Chun Wang

Shanghai University, Shanghai, Shanghai Shi, China

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Publications (74)125.74 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Purpose: For recipients of allogeneic hematopoietic stem-cell transplantation (alloHSCT), we hypothesized that prophylactic therapy during neutropenia with granulocyte-macrophage colony-stimulating factor (GM-CSF) decreases invasive fungal disease (IFD). Patients and methods: We randomly assigned 206 patients undergoing alloHSCT to receive once-daily subcutaneous GM-CSF (5 to 7 μg/kg per day), granulocyte colony-stimulating factor (G-CSF; 5 to 7 μg/kg per day), or a combination of G-CSF and GM-CSF (2 to 3 μg/kg per day each). Treatment was started on day 5 after transplantation and was continued until the absolute neutrophil count was ≥ 1.5 × 10(9)/L for 2 consecutive days. The primary outcomes were 100-day incidence of proven and probable IFD and response rate of antifungal treatment. Results: For the intent-to-treat population, there was no significant difference in 100-day incidences of proven and probable IFD among the three groups. The antifungal treatment response was better in the GM-CSF group and G-CSF+GM-CSF group than in G-CSF group from day 22 to day 100 (P = .009). The 100-day cumulative mortality after transplantation was lower in the GM-CSF group than in the G-CSF group (10.3% v 24.6%, respectively; P = .037). The GM-CSF and G-CSF+GM-CSF groups had lower 100-day transplantation-related mortality than the G-CSF group (8.8%, 8.7%, and 21.7%, respectively; P = .034). After a median follow-up of 600 days, IFD-related mortality was lower in the groups that received GM-CSF or G-CSF+GM-CSF compared with G-CSF (1.47%, 1.45%, and 11.59%, respectively; P = .016). There were no significant differences in relapse, graft-versus-host disease, or hemorrhage-related mortality among the three groups of patients. Conclusion: For recipients of alloHSCT, compared with G-CSF, prophylactic GM-CSF was associated with lower 100-day transplantation-related mortality, lower 100-day cumulative mortality, and lower 600-day IFD-related mortality.
    Journal of Clinical Oncology 09/2015; DOI:10.1200/JCO.2014.60.5121 · 18.43 Impact Factor
  • Zhigang Zhou · Liping Wan · Chun Wang · Kun Zhou ·
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    ABSTRACT: To investigate the spatial and temporal programmed expression of Shh and Wnt members during key stages of definitive hematopoiesis and the possible mechanism of Shh and Wnt signaling pathways regulating the proliferation of hematopoietic progenitor cells (HPCs). Spatial and temporal programmed gene expression of Shh and Wnt signaling during hematopoiesis corresponded with c-kit(+)lin(-) HPCs proliferation. C-kit(+)Lin(-) populations derived from aorta-gonad-mesonephros (AGM) of Balb/c mice at E10.5 with increased expression of Shh and Wnt3a demonstrated a greater potential for proliferation. Additionally, supplementation with soluble Shh N-terminal peptide promoted the proliferation of c-kit(+)Lin(-) populations by activating the Wnt signaling pathway, an effect which was inhibited by blocking Shh signaling. A specific inhibitor of wnt signaling was capable of inhibiting Shh-induced proliferation in a similar manner to shh inhibitor. Our results provide valuable information on Shh and Wnt signaling involved in hematopoiesis and highlight the importance of interaction of Shh and Wnt signaling in regulating HPCs proliferation.
    DNA and cell biology 09/2015; DOI:10.1089/dna.2015.2930 · 2.06 Impact Factor
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    Jixue Zou · Zhigang Zhou · Liping Wan · Yin Tong · Youwen Qin · Chun Wang · Kun Zhou ·
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    ABSTRACT: The complex mechanistic array underlying the pathogenesis of myelodysplastic syndrome (MDS) is still unclear. Although dysregulations of different signaling pathways involved in MDS have been described, the identification of specific biomarkers and therapy targets remains an important task in order to establish novel therapeutic approaches. Here, we demonstrated that the Shh signaling pathway is active in MDS and correlated it with disease progression. Additionally, the knockdown of Gli1 significantly inhibited cell proliferation in vitro and in vivo. Gli1 silencing also induced apoptosis and G0/G1 phase arrest. Furthermore, Gli1 silencing enhanced the demethylating effect of 5-aza-2'-deoxycytidine on the p15 gene promoter and subsequently promoted its expression by inhibiting DNA methyltransferase 1(DNMT1). Our findings show that the Shh signaling pathway plays a role in the pathogenesis and disease progression of MDS, and proceeds by modulating DNA methylation. This pathway may prove to be a potential therapeutic target for enhancing the therapeutic effects of 5-azacytidine on malignant transformation of MDS.
