scholarly journals Artesunate suppresses tumor growth and induces apoptosis through the modulation of multiple oncogenic cascades in a chronic myeloid leukemia xenograft mouse model

Oncotarget ◽  
2015 ◽  
Vol 6 (6) ◽  
pp. 4020-4035 ◽  
Author(s):  
Chulwon Kim ◽  
Jong Hyun Lee ◽  
Sung-Hoon Kim ◽  
Gautam Sethi ◽  
Kwang Seok Ahn
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Mouse Model ◽  
Tumor Growth ◽  
Myeloid Leukemia ◽  
Xenograft Mouse Model

scholarly journals Thymoquinone Inhibits Tumor Growth and Induces Apoptosis in a Breast Cancer Xenograft Mouse Model: The Role of p38 MAPK and ROS

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e75356 ◽  
Author(s):  
Chern Chiuh Woo ◽  
Annie Hsu ◽  
Alan Prem Kumar ◽  
Gautam Sethi ◽  
Kwong Huat Benny Tan
Keyword(s):  
Breast Cancer ◽  
Mouse Model ◽  
Tumor Growth ◽  
P38 Mapk ◽  
Xenograft Mouse Model ◽  
Breast Cancer Xenograft

scholarly journals Chronic myeloid leukemia-derived exosomes promote tumor growth through an autocrine mechanism

2015 ◽  
Vol 13 (1) ◽  
pp. 8 ◽  
Author(s):  
Stefania Raimondo ◽  
Laura Saieva ◽  
Chiara Corrado ◽  
Simona Fontana ◽  
Anna Flugy ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Tumor Growth ◽  
Myeloid Leukemia ◽  
Promote Tumor Growth ◽  
Autocrine Mechanism

scholarly journals An aging mouse model of human chronic myeloid leukemia

Oncogene ◽  
2021 ◽  
Author(s):  
Taisen Hao ◽  
Chunxiao Zhang ◽  
Zhiqiang Wang ◽  
Alison Buck ◽  
Steven L. Vonderfecht ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Mouse Model ◽  
Myeloid Leukemia ◽  
Aging Mouse

Synergic Effects of Proteasome Inhibitor PS-341 and Tyrosine Kinase Inhibitor STI571 on Chronic Myeloid Leukemia Cells and BCR-ABL Oncoprotein In Vitro and In Vivo.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4771-4771
Author(s):  
Guangbiao Zhou ◽  
Zheng Hu ◽  
Dapeng Liu ◽  
Fuqun Wu ◽  
Jiang Zhu ◽  
...  
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Tumor Growth ◽  
Proteasome Inhibitor ◽  
Myeloid Leukemia ◽  
K562 Cells ◽  
Leukemic Cells ◽  
Great Promise ◽  
Dependent Manner

Abstract STI571/Gleevec/imatinib, a rationally-designed agent that occupies the ATP-binding site of BCR-ABL and stabilizes the protein in its closed, inactive conformation, has been a remarkable success for the treatment of chronic myeloid leukemia (CML). However, a significant proportion of patients chronically treated with STI571 develop resistance because of the acquisition of mutations in the kinase domain of BCR-ABL. Furthermore, the effects of STI571 on CML patients in accelerated phase or blastic crisis are unsatisfactory since many patients relapse after transient remission. Hence, additional drugs or STI571-based combination regimens are desired to circumvent resistance and to improve response rates. Here we reported that PS-341, a proteasome inhibitor which offers great promise to patients with multiple myeloma (MM), significantly enhanced the antileukemia activity of STI571 in vitro and in vivo. We found a synergy exists between low concentrations of PS-341 (5–10 nM) and STI571 (0.1–0.2 μM) in inhibition of cell growth and induction of apoptosis in K562 cell line and CD34+ leukemic cells isolated from CML patients. In K562 cells, combined use of PS-341 and STI571 accelerated activation of caspase-3, 9, and facilitated cleavage of poly-(ADP-ribose) polymerase (PARP) as compared to those in cells treated with PS-341 or STI571 alone. Moreover, PS-341/STI571 combination resulted in potentiated degradation of BCR-ABL and downregulation of phosphorylated BCR-ABL as compared to those in mono treatment. In nude mice inoculated subcutaneously with K562 cells, treatment with PS-341 (injected intraperitoneally, ip) alone (at doses of 0.05, 0.5, 1 mg/kg/d, twice a week for 4 weeks, respectively) decreased tumor growth in a dose-dependent manner. STI571 (ip) at 10 mg/kg/d also inhibited tumor growth. Intriguingly, combinatory administration of low dose PS-341 (0.05 mg/kg/d, twice a week for 4 weeks) and STI571 (10 mg/kg/d) yielded a much more profound inhibition of tumor growth and even clearance of leukemic cells in mice compared to either monotherapy. Taken together, these results demonstrate synergic effects of PS-341 and STI571, and provide the rationale to evaluate PS-341/STI571 combination in treating CML aiming to further improve clinical outcome of patients.

