In vitro differentiation of Rauscher-virus-induced myeloid leukemia cells

1976 ◽  
Vol 17 (6) ◽  
pp. 789-797 ◽  
Author(s):  
Y. Ichikawa ◽  
M. Maeda ◽  
M. Horiuchi
Keyword(s):  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
In Vitro Differentiation ◽  
Rauscher Virus

AZD1152, a novel and selective aurora B kinase inhibitor, induces growth arrest, apoptosis, and sensitization for tubulin depolymerizing agent or topoisomerase II inhibitor in human acute leukemia cells in vitro and in vivo

Blood ◽  
2007 ◽  
Vol 110 (6) ◽  
pp. 2034-2040 ◽  
Author(s):  
Jing Yang ◽  
Takayuki Ikezoe ◽  
Chie Nishioka ◽  
Taizo Tasaka ◽  
Ayuko Taniguchi ◽  
...  
Keyword(s):  
Myeloid Leukemia ◽  
Topoisomerase Ii ◽  
Growth Arrest ◽  
Leukemia Cells ◽  
Aurora B ◽  
Thymidine Uptake ◽  
Aurora B Kinase ◽  
Aurora Kinases ◽  
Topoisomerase Ii Inhibitor

Abstract Aurora kinases play an important role in chromosome alignment, segregation, and cytokinesis during mitosis. We have recently shown that hematopoietic malignant cells including those from acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) aberrantly expressed Aurora A and B kinases, and ZM447439, a potent inhibitor of Aurora kinases, effectively induced growth arrest and apoptosis of a variety of leukemia cells. The present study explored the effect of AZD1152, a highly selective inhibitor of Aurora B kinase, on various types of human leukemia cells. AZD1152 inhibited the proliferation of AML lines (HL-60, NB4, MOLM13), ALL line (PALL-2), biphenotypic leukemia (MV4-11), acute eosinophilic leukemia (EOL-1), and the blast crisis of chronic myeloid leukemia K562 cells with an IC50 ranging from 3 nM to 40 nM, as measured by thymidine uptake on day 2 of culture. These cells had 4N/8N DNA content followed by apoptosis, as measured by cell-cycle analysis and annexin V staining, respectively. Of note, AZD1152 synergistically enhanced the antiproliferative activity of vincristine, a tubulin depolymerizing agent, and daunorubicin, a topoisomerase II inhibitor, against the MOLM13 and PALL-2 cells in vitro. Furthermore, AZD1152 potentiated the action of vincristine and daunorubicin in a MOLM13 murine xenograft model. Taken together, AZD1152 is a promising new agent for treatment of individuals with leukemia. The combined administration of AZD1152 and conventional chemotherapeutic agent to patients with leukemia warrants further investigation.

Lineage-specific expression of c-fos and c-fms in human hematopoietic cells: Discrepancies with the in vitro differentiation of leukemia cells

1987 ◽  
Vol 33 (3) ◽  
pp. 56-60
Author(s):  
Hans Kreipe ◽  
Heinz J. Radzun ◽  
Klaus Heidorn ◽  
Mohammad Reza Parwaresch ◽  
Bernard Verrier ◽  
...  
Keyword(s):  
Hematopoietic Cells ◽  
Leukemia Cells ◽  
In Vitro Differentiation ◽  
Specific Expression

siRNA/lipopolymer nanoparticles to arrest growth of chronic myeloid leukemia cells in vitro and in vivo

2018 ◽  
Vol 130 ◽  
pp. 66-70 ◽  
Author(s):  
Juliana Valencia-Serna ◽  
Hamidreza M. Aliabadi ◽  
Adam Manfrin ◽  
Mahsa Mohseni ◽  
Xiaoyan Jiang ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Arrest Growth

Augmentation of Hydroxyurea Cytotoxicity by Sintamil in Human Chronic Myeloid Leukemia Cells

1986 ◽  
Vol 72 (5) ◽  
pp. 507-510
Author(s):  
Seema G. Pradhan ◽  
Manik P. Chitnis ◽  
Vathsala S. Basrur ◽  
K. Satyamoorthy ◽  
Suresh H. Advani
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Nucleic Acids ◽  
Cytotoxic Activity ◽  
Exposure Time ◽  
Myeloid Leukemia ◽  
Exposure Dose ◽  
Leukemia Cells ◽  
Vitro Effect

The in vitro effect of sintamil, as a modulator alone and in combination with hydroxyurea (HU), on cytotoxicity was studied in 16 cases of human chronic myeloid leukemia (CML). We investigated the cytotoxicity of the drugs as a function of the exposure dose (HU, 10−4 M; sintamil, 10 μg/ml) and the exposure time (1 h) to the agent. Cytotoxicity was evaluated as the inhibition of incorporation of [3H-methyl]thymidine in the nucleic acids of CML cells. Cytotoxicity of HU was greatly enhanced (P < 0.001) by 1 h exposure of the CML cells to sintamil. The present data indicate that sintamil potentiates the cytotoxic activity of HU in CML cells.

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