scholarly journals C1206, a novel curcumin derivative, potently inhibits Hsp90 and human chronic myeloid leukemia cells in vitro

2017 ◽  
Vol 39 (4) ◽  
pp. 649-658 ◽  
Author(s):  
Ying-juan Fan ◽  
Yi-xiang Zhou ◽  
Lian-ru Zhang ◽  
Qiao-fa Lin ◽  
Ping-zhang Gao ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Curcumin Derivative

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.

Enhanced Growth Suppression of Philadephia1 Leukemia Cells in Mice by Targeting Both BCR-ABL and VEGF through the Antisense Strategy.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 5257-5257
Author(s):  
Zhong Chao Han ◽  
Xiu Li Cong ◽  
Bin Li ◽  
Ren Chi Yang
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Microvessel Density ◽  
Myeloid Leukemia ◽  
K562 Cells ◽  
Chemotherapeutic Agents ◽  
Leukemia Cells ◽  
Vegf Expression ◽  
Erythroleukemia Cell

Abstract The Philadephia chromosome (Ph1) translocation results in the formation of the BCR-ABL oncogene in over 95% patients with chronic myeloid leukemia (CML). VEGF levels are elevated both in the plasma of CML patients and in conditioned media taken from CML cells. Therefore, simultaneous targeting of BCR-ABL and VEGF might be a rational strategy for attempting treatment of Philadephia1 leukemia. To test this hypothesis, we used an antisense strategy to downregulate BCR-ABL and VEGF expression in K562 cells, a human erythroleukemia cell line. In vitro, combination of bcr/abl and VEGF antisense oligodeoxyribonucleotides (AS-ODNs) exerted a specific synergistic antiproliferative effect on K562 cells and prominently sensitized K562 cells to apoptosis-inducing stimuli. In vivo, nude mice injected with K562 cells were treated systemically with BCR-ABL or VEGF AS-ODNs or with both ODNs in combination. In comparison with the mice treated with individual agents, the mice treated with both ODNs showed a slower growth of leukemia tumors, a reduction of microvessel density and an increased apoptosis in the tumors. These results demonstrate that targeting both BCR-ABL and VEGF may represent an excellent strategy to overcome the resistance to chemotherapeutic agents and ultimately to augment the efficacy of chemotherapy in CML.

Inhibitory Effects of Homoharringtonine on Leukemic Stem Cells and BCR-ABL Induced Chronic Myeloid Leukemia and Acute Lymphoblastic Leukemia in Mice.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2912-2912 ◽  
Author(s):  
Yaoyu Chen ◽  
Yiguo Hu ◽  
Shawnya Michaels ◽  
Dennis Brown ◽  
Shaoguang Li
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Acute Lymphoblastic Leukemia ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cells ◽  
Leukemic Stem Cells ◽  
Lymphoid Leukemia

Abstract The Abl tyrosine kinase inhibitors (TKIs) imatinib mesylate (IM) and dasatinib, targeting BCR-ABL for the treatment of Philadelphia-positive (Ph+) leukemia including chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL), have produced impressive results in terms of therapeutic outcome and safety for patients. However, clinical resistance to these TKIs likely at the level of leukemic stem cell negates curative results in Ph+ leukemia. At present, an anti-stem cell strategy has not been developed for treating these leukemia patients. Homoharringtonine (HHT) (omacetaxine mepesuccinate - USAN/INN designation) has shown significant clinical activity in CML in combination with IM or alone for patients failing IM. However, little is known about whether HHT has an inhibitory effect on leukemic stem cells. The purpose of this study is to determine whether HHT inhibits BCR-ABL-expressing leukemic stem cells (Lin-c-Kit+Sca-1+) that we identified previously (Hu et al. Proc Natl Acad Sci USA 103(45):16870–16875, 2007) and to evaluate therapeutic effects of HHT on CML and B-ALL in mice. We find that in our in vitro stem cell assay, greater than 90% of leukemic stem cells were killed after being treating with HHT (12.5, 25, and 50 nM) for 6 days, and in contrast, greater than 75% or 92% of leukemic stem cells survived the treatment with dasatinib (100 nM) or imatinib (2 mM). We next treated CML mice with HHT (0.5 mg/kg, i.p., once a day). 4 days after the treatment, FACS analysis detected only 2% GFP+Gr–1+ myeloid leukemia cells in peripheral blood of HHT -treated CML mice and in contrast, 41% GFP+Gr–1+ myeloid leukemia cells in placebo-treated mice. We also treated mice with BCR-ABL induced B-ALL with HHT, and found that only 0.78% GFP+B220+ lymphoid leukemia cells were detected in peripheral blood compared to 34% GFP+B220+ lymphoid leukemia cells in placebo-treated mice. Furthermore, HHT significantly inhibited in vitro proliferation of K562 and B-lymphoid leukemic cells isolated from mice with B-ALL induced by BCR-ABL wild type and BCR-ABL-T315I resistant to both imatinib and dasatinib. In sum, HHT has an inhibitory activity against CML stem cells, and is highly effective in treating CML and B-ALL induced by BCR-ABL in mice.

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