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  • Cheng, Jian  (9)
  • Gao, Chong  (9)
  • 1
    Online Resource
    Online Resource
    Rapid Diagnosis of Multidrug Resistance In Leukemia by Electrochemical Biosensor Based on Carbon Nanotubes–Drug Supramolecular Interaction
    American Society of Hematology ; 2010
    In:  Blood Vol. 116, No. 21 ( 2010-11-19), p. 4856-4856
    Details
    In: Blood, American Society of Hematology, Vol. 116, No. 21 ( 2010-11-19), p. 4856-4856
    Abstract: Abstract 4856 Objective: The multidrug resistance (MDR) in leukemia is a major chemotherapy obstacle, rendering many currently available chemotherapeutic drugs ineffective. The aim of this study was to explore the new strategy to early diagnose the MDR by electrochemical biosensor based on carbon nanotubes–drug supramolecular interaction. Methods: The carbon nanotubes modified glassy carbon electrodes (CNTs/GCE) as a sensor were directly immersed into the cells suspension of the sensitive leukemia cells K562 and/or its MDR cells K562/A02 to detect the response of the electrochemical probe of daunorubicin (DNR) residues after incubated with cells. Results: The fresh evidence from the electrochemical studies based on CNTs/GCE demonstrated that the homogeneous, label-free strategy could directly measure the function of cell membrane transporters in MDR cancer cells, identify the cancer cell phenotype (sensitive or MDR). The cathodic peak current showed good linear response to the changes of the fraction of MDR with a correlation coefficient of 0.995 when we further took the different ratios of the sensitive leukemia cells K562 and its MDR ones K562/A02 as the model of MDR levels to simulate the MDR occurrence in leukemia. Then, we can easily predict the MDR fraction based on the calibration curve of the cathodic peak current versus the fraction of MDR according to the obtained peak current. Conclusion: These results indicated that the biosensing assay could provide a powerful tool for assessment of MDR in leukemia. The new electrochemical biosensor based on carbon nanotubes–drug supramolecular interaction could represent promising approach in the rapid diagnosis of MDR in leukemia. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V116.21.4856.4856
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 2
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    Clinical outcomes of transfusion-associated iron overload in patients with refractory chronic anemia
    Informa UK Limited ; 2014
    In:  Patient Preference and Adherence
    Details
    In: Patient Preference and Adherence, Informa UK Limited
    Type of Medium: Online Resource
    ISSN: 1177-889X
    URL: Journal
    URL: Article
    DOI: 10.2147/PPA
    DOI: 10.2147/PPA.S56238
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2014
    detail.hit.zdb_id: 2455848-5
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  • 3
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    Effect of YC-1, a HIF Inhibitor,On Apoptosis of Leukemia Cell.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 4432-4432
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 4432-4432
    Abstract: Abstract 4432 Object This study was purposed to investigate the expression of HIF-1α and VEGF in leukemia cell lines and the effect of YC-1 on the regulation of HIF-1α and VEGF and the induction of apoptosis in U937 cell, exploring the mechanism of apoptosis after treatment of YC-1. Methods RT-PCR was used to determine the levels of HIF-1α mRNA and VEGF mRNA in K562,U937 and Jurkat cells. After treatment of U937 cell with 4μmol/L YC-1 for 0 hour, 8 hours,16 hours and 24 hours respectively, the changes of morphologic features were observed by DAPI staining under fluorescent microscope and the apoptotic rates were assayed by flow cytometry with Annexin V-FITC/PI staining; the levels of HIF-1α mRNA and VEGF mRNA were measured with RT-PCR ; the protein expression of HIF-1α, VEGF, Bax,Bcl-2 and Caspase-3 were measured by Western blot. Results HIF-1α mRNA and VEGF mRNA were expressed in all three leukemia cell lines. After treatment of U937 cell with 4μmol/L YC-1 for 0 hour,8 hours,16hours and 24hours respectively, the typical apoptotic morphologic features of U937 cells were observed under fluorescent microscope and the apoptotic rates were significantly increased in a time-dependent manner, they were (4.87±0.70)%, (27.27±2.00)%, (51.53±2.81) and (60.5±3.20)% respectively, the level of VEGF mRNA reduced, while the level of HIF-1α mRNA had no obviously changes. Furthermore, the expression of HIF-1α, VEGF and Bcl-2 decreased, while the expression of Bax and Caspase-3 increased in a time-dependent manner. Conclusion HIF-1α mRNA and VEGF mRNA are expressed in leukemia, YC-1 has significant effect of down-regulation the protein expression of HIF-1α and VEGF and induction of apoptosis in U937, its mechanisms may involve in up-regulating Bax/Bcl-2 ratio and expression of Caspase-3. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.4432.4432
