Daiming Fan

Fourth Military Medical University, Xi’an, Liaoning, China

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Publications (450)1900.97 Total impact

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    ABSTRACT: Systematic review and meta-analysis were performed to evaluate the safety and efficacy of anticoagulation for the treatment of portal vein thrombosis (PVT) in cirrhotic patients. The PubMed, EMBASE, Cochrane Library, and ScienceDirect databases were searched. The rates of bleeding complications and portal vein recanalization in patients who received anticoagulant therapy were pooled. The odds ratio (OR) with 95% confidence interval (CI) was calculated to express the difference in the rate of portal vein recanalization between anticoagulation and non-anticoagulation groups. All meta-analyses were conducted by using a random-effects model. Sixteen of 960 initially identified papers were included. Two studies reported a low incidence of major anticoagulation-related complications (4% [2/55] and 3% [1/33]), but no lethal complications occurred. The rate of anticoagulation-related bleeding ranged from 0% to 18% with a pooled rate of 3.3% (95% CI=1.1%-6.7%). The heterogeneity was not significant in the meta-analysis. The total rate of portal vein recanalization ranged from 37% to 93% with a pooled rate of 66.6% (95% CI=54.7%-77.6%). The rate of complete portal vein recanalization ranged from 0% to 75% with a pooled rate of 41.5% (95% CI=29.2%-54.5%). However, the heterogeneity was significant in the 2 meta-analyses. The rate of complete portal vein recanalization was significantly higher in anticoagulation group than in non-anticoagulation group (OR=4.16, 95% CI=1.88-9.20, P=0.0004). The heterogeneity was not significant in the meta-analysis. Anticoagulation could achieve a relatively high rate of portal vein recanalization in cirrhotic patients with PVT. Given that only a small number of non-randomized comparative studies are reported, randomized controlled trials are warranted to confirm the risk-to-benefit of anticoagulation in such patients, especially anticoagulation-related bleeding. Copyright © 2014 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
    European Journal of Internal Medicine 01/2015; · 2.30 Impact Factor
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    ABSTRACT: Until now, no data on the routine screening for thrombotic risk factors in Chinese nonmalignant and noncirrhotic patients with portal vein thrombosis (PVT) have been reported. A total of 141 nonmalignant and noncirrhotic patients with PVT who underwent screening tests for thrombotic risk factors between September 2009 and August 2012 were included in this study. The JAK2 V617F mutation was found in 35 of the 141 patients tested. Neither the JAK2 exon 12 mutation nor the MPL W515 L/K mutation was found in any of the 50 patients tested. Overt myeloproliferative neoplasms (MPNs) were diagnosed in 13 patients (polycythemia vera, n=1; essential thrombocythemia, n=9; idiopathic myelofibrosis, n=3). Latent MPNs were considered in 23 patients with the JAK2 V617F mutation but without any significant abnormalities, as determined through regular blood tests. Anticardiolipin IgG antibodies were positive in none of the 136 patients tested. Paroxysmal nocturnal hemoglobinuria was not found in any of the 141 patients tested. Neither the factor V G1691A mutation nor the factor II G20210A mutation was found in any of the 72 patients tested. The C677T mutation in 5,10-methylenetetrahydrofolate reductase (MTHFR) was found in 29 of the 38 patients tested. Hyperhomocysteinemia was detected in eight of the 39 patients tested. MPNs are an important thrombotic risk factor in Chinese patients with PVT. However, the extreme rarity of paroxysmal nocturnal hemoglobinuria, anticardiolipin IgG antibodies, and factor V G1691A and factor II G20210A mutations has precluded any support for the implementation of routine screening for these thrombotic factors in such patients. Additional case-control studies should confirm the role of the MTHFR C677T mutation and hyperhomocysteinemia in the pathogenesis of PVT.
    European journal of gastroenterology & hepatology. 01/2015; 27(1):77-83.
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    ABSTRACT: Our previous work identified thioredoxin-like protein 2 (Txl-2), a novel thioredoxin family member, as the target of the monoclonal antibody MC3 which can detect colon cancer with high sensitivity and specificity. In the present study, the function of the most abundant isoform Txl-2b in cell proliferation and apoptosis were investigated. Txl-2 overexpression correlated with increased clinical stages. Inhibition of Txl-2b suppressed cell proliferation, induced cell cycle arrest at the G1/S phase, and led to the responsiveness to the vincristine-induced apoptosis in SW620 cells. Txl-2b overexpression in LoVo cells had the opposite effect, which was dependent of Trx domain function. In vivo studies validated that Txl-2b expression promoted colon cancer tumorigenesis in nude mice. Further studies revealed that nuclear factor-κB (NF-κB) signaling was activated by Txl-2b. Inhibition of NF-κB activation partly abrogated the pro-proliferation and anti-apoptotic phenotypes mediated by Txl-2b via reduced Cyclin D1, Bcl-2, Bcl-xL and Survivin expression and increased Caspase-3 activation. Overall, our results indicate that Txl-2b expression stimulates cancer cell proliferation, accelerates the cell cycle and contributes to apoptosis resistance in colon cancer and provides a potential therapeutic target for colon cancer treatment. Copyright © 2014. Published by Elsevier Ireland Ltd.
    Cancer Letters 12/2014; · 5.02 Impact Factor