    PLoS ONE 08/2015; 10(8):e0136843. DOI:10.1371/journal.pone.0136843 · 3.23 Impact Factor
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    ABSTRACT: In this study we investigated the correlation between donor chimerism status and disease relapse following allogeneic hematopoietic stem cell transplantation (allo-HSCT). The chimerism of Fluorescence-activated cell sorter (FACS) sorted CD3+T lymphocytes of 153 cases, CD56+CD16+NK lymphocytes of 153 cases and CD19+B lymphocytes of 31 cases with acute B lymphoblastic leukemia (B-ALL) was analyzed post-transplant utilizing polymerase chain reaction amplification of short tandem repeats (PCR-STR). A total of 33 patients (33/153, 21.6%) had recurrent disease. The positive predictive values of declining donor chimerism for hematologic and isolated extramedullary relapse were 58.8% and 10% (P=0.018, Chi-Square). The positive predictive values of declining donor chimerism in BMB, BMT, BMNK and PBB for hematologic relapse were 11.6%, 0%, 0% and 0% under close monitoring in patients with B-ALL. Only the donor chimerism in BMB significantly decreased in the group with hematologic relapse as compared with the group without hematologic relapse (P=0.00, Independent-samples T test) in patients with B-ALL. The median drop of donor chimerism in PBT, BMT, PBNK and BMNK were 0%, 0%, 5.9% and 2.8% one or two weeks prior to hematologic relapse in patients with non-B-ALL. The donor chimerism in PBNK significantly decreased prior to hematologic relapse in the group with hematologic relapse as compared with the group without hematologic relapse (P=0.022, Independent-samples T test).These data suggest donor chimerism of BMB can be used to predict the occurrence of hematologic relapse in patients with B-ALL. Donor chimerism decrease in PBNKwas associated with a somewhat increased risk of hematologic relapse in patients with non-B-ALL. Therefore, our results reveal a more effective path to individually predict for hematologic relapse by dynamic monitoring different cell lineages in different disease.
    PLoS ONE 08/2015; 10(7):e0133671. DOI:10.1371/journal.pone.0133671 · 3.23 Impact Factor
  • Chuxian Zhao · Chun Wang · Qi Cai ·

    Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 06/2015; 36(6):534-536. DOI:10.3760/cma.j.issn.0253-2727.2015.06.020
  • Youwen Qin · Xiaorui Wang · Chuxian Zhao · Chun Wang · Yining Yang ·
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    ABSTRACT: To assess the effect of JAK2V617F on different thrombotic risks in essential thrombocythemia (ET) patients, we identified eligible studies from several databases including Pubmed, Embase, and Cochrane Central Register of Controlled Trials (up to November 2014). Twenty-two studies of 2922 ET patients were included in exploring the relationship between JAK2V617F and the risk of thrombosis. Compared to JAK2V617F-negative ET patients, JAK2V617F-positive ET patients had higher odd risks (ORs) of arterial thrombosis [OR = 2.59 (1.84-3.65)] and venous thrombosis [OR = 2.10 (1.53-2.88)]. The JAK2V617F-positive group was also more prone to increased risk of microcirculatory disturbances [OR = 1.50 (0.97-2.32)]. Moreover, JAK2V617F may indicate increased risk of either arterial [OR = 1.71 (1.22-2.39)] or venous thrombosis [OR = 2.90 (1.54-5.46)] before diagnosis of ET. During follow-up, JAK2V617F might not be related to arterial thrombosis [OR = 1.90 (0.90-2.08)], but rather venous thrombosis [OR = 1.95 (1.08-3.53)]. In conclusion, JAK2V617F increased the risk of arterial and venous thrombosis in ET patients, while understanding its role in microcirculatory disturbances will require further studies.