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 4
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    Online Resource
    The interleukin-10-1082A〉G polymorphism and lymphoma risk: A meta-analysis
    IOS Press ; 2014
    In:  Cancer Biomarkers Vol. 14, No. 5 ( 2014-08-11), p. 381-388
    Details
    In: Cancer Biomarkers, IOS Press, Vol. 14, No. 5 ( 2014-08-11), p. 381-388
    Type of Medium: Online Resource
    ISSN: 1875-8592 , 1574-0153
    URL: Article
    DOI: 10.3233/CBM-140406
    Language: Unknown
    Publisher: IOS Press
    Publication Date: 2014
    detail.hit.zdb_id: 2525487-X
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  • 5
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    Association of Janus Kinase 2(JAK2) A830G Polymorphism with Acute Leukemia Susceptibility.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 1573-1573
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 1573-1573
    Abstract: Abstract 1573 Poster Board I-599 Background Aberrant activation of the The Janus kinase(JAK)/signal transducer and activator of transcription (STAT) pathway may predispose to leukemia cells due to deregulation of proliferation, differentiation or apoptosis. One of the members of this family, JAK2, plays a very important role in metabolizing carcinogens and medications. In this study, we aimed to determine whether any association exists between genetic polymorphism in JAK2 A830G and individual susceptibility to acute leukemia. Method We carried out a case-control study using a China sample set with 243 acute leukemia cases and 282 controls matched by age, ethnicity. 68 of the acute leukemia patients were diagnosed with acute lymphoblastic leukemia (ALL) and 175 patients with acute myeloid leukemia (AML). Genomic DNA was isolated from peripheral blood and genomic DNA samples were assayed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) in the A830G on JAK2 gene. The data were analyzed statistically employing chi-square and logistic regression analyses. Result The frequencies of G/G genotype (wild type) were 4%, 8% and 31.4% in ALL, AML and control groups, respectively. The frequencies of polymorphic G/A genotype (heterozygous variant) were found to be 69% in ALL patients, 71% in AML patients and 48.6% in controls. The A/A genotype (homozygous variant) were existed to be 69% in ALL patients, 20% in AML patients and 20% in controls. Logistic regression analyses showed a significant correlation between the JAK2 A830G polymorphism (G/G) and acute leukemia patients (OR = 1.309, 95% CI =0.839-2.043, p 〈 0.001). Conclusion Our findings indicate that G/G genotype may be an important genetic determinant for acute leukemias. According to our knowledge, this is the first report of an association between acute leukemia cases and the JAK2 A830G polymorphism. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.1573.1573
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 6
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    Effects of 5-Bromotetrandrine and Daunorubicin on the Expression of Survivin In K562/AO2 Cells
    American Society of Hematology ; 2010
    In:  Blood Vol. 116, No. 21 ( 2010-11-19), p. 4947-4947
    Details
    In: Blood, American Society of Hematology, Vol. 116, No. 21 ( 2010-11-19), p. 4947-4947
    Abstract: Abstract 4947 Objective: The aim of this study was to investigate the expression of survivin and the apoptosis induced by DNR and BrTet in the leukemic cells K562/A02. Methods: In a typical experiment, the K562/AO2 cells were treated with daunorubicin (DNR), 5-bromotetrandrine (BrTet), or DNR and BrTet for 48 hours, and the cells treated without any drugs were used as control group. Cell proliferation was analyzed by MTT assay. Cells apoptosis and the concentration of DNR within the cells were measured by Flow cytometry (FCM). The expressions of mRNA and protein of survivin were determined by semi-quantitative reverse transcription PCR (RT-PCR) and Western blot, respectively. Results: The results of MTT assay indicated that DNR and BrTet were both able to inhibit the proliferation of K562/AO2 cells in dose-dependent