26 results on '"Xu, Duo-Rong"'
Search Results
2. Negative implication of C-MYC as an amplification target in esophageal cancer
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Huang, Xiao-Ping, Rong, Tie-Hua, Wang, Jun-Ye, Tang, Ya-Qiong, Li, Bao-Jiang, Xu, Duo-Rong, Zhao, Mei-Qing, Zhang, Lan-Jun, Fang, Yan, Su, Xiao-Dong, and Liang, Qi-Wan
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- 2006
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3. Harvesting peripheral blood stem cells from major ABO mismatched donors using COM.TEC blood cell separator
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Wang, He-hua, Chen, Hui-zhen, Zou, Wai-yi, Xu, Duo-rong, and Chen, Yun-xian
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- 2011
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4. The VAD Scheme versus Thalidomide plus VAD for Reduction of Vascular Endothelial Growth Factor in Multiple Myeloma: A Meta-Analysis
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He, Gan-Lin, Xu, Duo-Rong, Zou, Wai-Yi, He, Sui-Zhi, and Li, Juan
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Article Subject ,parasitic diseases ,cardiovascular diseases ,biological phenomena, cell phenomena, and immunity - Abstract
The VAD (vincristine-doxorubicin-dexamethasone) regimen has been used for decades to treat multiple myeloma (MM). Based on reports that vascular endothelial growth factor- (VEGF-) mediated angiogenesis is critical for MM pathogenesis, the antiangiogenic compound thalidomide has been added to VAD (T-VAD). However, it remains unclear whether T-VAD is more efficacious than VAD for serum VEGF reduction or if the difference influences clinical outcome. Pubmed, Cochrane library, China Biomedical Literature (CBM) database, China National Knowledge Infrastructure (CNKI) database, Vip database, and Wanfang database were searched for relevant studies published up to June 2017. RevMan5.2 was used for methodological quality evaluation and data extraction. Thirteen trials (five randomized, seven nonrandomized, and one historically controlled) involving 815 cases were included. Serum VEGF was significantly higher in MM cases than non-MM controls (MD=353.01, [95%CI 187.52–518.51], P
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- 2018
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5. Inhibition of mitotic kinase Aurora suppresses Akt-1 activation and induces apoptotic cell death in all-trans retinoid acid-resistant acute promyelocytic leukemia cells
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Long Zi-Jie, Huang Shan, Xu Duo-Rong, Chen Jia-Jie, Zou Zheng-Zhi, Li Juan, Lin Dong-Jun, and Liu Quentin
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Medicine - Abstract
Abstract Background Aurora kinase ensures accurate chromosome segregation during cell cycle, maintaining genetic integrity in cell division. VX-680, a small-molecule Aurora kinase inhibitor, interferes with mitotic entry and formation of bipolar spindles. Here, we evaluated VX-680 as a potential agent for treatment of all-trans retinoid acid (ATRA)-resistant acute promyelocytic leukemia (APL) in vitro. Methods CD11b expression was utilized to assess cell differentiation by flow cytometry. Immunofluorescence staining was conducted to analyze formation of cell monopolar spindle. Cell proliferation was evaluated by MTT assay. Sub-G1 population and Annexin V/PI staining were used to measure cell apoptosis. Hoechst 33342 staining was applied for identifying morphological changes in nucleus of apoptotic cell. Aurora-A (Aur-A) activation and the signaling pathways involved in apoptosis were detected by Western blot. JC-1 probe was employed to measure mitochondrial depolarization. Results VX-680 inhibited Aur-A by reducing autophosphorylation at the activation site, Thr288, accompanied by producing monopolar mitotic spindles in APL cell line NB4-R2 that was resistant to ATRA. In addition, we found that VX-680 inhibited cell proliferation as assessed by MTT assay. Flow cytometry showed that VX-680 led to apoptotic cell death in both dose- and time-dependent manners by either Sub-G1 or Annexin V/PI analysis. Hoechst 33342 staining represented typical apoptotic cells with nuclear fragmentation in VX-680 treated cells. Importantly, VX-680 inhibition of Aurora kinase suppressed Akt-1 activation and induced mitochondrial depolarization, which eventually resulted in apoptosis by activation of caspase pathway, as indicated by increasing proteolytic cleavage of procaspase-3 and poly ADP ribose polymerase (PARP) in NB4-R2 cells. Conclusions Our study suggested potential clinical use of mitotic Aurora kinase inhibitor in targeting ATRA-resistant leukemic cells.