    International journal of hematology 05/2015; 102(2). DOI:10.1007/s12185-015-1808-y · 1.92 Impact Factor
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    Jixue Zou · Yan Hong · Yin Tong · Ju Wei · Youwen Qin · Shan Shao · Chun Wang · Kun Zhou ·
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    ABSTRACT: The role of marrow microenvironment in the pathogenesis of myelodysplastic syndrome (MDS) remains controversial. Therefore, we studied the influence of bone marrow-derived mesenchymal stromal cells (BMSCs) from patients with different risk types of MDS on the survival of the MDS cell lines SKM-1 and MUTZ-1. We first demonstrated that the expression of Sonic hedgehog (Shh), smoothened (Smo), and glioma-associated oncogene homolog 1 (Gli1) was increased in MDS patients ; the increase in expression was positively correlated with the presence of high-risk factors. The Shh signaling inhibitor, cyclopamine, inhibited high-risk MDS BMSC-induced survival of SKM-1 and MUTZ-1 cells, suggesting a role for Shh signaling in MDS cell survival. Furthermore, cyclopamine-mediated inhibition of Shh signaling in SKM-1 and MUTZ-1 cells resulted in decreased DNMT1 expression and cell survival; however, exogenous Shh peptide had the opposite effect, suggesting that Shh signaling could regulate the expression of DNMT1, thereby modulating cell survival in MDS. In addition, the apoptosis of SKM-1 and MUTZ-1 cell increased significantly when cultured with cyclopamine and a demethylation agent, 5-Aza-2′-deoxycytidine. These findings suggest that Shh signaling from BMSCs is important in the pathogenesis of MDS and could play a role in disease progression by modulating methylation.
    Stem cell International 04/2015; 2015:1-13. DOI:10.1155/2015/957502 · 2.81 Impact Factor
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    ABSTRACT: The China Assessment of Antifungal Therapy in Hematological Disease (CAESAR) study, the first large-scale observational study of invasive fungal disease (IFD) in China, enrolled 1401 patients undergoing haematopoietic stem cell transplantation (HSCT) (75.2% allogeneic, 24.8% autologous) at 31 hospitals across China. Overall incidence of proven or probable IFD was 7.7% (108/1401); there were another 266 cases (19.0%) of possible IFD. Following allogeneic or autologous HSCT, incidence of proven/probable IFD was 8.9% (94/1053) and 4.0% (14/348), respectively. Some cases (14/108) developed during conditioning before transplantation. Cumulative incidence of proven/probable IFD increased steeply the first month after transplantation, and after 6 months was significantly higher in allogeneic than autologous transplant recipients (9.2% versus 3.5%; P = 0.001) and when stem cells were derived from cord blood, or bone marrow and peripheral blood (P = 0.02 versus other sources). Independent risk factors for proven/probable IFD in allogeneic HSCT were diabetes, HLA-matched unrelated donor, prolonged severe neutropenia (absolute neutrophil count > 500/mm(3) for >14 days) and immunosuppressants (odds ratio = 2.0─3.4 for all). Antifungal prophylaxis was independently protective (P = 0.01). Previous IFD and prolonged severe neutropenia were significant independent risk factors among autologous transplant patients (P < 0.01, P = 0.04, respectively). In total, 1175 (83.9%) patients received antifungal prophylaxis (91.6% triazoles) and 514 (36.7%) were treated in hospital with therapeutic antifungals (89.1% triazoles; median 27 days). Empirical, pre-emptive and targeted antifungals were used in 82.3%, 13.6% and 4.1% of cases, respectively. Overall mortality (13.4%; 188 deaths) was markedly higher in patients with proven (5/16; 31.3%), probable (20/92; 21.7%) or possible (61/266; 22.9%) IFD; allogeneic (171/1053; 16.2%) rather than autologous (17/348; 4.9%) HSCT; and was significantly higher in patients receiving pre-emptive (18.6%) rather than empirical (6.1%) or targeted (9.5%) antifungal therapy (P = 0.002). Improvements in the selection and timing of prophylactic antifungals would be welcome. Healthcare providers should remain alert to the increased risk of IFD and associated mortality in allogeneic HSCT recipients, and the ongoing risk of IFD even after discharge from hospital. Copyright © 2015 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
    Biology of blood and marrow transplantation: journal of the American Society for Blood and Marrow Transplantation 03/2015; 21(6). DOI:10.1016/j.bbmt.2015.03.018 · 3.40 Impact Factor
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    ABSTRACT: To determine the sensitivity and significance of B-cell chimerism for the detection of early engraftment, transplant rejection, and disease relapse.
