold lower dose of ATRA. APX3330 alone did not induce differentiation and induced only minimal apoptosis but in combination with ATRA, increased the number of cells in G1/G0 phase significantly. 3) APX3330 + ATRA increased BLR-1 expression significantly by real time PCR suggesting enhanced activation of the MAPK pathway. Conclusions: APX3330 + ATRA limits HL60 growth and dramatically enhances terminal granulocytic differentiation. These finding may provide a therapeutic approach for prevention of the RAS. No significant financial relationships to disclose.

Continuous Monitoring of Enzymatic Reactions on Surfaces by Real-Time Flow Cytometry: Sortase A Catalyzed Protein Immobilization as a Case Study

2014 ◽  
Vol 25 (8) ◽  
pp. 1492-1500 ◽  
Author(s):  
Tobias Heck ◽  
Phu-Huy Pham ◽  
Frederik Hammes ◽  
Linda Thöny-Meyer ◽  
Michael Richter
Keyword(s):  
Flow Cytometry ◽  
Real Time ◽  
Continuous Monitoring ◽  
Protein Immobilization ◽  
Sortase A ◽  
Enzymatic Reactions ◽  
Time Flow

A quantitative method for measuring innate phagocytosis by human monocytes using real-time flow cytometry

2013 ◽  
Vol 85 (4) ◽  
pp. 313-321 ◽  
Author(s):  
Ben J. Gu ◽  
Chun Sun ◽  
Stephen Fuller ◽  
Kristen K. Skarratt ◽  
Steven Petrou ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Real Time ◽  
Quantitative Method ◽  
Human Monocytes ◽  
Time Flow

scholarly journals Shikonin Derivatives from Onsoma visianii Decrease Expression of Phosphorylated STAT3 in Leukemia Cells and Exert Antitumor Activity

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1147
Author(s):  
Zeljko Todorovic ◽  
Jelena Milovanovic ◽  
Dragana Arsenijevic ◽  
Nenad Vukovic ◽  
Milena Vukic ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Death ◽  
Antitumor Activity ◽  
Real Time ◽  
Leukemia Cells ◽  
Antitumor Effects ◽  
Shikonin Derivatives ◽  
Phosphorylated Stat3

Antitumor effects of shikonins on chronic lymphocytic leukemia (CLL) and B-cell prolymphocytic leukemia (B-PLL) are mostly unexplored. The antitumor activity of shikonins, isolated from Onosma visianii Clem (Boraginaceae), in BCL1, mouse CLL cells and JVM-13, human B-PLL cells was explored in this study. The cytotoxicity of shikonin derivatives was measured by an MTT test. Cell death, proliferation, cell cycle, and expression of molecules that control these processes were analyzed by flow cytometry. Expression of STAT3-regulated genes was analyzed by real-time q-RT-PCR (Quantitative Real-Time Polymerase Chain Reaction). The antitumor effects of shikonin derivatives in vivo were analyzed, using flow cytometry, by detection of leukemia cells in the peripheral blood and spleens of mice intravenously injected with BCL1 cells. The two most potent derivatives, isobutyrylshikonin (IBS) and α-methylbutyrylshikonin (MBS), induced cell cycle disturbances and apoptosis, inhibited proliferation, and decreased expression of phospho-STAT3 and downstream-regulated molecules in BCL1 and JVM-13 cells. IBS and MBS decreased the percentage of leukemia cells in vivo. The link between the decrease in phosphorylated STAT3 by MBS and IBS and BCL1 cell death was confirmed by detection of enhanced cell death after addition of AG490, an inhibitor of Jak2 kinase. It seems that IBS and MBS, by decreasing STAT3 phosphorylation, trigger apoptosis, inhibit cell proliferation, and attenuate leukemia cell stemness.

Antiproliferative Effects of Mitoxantrone in Adr-Sensitive and Adr-Resistant P388 Leukemia Cells Enhanced by Vitamin K3

1991 ◽  
Vol 77 (6) ◽  
pp. 484-490 ◽  
Author(s):  
Hemant Parekh ◽  
Surendra Chavan ◽  
Manik Chitnis
Keyword(s):  
Vitamin K ◽  
Multidrug Resistant ◽  
Dna Strand Breaks ◽  
Leukemia Cells ◽  
Vitamin K3 ◽  
Antitumor Effects ◽  
Antiproliferative Effects ◽  
Strand Breaks ◽  
P388 Leukemia ◽  
Dna Strand

Vitamin K3 was employed as a resistance-modifying agent to Investigate its activity in enhancing mitoxantrone (MITO)-induced cytotoxicity in parental (P388/S) and multidrug resistant (P388/ADR) P388 leukemia cells. Vitamin K3 potentiated the antitumor effects of MITO in P388/S and P388/ ADR tumor cells as monitored by inhibition of tumor cell survival (MTT assay). MITO and vitamin K3 in combination effected an enhanced inhibition of [3H]thymidine (DNA synthesis) and [3H]uridine (RNA synthesis) and also Increased the life span of the sensitive and resistant tumor-bearing animals. The effect of vitamin K3 on the induction of DNA strand breaks by MITO was also examined. Increased fragmentation of DNA was illustrated in the sensitive and resistant P388 leukemia cells exposed to the combination. Observations indicate the restoration of sensitivity in P388/ADR cells to MITO by vitamin K3 that may be due to its ability to increase the MITO-induced DNA strand breaks.

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