Chun Wang

The First People's Hospital of Changzhou, Wujin, Jiangsu Sheng, China

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Publications (68)91.13 Total impact

  • 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
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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; DOI:10.1007/s12185-015-1808-y · 1.68 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 · 3.35 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; DOI:10.1016/j.leukres.2015.02.005 · 2.69 Impact Factor
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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 01/2015; 2015:1-13. DOI:10.1155/2015/957502 · 2.81 Impact Factor
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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 · 1.68 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 · 2.84 Impact Factor
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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; DOI:10.1179/1607845414Y.0000000201 · 1.19 Impact Factor
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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 · 0.23 Impact Factor
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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 · 3.97 Impact Factor
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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 · 1.48 Impact Factor
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    ABSTRACT: This study mainly focused on the impact of Hepatitis B virus (HBV) infection on the prognosis of diffuse large B cell lymphoma (DLBCL) patients in rituximab era, using a Cox regression model to ascertain the prediction value of the serum HBV marker in survivals. Three hundred and eighty four DLBCL patients treated with rituximab, cyclophosphamide, doxorubicin/epirubicin, vincristine and prednisone (R-CHOP-like regimens) or CHOP-like regimens were included. Progression-free survival (PFS) and overall survival (OS) of the patients have or have not received rituximab were analyzed separately. In the CHOP group, HBV infection has not been found a profound impact on the survivals. In the R-CHOP group, PFS and OS were inferior in HBsAg-positive patients (p = 0.031 and p = 0.006, respectively); after adjusting for International Prognostic Index parameters, HBsAg is an independent unfavorable factor for both PFS (RR = 2.492) and OS (RR = 2.589).
    Medical Oncology 03/2014; 31(3):845. DOI:10.1007/s12032-014-0845-3 · 2.06 Impact Factor
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    ABSTRACT: Imatinib mesylate (IM), a targeted competitive inhibitor of the BCR-ABL tyrosine kinase, has revolutionized the clinical treatment of chronic myeloid leukemia (CML). However, resistance and intolerance are still a challenge in the treatment of CML. Autophagy has been proposed to play a role in IM resistance. To investigate the anti-leukemic activity of specific and potent autophagy inhibitor-1 (spautin-1) in CML, we detected its synergistic effect with IM in K562 and CML cells. Our results showed that spautin-1 markedly inhibited IM-induced autophagy in CML cells by downregulating Beclin-1. Spautin-1 enhanced IM-induced CML cell apoptosis by reducing the expression of the anti-apoptotic proteins Mcl-1 and Bcl-2. We further demonstrated that the pro-apoptotic activity of spautin-1 was associated with activation of GSK3β, an important downstream effector of PI3K/AKT. The findings indicate that the autophagy inhibitor spautin-1 enhances IM-induced apoptosis by inactivating PI3K/AKT and activating downstream GSK3β, leading to downregulation of Mcl-1 and Bcl-2, which represents a promising approach to improve the efficacy of IM in the treatment of patients with CML.
    International Journal of Oncology 02/2014; 44(5). DOI:10.3892/ijo.2014.2313 · 3.03 Impact Factor
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    ABSTRACT: To evaluate the correlation between chimerism status and acute graft-versus-host disease (aGVHD) following allogeneic hematopoietic stem cell transplantation. Chimerism of peripheral blood of 124 patients was monitored at regular intervals post-transplant. The chimerism of 124 post-transplant cases of CD3(+)T lymphocytes, 107 cases of CD3(-)CD56(+)CD16(+)NK lymphocytes, 49 cases of CD15(+) granulocytes, and 27 cases of CD19(+)B lymphocytes sorted by fluorescence-activated cell sorter were analyzed by polymerase chain reaction amplification of short tandem repeats. Differences were found in the time between establishment of full donor T-cell chimerism and the occurrence of aGVHD (P = 0.035, two related samples test). Patients with ≥69 % donor chimerism on day +7 in T-cells had higher rates of aGVHD. This study may provide a rational basis for treatment with adoptive immunotherapy at an earlier time, such as day 7 after SCT, than at present to prevent aGVHD.
    International journal of hematology 01/2014; 99(3). DOI:10.1007/s12185-014-1510-5 · 1.68 Impact Factor
  • Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi 12/2013; 34(12):1070-2. DOI:10.3760/cma.j.issn.0253-2727.2013.12.018
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    ABSTRACT: Previous studies have demonstrated that activator of G-protein signaling 3 (AGS3; also known as GPSM1), a member of the AGS family, plays an important anti-apoptotic role through enhancing the phosphorylation of cyclic AMP response element-binding protein (p-CREB). In this report, we delineate the anti-apoptotic role of AGS3 in multiple myeloma (MM). To do this, we developed a cell apoptotic model induced by doxorubicin in MM. Our data indicate that decreased expression of AGS3 is correlated with reduced levels of p-CREB in the apoptotic model. The negative role of AGS3 in cell apoptosis was further confirmed by knocking down AGS3. The microenvironment has been shown to influence tumor cell phenotype in response to chemotherapy. Since cell adhesion-mediated drug resistance remains a major obstacle for successful treatment of MM, we constructed a cell adhesion model in MM and detected the changing of AGS3 protein expression. AGS3 siRNA reversed the high rate of MM cell adhesion to either fibronectin or HS-5 cells. Consistent with the reduced adhesion rate, the cells also exhibited reduced drug resistance to doxorubicin, mitoxantrone, and dexamethasone. Collectively, these data indicate that AGS3 may be represented as a good candidate for pursuing clinical trials in MM. Moreover, our data provide a clinical therapeutic target for MM and potentially other tumors that home and/or metastasize to the bone.
    International journal of hematology 12/2013; 99(1). DOI:10.1007/s12185-013-1484-8 · 1.68 Impact Factor

Publication Stats

227 Citations
91.13 Total Impact Points


  • 2015
    • The First People's Hospital of Changzhou
      Wujin, Jiangsu Sheng, China
  • 2011–2015
    • Hangzhou First People's Hospital
      Hang-hsien, Zhejiang Sheng, China
  • 2007–2015
    • Shanghai Jiao Tong University
      Shanghai, Shanghai Shi, China
  • 2014
    • Renji Hospital
      Shanghai, Shanghai Shi, China
  • 2008–2014
    • Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
      Shanghai, Shanghai Shi, China
  • 2005–2014
    • Shanghai Putuo District People's Hospital
      Shanghai, Shanghai Shi, China
  • 2007–2009
    • First People's Hospital Chenzhou
      Chenchow, Hunan, China
  • 2006
    • Shanghai University
      Shanghai, Shanghai Shi, China