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- 2011
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6. Curcumin reduces expression of Bcl-2, leading to apoptosis in daunorubicin-insensitive CD34+ acute myeloid leukemia cell lines and primary sorted CD34+ acute myeloid leukemia cells
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Huang Sheng-Shan, Long Zi-Jie, Zheng Fei-Meng, Xu Duo-Rong, Rao Jia, Wu Xing, Zhou Wei-Hua, Huang Ren-Wei, and Liu Quentin
- Subjects
Medicine - Abstract
Abstract Background Acute myeloid leukemia (AML) is an immunophenotypically heterogenous malignant disease, in which CD34 positivity is associated with poor prognosis. CD34+ AML cells are 10-15-fold more resistant to daunorubicin (DNR) than CD34- AML cells. Curcumin is a major component of turmeric that has shown cytotoxic activity in multiple cancers; however, its anti-cancer activity has not been well studied in DNR-insensitive CD34+ AML cells. The aim of this study was to therefore to explore curcumin-induced cytotoxicity in DNR-insensitive CD34+ AML cell lines (KG1a, Kasumi-1), DNR-sensitive U937 AML cells, and primary CD34+ AML bone-marrow-derived cells. Methods Primary human CD34+ cells were isolated from peripheral blood mononuclear cells or bone marrow mononuclear cells using a CD34 MicroBead kit. The growth inhibitory effects of curcumin were evaluated by MTT and colony-formation assays. Cell cycle distribution was examined by propidium iodide (PI) assay. Apoptosis was analyzed by Wright-Giemsa, Hoechst 33342 and Annexin-V/PI staining assays. The change in mitochondrial membrane potential (MMP) was examined by JC-1 staining and flow cytometry. Expression of apoptosis-related proteins was determined by reverse transcription-polymerase chain reaction and Western blotting. Short interfering RNA (siRNA) against Bcl-2 was used in CD34+ KG1a and Kasumi-1 cells incubated with/without DNR. Results Curcumin inhibited proliferation and induced apoptosis and G1/S arrest in both DNR-insensitive KG1a, Kasumi-1 and DNR-sensitive U937 cells. Curcumin-induced apoptosis was associated with reduced expression of both Bcl-2 mRNA and protein, subsequent loss of MMP, and activation of caspase-3 followed by PARP degradation. Curcumin synergistically enhanced the cytotoxic effect of DNR in DNR-insensitive KG1a and Kasumi-1 cells, consistent with decreased Bcl-2 expression. Accordingly, siRNA against Bcl-2 increased the susceptibility of KG1a and Kasumi-1 cells to DNR-induced apoptosis. More importantly, curcumin suppressed Bcl-2 expression, selectively inhibited proliferation and synergistically enhanced the cytotoxicity of DNR in primary CD34+ AML cells, while showing limited lethality in normal CD34+ hematopoietic progenitors. Conclusion Curcumin down-regulates Bcl-2 and induces apoptosis in DNR-insensitive CD34+ AML cell lines and primary CD34+ AML cells.
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- 2011
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7. Allogeneic Bone-Marrow-Derived Mesenchymal stromal Cells Expanded in vitro for Treatment of Aplastic Anemia: A Multicenter Phase II Trial
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Pang, Yan, primary, Xiao, Hao-Wen, additional, Zhang, Hang, additional, Liu, Zeng-Hui, additional, Li, Li, additional, Gao, Yang, additional, Li, Hong-Bo, additional, Jiang, Zu-Jun, additional, Tan, Huo, additional, Lin, Jing-Ren, additional, Du, Xin, additional, Weng, Jian-Yu, additional, Nie, Da-Nian, additional, Lin, Dong-Jun, additional, Zhang, Xiang-Zhong, additional, Liu, Qi-Fa, additional, Xu, Duo-Rong, additional, Chen, Hai-Jia, additional, Ge, Xiao-Hu, additional, Wang, Xiao-Yan, additional, and Xiao, Yang, additional
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- 2017
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8. Targeting GLI1 Suppresses Cell Growth and Enhances Chemosensitivity in CD34+ Enriched Acute Myeloid Leukemia Progenitor Cells
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Long, Bing, primary, Wang, Le-Xun, additional, Zheng, Fei-Meng, additional, Lai, Shu-Ping, additional, Xu, Duo-Rong, additional, Hu, Yuan, additional, Lin, Dong-Jun, additional, Zhang, Xiang-Zhong, additional, Dong, Lin, additional, Long, Zi-Jie, additional, Tong, Xiu-Zhen, additional, and Liu, Quentin, additional
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- 2016
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9. Targeting GLI1 Suppresses Cell Growth and Enhances Chemosensitivity in CD34+ Enriched Acute Myeloid Leukemia Progenitor Cells.
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Long, Bing, Wang, Le-Xun, Zheng, Fei-Meng, Lai, Shu-Ping, Xu, Duo-Rong, Hu, Yuan, Lin, Dong-Jun, Zhang, Xiang-Zhong, Dong, Lin, Long, Zi-Jie, Tong, Xiu-Zhen, and Liu, Quentin
- Subjects
LEUKEMIA genetics ,STEM cells ,CANCER chemotherapy ,ACUTE myeloid leukemia ,DISEASE relapse ,MESSENGER RNA - Abstract
Resistance of leukemia stem cells (LSCs) to chemotherapy in patients with acute myeloid leukemia (AML) causes relapse of disease. Hedgehog (Hh) signaling plays a critical role in the maintenance and differentiation of cancer stem cells. Yet its role in AML remains controversial. The purpose of the present study is to investigate the role of GLI1, the transcriptional activator of Hh signaling, in AML progenitor cells and to explore the anti-AML effects of GLI small-molecule inhibitor GANT61. Methods: The expression of GLI1 mRNA and protein were examined in AML progenitor cells and normal cells. The proliferation, colony formation, apoptosis and differentiation of AML progenitor cells were also analyzed in the presence of GANT61. Results: Kasumi-1 and KG1a cells, containing more CD34
+ cells, expressed higher level of GLI1 compared to U937 and NB4 cells with fewer CD34+ cells. Consistently, a positive correlation between the protein levels of GLI1 and CD34 was validated in the bone marrow mononuclear cells (BMMC) of AML patients tested. GANT61 inhibited the proliferation and colony formation in AML cell lines. Importantly, GANT61 induced apoptosis in CD34+ enriched Kasumi-1 and KG1a cells, whereas it induced differentiation in U937 and NB4 cells. Furthermore, GANT61 enhanced the cytotoxicity of cytarabine (Ara-c) in primary CD34+ AML cells, indicating that inhibition of GLI1 could be a promising strategy to enhance chemosensitivity. Conclusions: The present findings suggested that Hh signaling was activated in AML progenitor cells. GLI1 acted as a potential target for AML therapy. [ABSTRACT FROM AUTHOR]- Published
- 2016
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10. Inhibition of mitotic kinase Aurora suppresses Akt-1 activation and induces apoptotic cell death in all-trans retinoid acid-resistant acute promyelocytic leukemia cells
- Author
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Xu, Duo-Rong, primary, Huang, Shan, additional, Long, Zi-Jie, additional, Chen, Jia-Jie, additional, Zou, Zheng-Zhi, additional, Li, Juan, additional, Lin, Dong-Jun, additional, and Liu, Quentin, additional
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- 2011
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11. Curcumin reduces expression of Bcl-2, leading to apoptosis in daunorubicin-insensitive CD34+ acute myeloid leukemia cell lines and primary sorted CD34+ acute myeloid leukemia cells
- Author
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Rao, Jia, primary, Xu, Duo-Rong, additional, Zheng, Fei-Meng, additional, Long, Zi-Jie, additional, Huang, Sheng-Shan, additional, Wu, Xing, additional, Zhou, Wei-Hua, additional, Huang, Ren-Wei, additional, and Liu, Quentin, additional
- Published
- 2011
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12. Inhibition of mitotic kinase Aurora suppresses Akt-1 activation and induces apoptotic cell death in all-trans retinoid acid-resistant acute promyelocytic leukemia cells.