Synergistic Effect of Sequential Combination of Decitabine and Idarubicin in Mouse Model of Human Acute Myeloid Leukemia

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1515-1515
Author(s):  
Hongyan Tong ◽  
Kongfei Li ◽  
Chen Mei ◽  
Chao Hu ◽  
Jie Jin
Keyword(s):  
Acute Myeloid Leukemia ◽  
Mouse Model ◽  
Synergistic Effect ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Myeloid Leukemia ◽  
Wnt Pathway ◽  
Sequential Combination ◽  
Acute Myeloid

Abstract Abstract 1515 Background: Decitabine is a prototype for epigenetic therapy in cancer which targets DNA methyltransferase. While it was known that decitabine monotherapy has been associated with a relative low rate of complete remission rates in acute myeloid leukemia and myelodysplastic syndrome. Several groups have attempted to increase the response rate with decitabine-based therapy by developing combinations. In the preliminary experiments, we investigated the effect of anti-leukemia drugs (idarubicin, daunorubicin, cytarabine, thalidomide and homoharringtonine) in combination simultaneously or sequentially with decitabine of inhibiting proliferation of acute myeloid leukemia cell lines. The result showed that sequential combination of decitabine and idarubicin induced a significant synergistic effect in cell apoptosis, inhibition of cell proliferation. With the gene chip technology, we found that the gene expression of Wnt pathway changed obviously after the treatment of DAC combined with IDA. Further we confirm that sequential combination of DAC and IDA caused depression of wnt pathway in vitro. In this study, we evaluate the anti-leukemic effect and the combination mechanism of DAC in sequential combination with IDA in vivo. Methods: The AML cell line U937 (14×107 cells per animal) were injected subcutaneously into the right flank of 6 to 8-week old NOD-SCID mice. After tumor growth, decitabine(0.5mg/kg/day) were injected intraperitoneal of a five consecutive days followed by a three days of idarubicin(0.5 mg/kg/day). The tumor growth inhibition effect was evaluated by microPET to reveal the synergistic effect of decitabine and idarubicin. Using TUNEL method and electron microscopy, we detected the apoptosis of leukemic cells from tumor bearing mice. The expression of β-catenin which is the key gene of Wnt/β-catenin pathway was also examined by immunochemistry. We then detected the expression of protein levels of the other genes(cyclinD1, c-myc, SFRP1,HDPR1 and DKK3) of Wnt/β-catenin pathway in tumor cells of tumor-bearing mice by western blot. Results: In vivo, the effect of sequential combination of decitabine and idarubicin was initially examined in a subcutaneous AML mouse model. The AML cell line U937(1×107 cell per animal) was transplanted subcutaneously into the right flank of 2-week-old female NOD-SCID mouse. The cell line developed into a rapidly growing tumor. Treatment was initiated in 7th days after injection of the leukemic cells, included with 5 days of decitabine alone, 3 days of idarubicin alone and 5 days of decitabine followed by 3 days of idarubicin. A significant inhibition of tumor growth was demonstrated with microPET in animals treated with sequential combination of decitabine and idarubicin compared with the other treatment and control group animals. The apoptosis of tumor cells was also significantly increased in the sequential combination treatment group detected by TUNEL and electron microscope. We also found that the sequential treatment group induced synergistic effect in re-expression or up-expression of the Wnt inhibitor genes (SFRP1, HDPR1 and DKK3) in tumor cells. Furthermore, the down-steam genes of wnt pathway including β-catenin, c-myc and cyclinD1 were down-regulated which suggest depression of wnt/β-catenin pathway. These results suggest that sequential combination of decitabine and idarubicin has a powerful anti-leukemic effect not only in vitro but also in vivo. Conclusion: Our results demonstrate decitabine in sequential combination with idarubicin in mouse model of AML and suggest that this combination may be of clinical value in the treatment of patients with AML. Disclosures: No relevant conflicts of interest to declare.

Multiparameter urine analysis for quantitative bladder cancer surveillance of orthotopic xenografted mice

Lab on a Chip ◽  
2020 ◽  
Vol 20 (3) ◽  
pp. 634-646 ◽  
Author(s):  
Xiaotian Tan ◽  
Luke J. Broses ◽  
Menglian Zhou ◽  
Kathleen C. Day ◽  
Wenyi Liu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Mouse Model ◽  
Tumor Growth ◽  
Urine Analysis ◽  
Cancer Surveillance ◽  
Cancer Markers ◽  
Xenograft Mouse Model ◽  
Orthotopic Xenograft

A method utilizing urinary cancer markers to monitor tumor growth in a bladder cancer orthotopic xenograft mouse model.

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