manner. The fresh evidence from flow cytometry showed that a higher apoptosis rate could be induced and a higer concentration of DNR could be detected in K562/AO2 cells by DNR and BrTet as compared with those by DNR or BrTet in the same concentrations(P 〈 0.01). RT-PCR revealed that the expression of survivin mRNA, a higer expression in K562/AO2 cells with acquired resistance to adriamycin than that in parent K-562 cells, decreased in the DNR and BrTet group (P 〈 0.05), but there was no obvious change in other groups(P 〉 0.05). Western bolt demonstrated that the expression of survivin protein was much lower in the DNR and BrTet group(P 〈 0.05). Conclusion: BrTet could increase the concentration of DNR and reverse the multidrug resistance(MDR) in the K562/AO2 cells. Survivin may play an important role in apoptosis induced by DNR. Survivin could be a target for the treatment of MDR in haematopoietic malignancies. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V116.21.4947.4947
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 7
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    Ultrasound Mediated Drug-Loaded Nanoparticles Crossing Cell Membranes as a New Strategy to Reverse Multidrug Resistance In Human Leukemia Cell Line K562/A02
    American Society of Hematology ; 2010
    In:  Blood Vol. 116, No. 21 ( 2010-11-19), p. 3969-3969
    Details
    In: Blood, American Society of Hematology, Vol. 116, No. 21 ( 2010-11-19), p. 3969-3969
    Abstract: Abstract 3969 Objective: Although many strategies have been explored to overcome the multidrug resistance (MDR) in leukemia which has rendered many currently available chemotherapeutic drugs ineffective, the results have been disappointing to the obstacle. The aim of this study was to investigate whether the new strategy of combining drug-loaded nanoparticles (Nps) and ultrasound (US) would show useful effects on the reversal of MDR in human leukemia cell line K562/A02. Methods: In this study, daunorubicin (DNR), a frequently chemotherapeutic agent known to cause DNA damage and induce apoptosis and cell death, was loaded on the TiO2 Nps which is chemically stable, environmental friendly, and shows weak or non cytotoxic to apply as the nano-drug carrier. The MDR leukemia K562/A02 cells were treated with the DNR-loaded TiO2 Nps drug carrier and US exposure. Then, we examined the effectiveness of delivering DNR into the MDR leukemia K562/A02 cells with the electrochemical studies, observed the bio-effects on the cell viability by MTT assays, investigated the induced apoptosis, and assessed the reversal ability and the mechanism of MDR by combining the drug-loaded Nps and US. Results: We observed good biocompatibility of the therapeutic approach. When the K562/A02 cells were incubated with DNR only, the cathodic current decreased by only 10% normalized to the DNR (10 μg/mL) standard, indicating less DNR was absorbed by the MDR cells. The cathodic current decreased by 39% and 63% in the presence of US or DNR-loaded TiO2 Nps, respectively. In comparison, when the cells were treated by the novel strategy of US mediated drug-loaded Nps crossing cell membranes, the cathodic current of DNR in the supernatant decreased greatly by 82% and became the minimal, which suggesting the least amount of DNR remained outside the MDR cells in this case and the largest uptake into the cells by this new strategy. These observations demonstrated that the remarkable synergistic effect of the novel strategy facilitated the accumulation of DNR in the MDR K562/A02 cells. In addition, our MTT assay illustrated comparative sensitization of the MDR K562/A02 cells under the treatment of US or drug-loaded Nps, but especially enhanced effect by combining drug-loaded Nps and US. The resisting fold of the MDR leukemia K562/A02 became obviously lower, decreasing from 58.71 to 16.69. The fresh evidence from caspase-3 immunocytochemistry demonstrated that the strategy could induce the apoptosis in the cells as well. Conclusion: It was therefore concluded that the strategy could have good reversal ability of MDR in tumor. These findings reveal that the reversal of MDR in tumor by US mediated drug-loaded Nps crossing cell membranes could represent promising approach in cancer therapy. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V116.21.3969.3969
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 8
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    Online Resource
    Microarray-Based Method for Quantificationally Detecting Methylation Changes of E-Cadherin Gene in Acute Leukemia.