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Duo-Rong Xu, Shan Huang, Zi-Jie Long, Jia-Jie Chen, Zheng-Zhi Zou, Juan Li, Dong-Jun Lin, Quentin Liu, Xu, Duo-Rong, Huang, Shan, Long, Zi-Jie, Chen, Jia-Jie, Zou, Zheng-Zhi, Li, Juan, Lin, Dong-Jun, and Liu, Quentin
- Subjects
MITOSIS ,APOPTOSIS ,CELL death ,LEUKEMIA ,SPINDLE apparatus - Abstract
Background: Aurora kinase ensures accurate chromosome segregation during cell cycle, maintaining genetic integrity in cell division. VX-680, a small-molecule Aurora kinase inhibitor, interferes with mitotic entry and formation of bipolar spindles. Here, we evaluated VX-680 as a potential agent for treatment of all-trans retinoid acid (ATRA)-resistant acute promyelocytic leukemia (APL) in vitro.Methods: CD11b expression was utilized to assess cell differentiation by flow cytometry. Immunofluorescence staining was conducted to analyze formation of cell monopolar spindle. Cell proliferation was evaluated by MTT assay. Sub-G1 population and Annexin V/PI staining were used to measure cell apoptosis. Hoechst 33342 staining was applied for identifying morphological changes in nucleus of apoptotic cell. Aurora-A (Aur-A) activation and the signaling pathways involved in apoptosis were detected by Western blot. JC-1 probe was employed to measure mitochondrial depolarization.Results: VX-680 inhibited Aur-A by reducing autophosphorylation at the activation site, Thr288, accompanied by producing monopolar mitotic spindles in APL cell line NB4-R2 that was resistant to ATRA. In addition, we found that VX-680 inhibited cell proliferation as assessed by MTT assay. Flow cytometry showed that VX-680 led to apoptotic cell death in both dose- and time-dependent manners by either Sub-G1 or Annexin V/PI analysis. Hoechst 33342 staining represented typical apoptotic cells with nuclear fragmentation in VX-680 treated cells. Importantly, VX-680 inhibition of Aurora kinase suppressed Akt-1 activation and induced mitochondrial depolarization, which eventually resulted in apoptosis by activation of caspase pathway, as indicated by increasing proteolytic cleavage of procaspase-3 and poly ADP ribose polymerase (PARP) in NB4-R2 cells.Conclusions: Our study suggested potential clinical use of mitotic Aurora kinase inhibitor in targeting ATRA-resistant leukemic cells. [ABSTRACT FROM AUTHOR]- Published
- 2011
- Full Text
- View/download PDF
13. Curcumin reduces expression of Bcl-2, leading to apoptosis in daunorubicin-insensitive CD34+ acute myeloid leukemia cell lines and primary sorted CD34+ acute myeloid leukemia cells.
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Jia Rao, Duo-Rong Xu, Fei-Meng Zheng, Zi-Jie Long, Sheng-Shan Huang, Xing Wu, Wei-Hua Zhou, Ren-Wei Huang, Quentin Liu, Rao, Jia, Xu, Duo-Rong, Zheng, Fei-Meng, Long, Zi-Jie, Huang, Sheng-Shan, Wu, Xing, Zhou, Wei-Hua, Huang, Ren-Wei, and Liu, Quentin
- Subjects
ACUTE myeloid leukemia ,APOPTOSIS ,CELL lines ,IMMUNOPHENOTYPING ,CD antigens - Abstract
Background: Acute myeloid leukemia (AML) is an immunophenotypically heterogeneous malignant disease, in which CD34 positivity is associated with poor prognosis. CD34+ AML cells are 10-15-fold more resistant to daunorubicin (DNR) than CD34- AML cells. Curcumin is a major component of turmeric that has shown cytotoxic activity in multiple cancers; however, its anti-cancer activity has not been well studied in DNR-insensitive CD34+ AML cells. The aim of this study was to therefore to explore curcumin-induced cytotoxicity in DNR-insensitive CD34+ AML cell lines (KG1a, Kasumi-1), DNR-sensitive U937 AML cells, and primary CD34+ AML bone-marrow-derived cells.Methods: Primary human CD34+ cells were isolated from peripheral blood mononuclear cells or bone marrow mononuclear cells using a CD34 MicroBead kit. The growth inhibitory effects of curcumin were evaluated by MTT and colony-formation assays. Cell cycle distribution was examined by propidium iodide (PI) assay. Apoptosis was analyzed by Wright-Giemsa, Hoechst 33342 and Annexin-V/PI staining assays. The change in mitochondrial membrane potential (MMP) was examined by JC-1 staining and flow cytometry. Expression of apoptosis-related proteins was determined by reverse transcription-polymerase chain reaction and Western blotting. Short interfering RNA (siRNA) against Bcl-2 was used in CD34+ KG1a and Kasumi-1 cells incubated with/without DNR.Results: Curcumin inhibited proliferation and induced apoptosis and G1/S arrest in both DNR-insensitive KG1a, Kasumi-1 and DNR-sensitive U937 cells. Curcumin-induced apoptosis was associated with reduced expression of both Bcl-2 mRNA and protein, subsequent loss of MMP, and activation of caspase-3 followed by PARP degradation. Curcumin synergistically enhanced the cytotoxic effect of DNR in DNR-insensitive KG1a and Kasumi-1 cells, consistent with decreased Bcl-2 expression. Accordingly, siRNA against Bcl-2 increased the susceptibility of KG1a and Kasumi-1 cells to DNR-induced apoptosis. More importantly, curcumin suppressed Bcl-2 expression, selectively inhibited proliferation and synergistically enhanced the cytotoxicity of DNR in primary CD34+ AML cells, while showing limited lethality in normal CD34+ hematopoietic progenitors.Conclusion: Curcumin down-regulates Bcl-2 and induces apoptosis in DNR-insensitive CD34+ AML cell lines and primary CD34+ AML cells. [ABSTRACT FROM AUTHOR]- Published
- 2011
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14. Significance of sRANKL/OPG Ratio in Diagnosis of Multiple Myeloma Bone Disease.