    03/2015; 1(1):48-54. DOI:10.1016/j.cdtm.2015.02.004
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    ABSTRACT: In an attempt to establish the advantages of fluorescence in situ hybridization (FISH) studies over conventional cytogenetic (CC) analysis, a total of 2302 de novo MDS patients from 31 Chinese institutions were prospectively selected in the present study for both CC and standardized FISH analysis for +8, -7/7q-, -5/5q-, 20q- and-Y chromosomal abnormalities. CC analysis was successful in 94.0% of the patients; of these patients, 35.9% of the cases were abnormal. FISH analysis was successful in all 2302 patients and detected at least one type of common cytogenetic abnormality in 42.7% of the cases. The incidences of +8, -7/7q-, -5/5q-, 20q- and-Y chromosomal abnormalities by FISH were 4.1% to 8.7% higher than those by CC. FISH identified abnormalities in 23.6% of the patients exhibiting normal CC results and revealed that 20.7% of the patients with adequate normal metaphases (≥20) had abnormal clones. FISH identified cytogenetic abnormalities in 50.4% of the patients with failed CC analysis. In summary, our multicenter studies emphasised and confirmed the importance of applying standardized FISH testing based on an appropriate panel of probes to detect common cytogenetic abnormalities in Chinese de novo MDS patients, particularly those with normal or failed CC results. Copyright © 2015. Published by Elsevier Ltd.
    Leukemia research 02/2015; 39(5). DOI:10.1016/j.leukres.2015.02.005 · 2.35 Impact Factor
  • Yining Yang · Xiaorui Wang · Chun Wang · Youwen Qin ·
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    ABSTRACT: A systematic review and meta-analysis were carried out to compare the clinical features and outcomes in calreticulin (CALR)-mutated and JAK2V617F patients of essential thrombocythemia (ET). Compared with JAK2V617F ET patients, CALR-mutated ET was associated with a clear increase in male predominance [OR 1.71 (95 % CI 1.28–2.28), P < 0.001, I 2 = 51.6] and a significant decrease in thrombosis events [OR 0.40 (95 % CI 0.32–0.50), P < 0.001, I 2 = 0]. No difference was observed in hemorrhagic events [OR 0.86 (95 % CI 0.52–1.42), P = 0.558, I 2 = 0] or splenomegaly [OR 0.8 (95 % CI 0.55–1.14), P = 0.217 I 2 = 42.9]. CALR-mutated ET did not show better overall survival (OS) [HR 1.03 (95 % CI 0.74–1.44) P = 0.854, I 2 = 47.6] but showed better thrombosis-free survival (TFS) [HR 0.62 (0.44–0.87), P = 0.005, I 2 = 0] than JAK2V617F ET. In conclusion, CALR-mutated ET and JAK2V617F ET may represent two different subgroups of essential thrombocythaemia with respect to clinical features and outcomes.
    International Journal of Hematology 12/2014; 101(2). DOI:10.1007/s12185-014-1724-6 · 1.92 Impact Factor
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    ABSTRACT: This stud y examined the epidemiology, risk factors, management, and outcome of invasive fungal infection (IFI) in patients receiving chemotherapy for hematological malignancy in China. IFI risk factors were analyzed using univariate analysis and multivariate logistic regression. In total, 4,192 patients receiving 4,889 chemotherapy courses were enrolled [mean age 40.7 years, 58.4 % male, 16.9 % children (<18 years)]. The most common hematological diseases were acute myeloid leukemia (AML, 28.5 %), non-Hodgkin lymphoma (NHL, 26.3 %), and acute lymphoblastic leukemia (ALL, 20.2 %). Severe neutropenia (absolute neutrophil count [ANC] <500/mm(3)) occurred after one third (1,633/4,889, 33.4 %) of chemotherapy courses. Incidence of proven/probable IFI was 2.1 % per chemotherapy course and higher in patients with myelodysplastic syndrome (MDS, 4.94 %), acute hyperleukocytic leukemia (AHL, 4.76 %), AML (3.83 %), or induction chemotherapy. Risk factors included ANC <500/mm(3) [odds ratio (OR) 3.60], AML or MDS (OR 1.97), induction chemotherapy (OR 2.58), previous IFI (OR 3.08), and being male (OR 1.74). Antifungal agents, prescribed in one quarter (1,211/4,889, 24.8 %) of chemotherapy courses, included primary/secondary prophylaxis (n = 827, 16.9 %) and/or treatment (n = 655, 13.4 %; 86.9 % triazoles), which was empirical (84.3 %), pre-emptive (8.6 %), or targeted (7.1 %). Overall mortality following each chemotherapy course (1.5 %) increased in proven/probable (11.7 %) and possible IFI (8.2 %). In summary, IFI was more common in MDS, AHL, AML, or induction chemotherapy, and substantially increased mortality. Neutropenic patients receiving induction chemotherapy for AML or MDS and those with previous IFI were at particular risk. Antifungal prophylaxis showed an independent protective effect but was not commonly used, even in high-risk patients. By contrast, empiric antifungals were widely used.