    American Society of Hematology ; 2006
    In:  Blood Vol. 108, No. 11 ( 2006-11-16), p. 4406-4406
    Details
    In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 4406-4406
    Abstract: Aberrant DNA methylation of CpG sites is among the earliest and most frequent alterations in cancer. Several studies suggest that aberrant methylation of the CpG sites of the tumor suppressor gene is closely associated with carcinogenesis. So methylation detection is very important. The aim of this study was to describe a microarray-based method for quantificationally detecting changes of E-cadherin methylation in acute leukemia and to simply discuss the effect of microarray on detecting tumor methylation. This method used bisulfite-modified DNA as a template for PCR amplification, resulting in conversion of unmethylated cytosine, but not methylated cytosine, into thymine within CpG islands of interest. Five sets of oligonucleotide probes were designed to fabricate a DNA microarray to detect the methylation changes of E-cadherin gene CpG islands in acute leukemia. Each set contained a pair of methylated and unmethylated oligonucleotides for interrogating 3 or 4 CpG sites in close proximity. By TA cloning, PCR, sequencing, positive and negative DNA targets were obtained. A series of microarray hybridization were performed with mixtures of Cy3 labeled positive and negative DNA targets at different proportions. Next draw a standard curve by fluorescence intensity. Then leukemia samples DNA were abstracted and bisulfite-modified. Sample DNA targets were obtained by PCR amplification and were hybridized with the microarry. Finally the microarry was scanned with ScanArray Lite microarray analysis systems. Five linear relationships(R2=0.9660~0.9963) was established, which said the accuracy and reproducibility of the probes designed for microarray hybridization was good and could be used to eliminate background noise. The experimental results showed that the microarray assay could successfully detect five regions methylation changes of E-cadherin gene in every acute leukemia sample quantificationally. There were different degree of methylation in five acute leukemia samples and the hypermethylation region was the same. The test result was validated by gene sequencing. In tumors E-cadherin expression frequently is reduced, an event that contributes to tumor invasion and metastasis. The methylation of E-cadherin gene promoter is one important reason resulting in the silencing of expression. In normal peripheral blood mononuclear cells and bone marrow, E-cadherin is completely unmethylated. In our results, the methylation of E-cadherin is related to acute leukemia. And the same hypermethylation region may be the critical sites of methylation sites. As shown in this study, the use of a simple control system could test the accuracy and reproducibility of the probes designed for microarray hybridization. This control system can also be used to calibrate the levels of methylation changes detected in the investigated samples by microarray assay. With more and more methylated genes are found, microarray assay could be applied as a useful tool for mapping methylation changes in multiple CpG loci. It’s more time-saving and more labor-saving than gene sequencing and can be readily used to high throughput analysis of DNA methylation. It will contribute significant information to our understanding of CpG island methylation in acute leukemia.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V108.11.4406.4406
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2006
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 9
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    Reversal of Multidrug Resistance by Magnetic Fe3O4 Nanoparticle Copolymerizating Daunorubicin and mdr1-shRNA Expression Vetor in Leukemia Cells.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 4829-4829
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 4829-4829
    Abstract: Abstract 4829 Object In many instances, Multidrug resistance (MDR) is mediated by increased expression at the cell surface of the MDR1 gene product, P-glycoprotein (P-gp), a 170-kD energy-dependent efflux pump. The aim of this study was to investigate the potential benefit of combination therapy with magnetic nanoparticle of Fe3O4 (MNP(Fe3O4)) and mdr1-shRNA Expression vetor.in K562/A02 leukemic cells. Methods To synthesis short hairpin RNA (shRNA)aiming divectly at the target sequence,we choice the 3491-3509,1539-1557and 3103-3121 nucleotide of mdr-1 mRNA as targets. Cloning in the plasmid vetor PGCSilencer-U6-neo-GFP, The recombinant plasmid vetors were called for PGY1-1,PGY1-2 and PGY1-3.The recombinant plasmid vetors were transfected into the cell 1ines K562/A02 by lipofection. After transfected 48 hours,the inhibition of mdr-1mRNA expression and the expression of P-gp was detected by realtime–PCR and Weston-blot, screening the recombinant plasmid vetor which has the most greatest mdr-1 gene inhibition ratio is PGY1-2.Analysis of the reveral ratio of multidrug resistance, the concentration of DNR and the content of mdr-1 gene and P-gp in K562/A02 cell line. Results The combination of daunorubicin (DNR) with either MNP(Fe3O4) or PGY1-2 exerted a potent cytotoxic effect on K562/A02 cells, while MNP(Fe3O4) and PGY1-2 cotreatment can synergistically down regulation the expression of mdr-1 gene and the expression of P-gp(P 〈 0.05). The transfection efficiency was 20%; the concentration of DNR in K562/A02 cell line was obviously elevated (P 〈 0.05);the multidrug resistance index of K562/A02 cell line was obviously decreased (P 〈 0.05). Conclusion MNP(Fe3O4) and PGY1-2 cotreatment can synergistically reveral multidrug resistance. Thus our in vitro data strongly suggests a potential clinical application of MNP(Fe3O4) and PGY1-2 combination on CML. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.4829.4829
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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