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XU Duo-Rong, SU Chang, ZOU Wai-Yi, XU Hui-Ru, HUANG Shan, LI Juan, and LUO Shao-Kai
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- 2010
15. [Effects of Prostaglandin E 2 Receptor 4 Agonist on the Expression of Stem Factors in Human CD34 + Cells].
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Li CM, Liu FJ, Wang YQ, Tang J, Chen HZ, Li J, and Xu DR
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- Antigens, CD34, Cell Movement, Granulocyte Colony-Stimulating Factor, Humans, Nanog Homeobox Protein, Octamer Transcription Factor-3, Prostaglandins, RNA, Messenger, T-Lymphocytes, Receptors, Prostaglandin E, EP4 Subtype metabolism
- Abstract
Objective: To investigate the effect of prostaglandin E
2 recoptor 4 antagonist (EP4 A) on the self-renewal ability of human CD34+ cells and its mechamism., Methods: The peripheral blood hematopoietic stem cell of 20 healthy donors received the G-CSF-mobilization were collected, then the human CD34+ cells were sorted out by MACS microbead kit. The human CD34+ cells were treated with DMSO (control group), EP4 A (EP4 A group) and EP4 A+EP4 A antagonist (EP4 A+EP4 A group) for 72 hours. The differential genes and pathways related with CD34+ cell stemness were detected by Thermogram and Pathway enrichment analysis. and then the expression levels of protein and gene (β-catenin, Nanog, Oct4, Sox2, Stat3, AKT, P38) were detected by qRT-PCR and Western blot respectively., Results: EP4 A could elevate the mRNA and protein expression of β-catenin, Nanog, Oct4, Sox2, in comparison with control group, however, mRNA and protein expression of STAT3, AKT, P38 were not changed. When human CD34+ cell were cultured with EP4 A+XAV939 it was found that the mRNA and protein expression of β-catenin was downregulated, moreover the mRNA and protein expression of Nanog, Oct4, Sox2 were reduced., Conclusion: EP4 A can upregulate stemness factors-β-catenin, Nanog, Oct4 and Sox2 in human CD34+ cell in vitro, but not STAT3, AKT and P38.- Published
- 2020
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16. [Prostaglandin E2 Receptor 4 Agonist Promotes Human CD34 + Cell Proliferation in vitro by Activating Wnt/β-Catenin Signaling Pathway].
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Wang YQ, Liu FJ, Chen HZ, Wang HH, Zou WY, Su C, Li J, and Xu DR
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- Antigens, CD34, Dinoprostone, Glycogen Synthase Kinase 3 beta, Humans, Receptors, Prostaglandin, beta Catenin, Cell Proliferation, Receptors, Prostaglandin E, EP4 Subtype agonists, Wnt Signaling Pathway
- Abstract
Objective: To investigate the potential signaling pathway that regulates the proliferation of human CD34
+ cells stimulated by prostaglandin E2 receptor 4 agonist (EP4A) in vitro., Methods: Twenty samples of peripheral blood containing stem cells were collected from the G-CSF mobilized healthy donors in our department of hematology. Human CD34+ cells were isolated by magnetic activated cell sorting (MACS) microbeads kit. The Cell Counting Kit-8 (CCK8) assay was used to determine the optimal concentration and time of EP4A to promote human CD34+ cell proliferation in vitro. Under the optimal condition, quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect mRNA level of β-catenin, and Western blot was used to assay protein expression of β-catenin and P-GSK-3β in human CD34+ cells treated with EP4A., Results: Culturing with 10 µmol/L EP4A for 72 h, it was found that EP4A promoted human CD34+ cell proliferation significantly, and the proliferation rate of human CD34+ cells was 1.36 times higher than that of the control(P=0.002). Under the optimal condition, it was also found that EP4A enhanced the β-catenin expression at both mRNA and protein levels, and up-regulated phosphorylation of GSK-3β in human CD34+ cells, but these effects could be inhibited by the EP4A antagonist EP4AA., Conclusion: EP4A can enhance human CD34+ cell proliferation in vitro by activating Wnt/β-catenin signaling pathway.- Published
- 2017
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17. Prophylactic antiviral therapy in allogeneic hematopoietic stem cell transplantation in hepatitis B virus patients.