    Tumor Biology 10/2014; 36(2). DOI:10.1007/s13277-014-2649-7 · 3.61 Impact Factor
  • Lili Zhou · Haitao Bai · Chong Deng · Chun Wang · Rang Xu · Shan Shao ·
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    ABSTRACT: Background: Many studies have demonstrated that microRNA-21 (miR-21) acts as an oncogene in the tumourigenesis of a variety of tumours and may be involved in the chemotherapeutic drug resistance of tumour cells. In this study, we utilized the leukaemia cell line K562 as an in vitro cell model to investigate whether miR-21 is involved in X-ray irradiation resistance. Methods: Retroviral transduction and antisense oligonucleotide transfection were used to overexpress or knock down miR-21 expression, respectively. An MTT assay was used to measure cell viability, and western blotting was performed to detect the expression of the miR-21 target gene, PTEN (phosphatase and tensin homologue), and its downstream signalling components, phosphatidylinositol 3-kinase (PI3K), and AKT. Results: The overexpression of miR-21 decreased the protein expression levels of PTEN, increased the phosphorylation level of AKT, and enhanced the X-ray irradiation resistance in K562 cells. In contrast, the knockdown of miR-21 increased the PTEN protein expression, reduced the phosphorylation levels of the AKT, and increased the sensitivity of K562 cells to X-ray irradiation. The overexpression of PTEN or the knockdown of AKT also increased the sensitivity of K562 cells to X-ray irradiation. Conclusion: By regulating the expression of its target gene PTEN, which subsequently affects the PI3K/AKT signalling pathway, miR-21 exerts its regulatory role on the radiation sensitivity of K562 cells. These results may help to provide the basis for microRNA-based targeted therapies to overcome radiation resistance in tumour cells.
    Hematology (Amsterdam, Netherlands) 09/2014; 20(6). DOI:10.1179/1607845414Y.0000000201 · 1.25 Impact Factor
  • Daolin Wei · Chuxian Zhao · Min Zhao · Ju Wei · Yanrong Gao · Qi Cai · Chun Wang ·

    Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 09/2014; 35(9):854-856. DOI:10.3760/cma.j.issn.0253-2727.2014.09.017
  • You-Wen Qin · Yi-Ning Yang · Su Li · Chun Wang ·
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    ABSTRACT: In 2012, a 25-years-old pregnant woman presented with thromocytosis for 4 months, blood counts showed platelets 701 × 10(9)/L. Bone marrow examination disclosed a feature of hypercellular marrow in erythrocytic,granulocytic and megakaryocytic series. Cytogenetic analysis showed t(9;22)(q34;q11) in 100 % of metaphase. The percentage of BCR-ABL-positive FISH signals was 37 % in the peripheral blood. Molecular analysis showed the presence of the JAK2V617F mutation and BCR-ABL mRNA b3a2 transcript. A diagnosis of concomitant presence of essential thrombocythemia and chronic myelocytic leukemia was made. Based on this case and literatures reported before, it might be necessary to detect JAK2-V617F mutation and BCR-ABL fusion gene concomitantly in myeloproliferative neoplasms patients.
    Indian Journal of Hematology and Blood Transfusion 09/2014; 30(Suppl 1):331-4. DOI:10.1007/s12288-014-0385-1 · 0.20 Impact Factor

  • Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 08/2014; 35(8):774. DOI:10.3760/cma.j.issn.0253-2727.2014.08.028
  • Daolin Wei · Xin Pan · Shike Yan · Yanrong Gao · Qi Cai · Chun Wang ·

    Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 08/2014; 35(8):763-6. DOI:10.3760/cma.j.issn.0253-2727.2014.08.024
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    ABSTRACT: Objective Atherosclerosis is a chronic inflammatory and immune vascular disease, and clinical and experimental evidence has indicated an important role of complement activation products, including the terminal membrane attack complex (MAC), in atherogenesis. Here, we investigated whether complement inhibition represents a potential therapeutic strategy to treat/prevent atherogenesis using CR2-Crry, a recently described complement inhibitor that specifically targets to sites of C3 activation. Methods and results Previous studies demonstrated that loss of CD59 (a membrane inhibitor of MAC formation) accelerated atherogenesis in Apoe deficient (Apoe−/−) mice. Here, both CD59 sufficient and CD59 deficient mice in an Apoe deficient background (namely, mCd59 ab+/+/Apoe−/− and mCd59 ab−/−/Apoe−/−) were treated with CR2-Crry for 4 and 2 months respectively, while maintained on a high fat diet. Compared to control treatment, CR2-Crry treatment resulted in significantly fewer atherosclerotic lesions in the aorta and aortic root, and inhibited the accelerated atherogenesis seen in mCd59 ab+/+/Apoe−/− and mCd59 ab−/−/Apoe−/− mice. CR2-Crry treatment also resulted in significantly reduced C3 and MAC deposition in the vasculature of both mice, as well as a significant reduction in the number of infiltrating macrophages and T cells. Conclusion The data demonstrate the therapeutic potential of targeted complement inhibition.