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Liao YP, Jiang JL, Zou WY, Xu DR, and Li J
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- Adult, Antiviral Agents adverse effects, Biomarkers blood, Case-Control Studies, Chemical and Drug Induced Liver Injury etiology, China, Chronic Disease, DNA, Viral blood, Drug Administration Schedule, Female, Graft vs Host Disease etiology, Hematologic Neoplasms complications, Hematologic Neoplasms diagnosis, Hematologic Neoplasms mortality, Hepatitis B complications, Hepatitis B diagnosis, Hepatitis B mortality, Hepatitis B Antibodies blood, Hepatitis B Surface Antigens blood, Hepatitis B virus drug effects, Hepatitis B virus genetics, Hepatitis B virus immunology, Humans, Immunosuppressive Agents administration & dosage, Kaplan-Meier Estimate, Male, Prospective Studies, Recurrence, Risk Factors, Time Factors, Transplantation, Homologous, Treatment Outcome, Viral Load, Virus Activation drug effects, Young Adult, Antiviral Agents administration & dosage, Hematologic Neoplasms surgery, Hematopoietic Stem Cell Transplantation adverse effects, Hematopoietic Stem Cell Transplantation mortality, Hepatitis B drug therapy
- Abstract
Aim: To investigate the timing, safety and efficacy of prophylactic antiviral therapy in patients with hepatitis B virus (HBV) infection undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT)., Methods: This prospective study recruited a total of 57 patients diagnosed with malignant hematological diseases and HBV infection at the First Affiliated Hospital of Sun Yat-sen University between 2006 and 2013. The patients were classified as hepatitis B surface antigen (HBsAg)-positive or HBsAg-negative/ antiHBc-positive. Patients were treated with chemotherapy followed by antiviral therapy with nucleoside analogues. Patients underwent allo-HSCT when serum HBV DNA was < 10(3) IU/mL. Following allo-HSCT, antiviral therapy was continued for 1 year after the discontinuation of immunosuppressive therapy. A total of 105 patients who underwent allo-HSCT and had no HBV infection were recruited as controls. The three groups were compared for incidence of graft-vs-host disease (GVHD), drug-induced liver injury, hepatic veno-occlusive disease, death and survival time., Results: A total of 29 of the 41 subjects with chronic GVHD exhibited extensive involvement and 12 exhibited focal involvement. Ten of the 13 subjects with chronic GVHD in the HBsAg(-)/hepatitis B core antibody(+) group exhibited extensive involvement and 3 exhibited focal involvement. Five of the 10 subjects with chronic GVHD in the HBsAg(+) group exhibited extensive involvement and 5 exhibited focal involvement. The non HBV-infected group did not differ significantly from the HBsAg-negative/antiHBc-positive and the HBsAg-positive groups which were treated with nucleoside analogues in the incidence of graft-vs-host disease (acute GVHD; 37.1%, 46.9% and 40%, respectively; P = 0.614; chronic GVHD; 39%, 40.6% and 40%, respectively; P = 0.98), drug-induced liver injury (25.7%, 18.7% and 28%, respectively; P = 0.7), death (37.1%, 40.6% and 52%, respectively; P = 0.4) and survival times (P = 0.516). One patient developed HBV reactivation (HBsAg-positivity) due to early discontinuation of antiviral therapy., Conclusion: Suppression of HBV DNA to < 10(3) IU/mL before transplantation, continued antiviral therapy and close monitoring of immune markers and HBV DNA after transplantation may assure the safety of allo-HSCT.
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- 2015
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18. [Clinical significance of abnormal protein bands in multiple myeloma treated with bortezomib-based induction regimen and autologous stem cell transplantation].
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Wang HH, Li J, Liu JR, Zheng D, Gu JL, Yan MS, Zou WY, and Xu DR
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- Adult, Aged, Bortezomib, Female, Humans, Male, Middle Aged, Multiple Myeloma metabolism, Prognosis, Retrospective Studies, Transplantation, Autologous, Boronic Acids therapeutic use, Hematopoietic Stem Cell Transplantation, Multiple Myeloma therapy, Myeloma Proteins metabolism, Pyrazines therapeutic use
- Abstract
Objective: To study the clinical significance of abnormal protein bands (APB) in multiple myeloma (MM) patients treated with bortezomib-based induction regimen and autologous stem cell transplantation (ASCT)., Methods: Sixty-eight MM patients submitted to bortezomib-based induction therapy and ASCT from January 2007 to July 2012 were retrospectively studied. Monoclonal protein was detected by immunofixation electrophoresis (IFE)., Results: Of all 68 patients, 33 (48.5%) patients had APB. At the first emergence of an APB, two patients with light chain type achieved CR and before transplantation, and thirty-one patients were after transplantation with median time of 104 (ranged 33-404) days. The median duration of APB appearance was 105 (ranged 35-801) days. Patients who developed APB compared with those without APB, had a significantly higher CR plus very good partial response (VGPR) rates (100.0% vs 85.7%%, P=0.017) and CR rates (87.9% vs 62.9%) (P=0.03). There were no significant differences in gender, age, HGB, ALB, β2-microglobulin, M protein type, Durie-Salmon and ISS stages, the case number of first line or second line treatment, induction courses of bortezomib-based regimen, and the mode of ASCT. With a median follow-up of 33.4 (ranged 7.0-71.7) months, patients with APB tended to have a longer overall survival (OS) versus non-APB patients, although no significant difference obtained (P>0.05). Among APB patients, OS was longer in patients whose appearance of APB occurred <6 months after transplantation than those ≥ 6 months, but the significant difference was not obtained yet (P>0.05)., Conclusions: Patients who developed APB had a significantly better response to bortezomib-based induction regimen followed ASCT. APB emergence has a good prognostic significance.
- Published
- 2013
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19. [Observation of humoral immunity reconstitution and its relationship with infection after autologous hematopoietic stem cell transplantation for patients with multiple myeloma].
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Liu JR, Li J, Shang JJ, Zheng D, Gu JL, Zou WY, and Xu DR
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- Adult, Aged, Female, Humans, Male, Middle Aged, Multiple Myeloma therapy, Transplantation, Autologous, Virus Diseases immunology, Hematopoietic Stem Cell Transplantation, Immunity, Humoral, Multiple Myeloma immunology
- Abstract
Objective: To study the humoral immunity reconstitution and its relationship with infection in patients with multiple myeloma (MM) after undergoing autologous hematopoietic stem cell transplantation (auto-HSCT)., Methods: Forty-two MM patients undergoing auto-HSCT were included in this study. Peripheral blood were obtained for immunoglobulin detection, including IgG, IgA and IgM before transplantation and 1, 3, 6, 12, 18 and 24 months after transplantation. The time, type, pathogen of infection between 1 and 24 month after transplantation were analyzed., Results: The level of IgA at 6 month [(0.75±0.59) g/L] after auto-HSCT was lower than that of pre-auto-HSCT [(1.04±0.70) g/L], and reached the level of pre-auto-HSCT at 9 months [(0.99±0.52) g/L] after auto-HSCT. The level of IgM reached the level of pre-auto-HSCT [(0.45±0.26) g/L] at 3 months after auto-ASCT [(0.50±0.26) g/L]. The level of IgG reached the level of pre-auto-HSCT [(9.80±2.98) g/L] at 1 month after auto-HSCT [(11.09±2.69) g/L], and higher than that of pre-auto-HSCT at 9 months after auto-HSCT [(12.07±3.57) g/L]. The level of IgG with IgG-type MM was higher than that of patients with light-chain type and IgD-type MM at 6, 9 and 12 months after auto-HSCT. The IgA level of patients who obtained complete remission (CR) is much higher than that of patients who obtained nCR in IgG-type patients. The incidence of infection in 6 month after auto-HSCT was higher than that of (6-12) month and >12 month after auto-HSCT. The incidence of infection was strongly negative correlated with IgA (r =-0.943, P=0.005) and IgG (r=-0.943, P=0.005) level. The frequency of viral infection was also negatively correlated with IgA and IgG., Conclusion: The reconstitution time of IgG, IgA and IgM was different in MM patients after auto-HSCT. IgG recovered first, then IgM, and IgM the last. The incidence of infection was negatively correlated with IgA and IgG. With the recovery of IgG and IgA, the incidence of infection was decreased accordingly.
- Published
- 2013
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20. [The efficacy and safety of bortezomib-based induction regimen before autologous hematopoietic stem cell transplantation in patients with multiple myeloma].
- Author
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Li J, Liu JR, Huang BH, Chen M, Zheng D, Xu DR, and Zou WY
- Subjects
- Adult, Aged, Boronic Acids administration & dosage, Bortezomib, Female, Humans, Male, Middle Aged, Multiple Myeloma drug therapy, Multiple Myeloma surgery, Pyrazines administration & dosage, Retrospective Studies, Transplantation, Autologous, Treatment Outcome, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Boronic Acids therapeutic use, Hematopoietic Stem Cell Transplantation, Multiple Myeloma therapy, Pyrazines therapeutic use
- Abstract
Objective: To investigate the efficacy and safety of bortezomib-based induction regimen followed by autologous hematopoietic stem cell transplantation (ASCT) in patients with multiple myeloma (MM)., Methods: A retrospective analysis was performed upon clinical data of 62 MM patients who received bortezomib-based induction regimen followed by ASCT from June 2006 to June 2011. All patients were followed up to September 30, 2011., Results: Overall response rate [complete remission (CR) + near complete remission (nCR) + partial remission (PR)], ≥ nCR rate (CR/nCR) and CR rate of post-induction with bortezomib-based regimen were 88.7%, 66.1% and 24.2%, respectively. After ASCT, CR rate and CR/nCR rate were increased to 50.0% and 82.3%, respectively, with significant differences (P = 0.003 and P = 0.032). The median time of neutrophil and platelet engraftment was 12.0 (9 - 43) days and 13.5 (0 - 120) days, respectively. Significances were found in neutrophil and platelet engraftment between MM patients with and without prior exposure to alkylating agents. Furthermore, engraftment of neutrophil and platelet in patients receiving peripheral blood stem cell transplantation were faster than those receiving bone marrow transplantation. No unexpected side effects occurred. The median time of follow-up was 26.5 (7-61) months. The median overall survival (OS) was not reached and the median progression-free survival (PFS) was 30 months. There were significant differences in OS and PFS between patients obtaining CR/nCR and those with ≤ PR before ASCT., Conclusions: Bortezomib-based induction regimen can improve the efficacy of ASCT in MM patients. The side effects are tolerant. Higher response quality before ASCT can translate to high rates of OS and PFS following high-dose therapy and stem cell transplantation.
- Published
- 2012
21. [The clinical features of infection in multiple myeloma undergoing autologous hematopoietic stem cell transplantation].
- Author
-
Li J, Huang BH, Zhou ZH, Zheng D, Xu DR, and Zou WY
- Subjects
- Adult, Aged, Female, Humans, Incidence, Infections complications, Male, Middle Aged, Multiple Myeloma complications, Multiple Myeloma microbiology, Retrospective Studies, Transplantation, Autologous, Treatment Outcome, Hematopoietic Stem Cell Transplantation, Infections diagnosis, Multiple Myeloma surgery
- Abstract
Objective: To explore the clinical features of infection in multiple myeloma (MM) undergoing autologous hematopoietic stem cell transplantation (ASCT)., Methods: Thirty-seven patients with MM undergoing ASCT were retrospectively analyzed for type and time of infection, pathogen, and outcome., Results: Fifty-nine cases of infectious complications occurred in 33 patients (89.2%) after ASCT, with 34 cases (57.6%) of bacterial infections in 30 patients, 15 cases (25.4%) of fungal infections in 12 patients, 4 cases (6.8%) of cytomegalovirus (CMV) infection, 3 cases (5.1%) of herpes zoster virus infection and 3 cases (5.1%) of HBV reactivation. The proportion of bacterial infection, fungal infection and virus infection were 62.8%, 28.6% and 8.6% respectively in the early stage after ASCT, and 50.0%, 20.8% and 29.3% respectively in the median stage. Response to first-line antibiotic therapy was seen in 38 cases (64.4%). Infection-related mortality was 8.1% (3 cases)., Conclusions: The incidence of infection in MM patients undergoing ASCT is high and they are susceptible to all pathogens. It is important to choose the right antifungal agents as quickly as possible to reduce infection-related mortality.
- Published
- 2011
22. [Dynamic observations of beta-catenin in chronic myeloid leukemia and its relationship with cytogenetic response].