    Atherosclerosis 05/2014; 234(1):237–243. DOI:10.1016/j.atherosclerosis.2014.03.004 · 3.99 Impact Factor
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    ABSTRACT: Invasive Fungal Disease (IFD) is a major cause of death in severe neutropenic patients with hematologic malignancies. Micafungin, a new echinocandin antifungal drug, is effective in treating IFD. However, the efficacy and safety of micafungin in preventing IFD in severe neutropenic patients with hematologic malignancies have not been demonstrated. A prospective and multicenter clinical study was conducted to evaluate the efficacy and safety of micafungin as prophylaxis for IFD. Micafungin 50 mg daily was administered intravenously to 117 high-risk patients with hematologic malignancies undergoing intensive chemotherapy or Hematopoietic Stem Cell Transplantation (HSCT), for a median of 24 days. Successful prophylaxis (no proven, probable or possible IFD up to 1 week after the end of prophylactic treatment) was achieved in 88.54% patients. No patient developed proven IFD during treatment and only 2.08% had probable IFD and 9.38% possible IFD. Micafungin potentially accounted for adverse events in 6.84% of patients. No severe adverse events attributable to micafungin were seen. Micafungin 50 mg daily is a promising prophylactic antifungal therapy for neutropenic patients with hematologic malignancies.
    International Journal of Pharmacology 04/2014; 10(4):231-236. DOI:10.3923/ijp.2014.231.236 · 0.71 Impact Factor
  • Lili Zhou · Haitao Bai · Chun Wang · Daolin Wei · Youwen Qin · Xiaowei Xu ·
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    ABSTRACT: microRNA‑125b (miR‑125b) is overexpressed in several types of cancer and contributes to tumor resistance to chemotherapy. The present study investigated the effect of miR‑125b on the resistance of leukemia cell lines to the chemotherapeutic agent daunorubicin (DNR). miR‑125b expression was found to be upregulated in patients who had failed therapy compared with those who demonstrated event‑free survival. The overexpression of miR‑125b was observed to induce DNR resistance in K562, THP‑1 and Jurkat cells by reducing apoptosis, whereas the suppression of miR‑125b was found to enhance DNR cytotoxicity in REH cells. Furthermore, miR‑125b was observed to mediate DNR resistance in leukemia cell lines through decreasing expression of G protein‑coupled receptor kinase 2 and p53‑upregulated modulator of apoptosis, which were shown to be direct targets of miR‑125b using a dual‑luciferase reporter. The present study provides a novel mechanism for understanding leukemia drug resistance and provides a novel method for calculating patient prognosis.
    Molecular Medicine Reports 03/2014; 9(5). DOI:10.3892/mmr.2014.2011 · 1.55 Impact Factor

Publication Stats

333 Citations
125.74 Total Impact Points


  • 2015
    • Shanghai University
      • Department of Hematology
      Shanghai, Shanghai Shi, China
    • The First People's Hospital of Changzhou
      Wujin, Jiangsu Sheng, China
  • 2014-2015
    • Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
      Shanghai, Shanghai Shi, China
    • Renji Hospital
      Shanghai, Shanghai Shi, China
  • 2008-2015
    • Shanghai Jiao Tong University
      • • Department of Rheumatology
      • • Shanghai First People's Hospital
      Shanghai, Shanghai Shi, China
  • 2007-2015
    • Hangzhou First People's Hospital
      Hang-hsien, Zhejiang Sheng, China
    • Tianjin Medical University
      T’ien-ching-shih, Tianjin Shi, China
  • 2005-2014
    • Shanghai Putuo District People's Hospital
      Shanghai, Shanghai Shi, China
  • 2007-2009
    • First People's Hospital Chenzhou
      Chenchow, Hunan, China