- Author
-
Zou WY, Xu DR, Su C, Chen M, Li J, and Luo SK
- Subjects
- Adolescent, Adult, Benzamides therapeutic use, Blast Crisis drug therapy, Blast Crisis genetics, Blast Crisis metabolism, Case-Control Studies, Female, Humans, Imatinib Mesylate, Leukemia, Myelogenous, Chronic, BCR-ABL Positive drug therapy, Leukemia, Myelogenous, Chronic, BCR-ABL Positive pathology, Male, Middle Aged, Piperazines therapeutic use, Pyrimidines therapeutic use, RNA, Messenger genetics, Young Adult, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, Leukemia, Myelogenous, Chronic, BCR-ABL Positive metabolism, beta Catenin metabolism
- Abstract
Objective: To investigate the changes in the expression of beta-catenin in patients with chronic myeloid leukemia (CML) in different phases, and explore the relationship between beta-catenin and the cytogenetic response to imatinib mesylate., Methods: Beta-catenin mRNA and protein expressions were detected by RT-PCR and Western blotting in the bone marrow mononuclear cells (BMMNCs) from 99 CML patients. The expressions of BCR-ABL fusion gene at both the mRNA and protein levels were detected by fluorescence in situ hybridization (FISH) in 94 patients before and during the one-year treatment with imatinib mesylate at the interval of 3 months, and the relationship between beta-catenin and cytogenetic response to imatinib mesylate was analyzed., Results: The expression of beta-catenin increased significantly in patients with blast crisis and accelerated phase (P<0.001), but showed no significant difference between normal subjects and CML patients in the chronic phase (P>0.05). The main cytogenetic remission rate was significantly higher in patients who were consistently negative for beta-catenin than in those consistently positive for beta-catenin or those with a positive transformation (P<0.001)., Conclusion: Beta-catenin overexpression in the progression of CML, consistent high level of beta-catenin or a positive transformation may indicate a poor response to imatinib, and early measures should be taken to increase the remission rate.
- Published
- 2010
23. [Osteoclast differentiation regulated by receptor activator of nuclear factor kappaB probably through a novel signaling pathway].
- Author
-
Xu DR, Chen HZ, Wang HH, Li J, and Luo SK
- Subjects
- Animals, Cell Differentiation drug effects, Cell Line, Tumor, Extracellular Signal-Regulated MAP Kinases metabolism, JNK Mitogen-Activated Protein Kinases metabolism, Mice, Mice, Knockout, NF-kappa B metabolism, Osteoclasts cytology, Phosphorylation, Tumor Necrosis Factor-alpha pharmacology, p38 Mitogen-Activated Protein Kinases metabolism, Osteoclasts drug effects, Osteoclasts metabolism, Receptor Activator of Nuclear Factor-kappa B pharmacology, Signal Transduction drug effects
- Abstract
This study was aimed to investigate the signaling pathways regulating osteoclast (OC) differentiation by receptor activator of nuclear factor kappa (RANK) under physiological condition so as to provide some theoretical basis for clarifying mechanism of bone destruction in multiple myeloma. A mutant TNFR(1)/RANK(2) (named RANK-Mu) chimera consisting of tumor necrosis factor receptor 1 (TNFR(1)) and RANK intramembrane domain was constructed by using deletion mutation for deleting IVVY amino acids in RANK intramembrane domain in accordance with (535-)IVVY(-538) as specific domain regulating OC differentiation by RANK. The RANK-Mu and TNFR(1)/RANK chimera without mutation (RANK-WT) were packaged by using plat E cell line to produce the retrovirus, which were transfected into bone marrow macrophages (BMMs) of TNFR(1)/TNFR(2) double knockout mice. After stimulation of these transfected BMMs with TNF-alpha, the differentiation of BMMs into OCs were observed, meanwhile the phosphorylation of NF-kappab, JNK, p38 and ERK was detected by Western blot after stimulation of these BMMs with TNF-alpha. The results showed that BMMs transfected with RANK-WT could be differentiated into OCs and phosphorylation of NF-kappaB, JNK, P38 and ERK were activated at 5 - 10 minutes after being stimulated by TNFalpha. BMMs transfected with RANK-Mu could not be differentiated into OCs, but phosphorylation of NF-kappaB, JNK, P38 and ERK were activated also. It is concluded that RANK regulates osteoclast differentiation probably not through 4 typical signaling pathways, named as NF-kappaB, JNK, P38 and ERK, in this process other new signaling pathways maybe participate.
- Published
- 2009
24. [The clinical features, chemotherapy responses and survival of 223 patients with newly diagnosed multiple myeloma].
- Author
-
Li J, Zhao Y, Luo SK, Huang BH, Zhang GC, Peng AH, Zheng D, Su C, Xu DR, Tong XZ, Gu JL, and Ding Y
- Subjects
- Adult, Aged, Aged, 80 and over, Disease-Free Survival, Female, Follow-Up Studies, Humans, Immunoglobulin Isotypes immunology, Male, Middle Aged, Multiple Myeloma diagnosis, Retrospective Studies, Treatment Outcome, Young Adult, Multiple Myeloma drug therapy, Multiple Myeloma immunology
- Abstract
Objective: To explore the proportion, clinical and laboratory features, chemotherapy responses and long term survival of different kinds of newly diagnosed multiple myeloma (MM) in China., Methods: The clinical data of 223 cases of newly diagnosed MM patients were gathered in the First Affiliated Hospital of Sun Yat-sen University from Jan, 2000 to Seb, 2007 were retrospectively analyzed., Results: The proportions of each kind of MM including IgG, IgA, light chain, IgD, IgM and biclonal MM were 48.0%, 20.6%, 25.6%, 4.0%, 0.9% and 0.9% respectively. No IgE and nonsecretory myeloma was found. The median age of onset was 58 years, of which that of the IgA type was the oldest one and the light chain type was the youngest (P = 0.004). Bone pain, renal insufficiency, and anemia were the most common symptoms which accounted for 67.7%, 61.0% and 45.3% respectively. The incidences of renal inadequacy, hypercalcemia and pathological fracture in light chain type were higher than those in IgG and IgA types. Besides, no M protein were found in serum protein electrophoresis and no elevation of total globulin. The clinical features of IgD type were similar to that of the light-chain type. The total chemotherapy efficacy rate of 89 patients who were treated with more than 3 cycles in our hospital is 61.8%, which has no difference in all types. Median overall survival of the 89 patients was 33.0 months., Conclusion: IgG is the most common type in MM. Bone pain, anemia, hypercalcemia and renal insufficiency are common symptoms. Immunofixation electrophoresis should be performed routinely to avoid missed diagnosis of light-chain and IgD types of MM.
- Published
- 2008
25. [Therapeutic effects of imatinib on chronic myeloid leukemia in different phases and the factors affecting the effects].
- Author
-
Zou WY, Xu DR, Su C, Li J, and Luo SK
- Subjects
- Antineoplastic Agents therapeutic use, Benzamides, Female, Humans, Imatinib Mesylate, Male, Treatment Outcome, Leukemia, Myelogenous, Chronic, BCR-ABL Positive drug therapy, Leukemia, Myeloid, Chronic-Phase drug therapy, Piperazines therapeutic use, Pyrimidines therapeutic use
- Abstract
Objective: To evaluate the therapeutic effect of imatinib on chronic myeloid leukemia (CML) in different phases and analyze the factors that may affect the effects., Methods: Eighty-five patients with CML in chronic phase, 24 in accelerated phase and 19 in blastic phase patients were treated with imitinib. The hematologic response, cytogenetic response, molecular response, overall survival (OS), progression-free survival (PFS) and adverse events were analyzed in these groups., Results: The rates of complete hematologic response (CHR), complete cytogenetic response (CCyR) and complete molecular response (CMoR) of the patients in chronic phase were 100%, 82.4% and 21.2%, respectively, and the 5-year OS and PFS of these patients were 92.1% and 84.7%. All these rates were significantly higher than those in patients in accelerated and blastic phases (P<0.0001). The CCyR, CMoR, 5-year OS and PFS in the 42 newly diagnosed patients in chronic phase were 92.9%, 26.3%, 100% and 95.2%, respectively, all significantly higher than those in patients with interferon therapy failure (P<0.001). Severe leukocytopenia and thrombocytopenia occurred at greater frequencey in AP and BP patients than in chronic phase patients (P<0.0001). Non-hematologic toxicity was rarer and milder in patients in chronic phase. Multivariate analysis showed that interferon therapy prior to imitinib treatment and prolonged drug cessation were the independent factors that affected the achievement of cytogenetic response and PFS., Conclusion: Early imitinib therapy can be effective and safe, and should be used as the first line drug for CML.
- Published
- 2008
26. [Efficacy and toxicity of intravenous busulfan-based conditioning before allogeneic peripheral blood stem cell transplantation for leukemia].
- Author
-
Tong XZ, Xu DR, Zou WY, Li J, Luo SK, Peng AH, Zhang GC, and Zheng D
- Subjects
- Adolescent, Adult, Busulfan administration & dosage, Busulfan adverse effects, Cyclophosphamide administration & dosage, Cyclophosphamide adverse effects, Cyclophosphamide therapeutic use, Female, Follow-Up Studies, Graft vs Host Disease prevention & control, Humans, Immunosuppressive Agents administration & dosage, Immunosuppressive Agents adverse effects, Injections, Intravenous, Leukemia drug therapy, Male, Middle Aged, Mucositis chemically induced, Transplantation, Homologous, Vomiting chemically induced, Young Adult, Busulfan therapeutic use, Immunosuppressive Agents therapeutic use, Leukemia therapy, Peripheral Blood Stem Cell Transplantation, Transplantation Conditioning
- Abstract
Background & Objective: Busulfan (Bu) is commonly used as a component of conditioning regimens for hematopoietic stem cell transplantation. Erratic gastrointestinal absorption as a result of oral administration of Bu not only affects the efficacy, but also increases the risk of toxicity. This study was to analyze the efficacy and toxicity of intravenous Bu and cyclophosphamide (Cy) conditioning before allogeneic peripheral blood stem cell transplantation (allo-PBSCT) for leukemia., Methods: Fifteen leukemia patients received intravenous Bu/Cy conditioning before allo-PBSCT, while 20 patients received oral Bu/Cy conditioning. The responses and adverse events of the 2 groups were assessed., Results: All 15 patients in intravenous Bu/Cy group had hematopoietic engraftment. The median time of engraftment was 12 (9-15) days for neutrophils and 15 (11-24) days for platelets. Of the 15 patients, 6 (40.0%) developed acute graft-versus-host disease (aGVHD), including 4 cases of grade I-II aGVHD and 2 cases of grade III-IV aGVHD; during conditioning, 7 (46.6%) had vomiting, 1 (6.7%) had oral mucositis, 1 (6.7%) had hemorrhagic cystitis, 2 (13.3%) had hepatic damage, none developed seizure. With a median follow-up of 180 days (range, 35-420 days), 14 (93.3%) patients were alive, 1 died of severe aGVHD accompanied fungal infection of the lung and central nerve system. The occurrence rates of hepatic damage and oral mucositis were significantly lower in intravenous Bu/Cy group than in oral Bu/Cy group (13.3% vs. 60.0%, 6.7% vs. 80.0%, P<0.01). There were no significant differences in hematopoietic reconstruction, aGVHD, stomatitis, gastrointestinal reaction, and hemorrhagic cystitis between the 2 groups (P>0.05)., Conclusion: The intravenous Bu/Cy conditioning before allo-PBSCT for leukemia has clear efficacy with low extramedullary toxicity.
- Published
- 2007
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