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    ABSTRACT: Inconsistent results of SOX2 expression have been reported in gastric cancer (GC). Here, we demonstrated that SOX2 was progressively downregulated during GC development via immunochemistry in 755 human gastric specimens. Low SOX2 levels were associated with pathological stage and clinical outcome. Multivariate analysis indicated that SOX2 protein expression served as an independent prognostic marker for GC. Gain-and loss-of function studies showed the anti-proliferative, anti-metastatic, and pro-apoptotic effects of SOX2 in GC. PTEN was selected as SOX2 targets by cDNA microarray and ChIP-DSL, further identified by luciferase assays, EMSA and ChIP-PCR. PTEN upregulation in response to SOX2-enforced expression suppressed GC malignancy via regulating Akt dephosphorylation. PTEN inhibition reversed SOX2-induced anticancer effects. Moreover, concordant positivity of SOX2 and PTEN proteins in nontumorous tissues but lost in matched GC specimens predicted a worse patient prognosis. Thus, SOX2 proved to be a new marker for evaluating GC outcome. Copyright © 2014. Published by Elsevier Ireland Ltd.
    Cancer Letters 12/2014; · 5.02 Impact Factor
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    ABSTRACT: STIM1 (stromal interaction molecule 1), an endoplasmic reticulum Ca(2+) sensor that triggers the store-operated Ca(2+) entry activation, has recently been implicated in cancer progression. However, the role of STIM1 in the progression and metastasis of colorectal cancer (CRC) has not been addressed. In this study, we confirmed increased expression of STIM1 in highly invasive CRC cell lines. Enhanced expression of STIM1 promoted CRC cell metastasis in vitro and in vivo, whereas silencing of STIM1 with small interfering RNA resulted in reduced metastasis. Ectopic expression of STIM1 in CRC cells induced epithelial-to-mesenchymal transition (EMT), whereas silencing of STIM1 had the opposite effect. Furthermore, STIM1 expression was markedly higher in CRC tissues than in adjacent noncancerous tissues. STIM1 overexpression correlated with poor differentiation and higher tumor node metastasis stage. CRC patients with positive STIM1 expression had poorer prognoses than those with negative STIM1 expression. Moreover, STIM1 was found to be a direct target of miR-185, a microRNA (miRNA) that has not previously been reported to be involved in EMT, in both CRC tissues and cell lines. Taken together, these findings demonstrate for the first time that STIM1 promotes metastasis and is associated with cancer progression and poor prognosis in patients with CRC. In addition, we show that expression of STIM1 is regulated by a posttranscriptional regulatory mechanism mediated by a new EMT-related miRNA. This novel miR-185-STIM1 axis promotes CRC metastasis and may be a candidate biomarker for prognosis and a target for new therapies.Oncogene advance online publication, 22 December 2014; doi:10.1038/onc.2014.404.
    Oncogene 12/2014; · 8.56 Impact Factor
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    ABSTRACT: Loss of cell-cell adhesion is important for the development of cancer invasion and metastasis. Vinculin, a key adhesion-related protein, can affect metastasis and prognosis in several tumours. Here, we determined the biological roles of vinculin in the metastasis of colorectal cancer (CRC) and evaluated its clinical significance as a potential disease biomarker. The expression level of vinculin in CRC cell lines and tissues was measured using Real-Time PCR and western blotting. Moreover, vinculin function was analysed using Transwell assays and in vivo metastasis assays in gain- and loss-of-function experiments. Furthermore, the impact of vinculin together with membrane-bound beta-catenin on the prognosis of 228 CRC patients was investigated by immunohistochemistry. Additionally, the expression of epithelial-mesenchymal transition (EMT) indicators was verified by immunohistochemistry in CRC tissues obtained from these patients.Result: Vinculin expression was found to be significantly downregulated in highly metastatic CRC cell lines and metastatic tissues. Both in vitro and in vivo experiments showed that vinculin suppressed invasion, migration and metastasis in CRC cells and that this suppression could be attenuated by silencing beta-catenin. Moreover, the expression of vinculin and membrane-bound beta-catenin were positively correlated in CRC tissues, and lack of vinculin expression emerged as an independent prognostic factor in patients with CRC. Finally, the loss of vinculin and membrane-bound beta-catenin was associated with node metastasis, organ metastasis and expression of EMT indicators. Our results suggest that vinculin may play specific roles in the EMT and metastasis of CRC and that loss of vinculin could be used as a prognostic factor for CRC.
    Molecular cancer. 12/2014; 13(1):263.
  • Xiangqiang Liu, Daiming Fan
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    ABSTRACT: The epithelial-mesenchymal transition (EMT) is a highly conserved cellular process that transforms epithelial cells into mesenchymal cells; EMT is involved in normal embryogenesis and tissue repair and contributes to tumor progression, including tumor metastasis, therapy resistance and disease recurrence. Cancer stem cells (CSCs) represent a fraction of undifferentiated cancer cells that exhibit stem cell-like features. They have the ability to self-renew and can seed new tumors. Thus, CSCs might represent the cellular resource that causes metastases and accounts for therapy resistance. Recent studies have highlighted a link between EMT and CSC formation. EMT is relevant to the acquisition and maintenance of stem cell-like characteristics and is sufficient to endow differentiated normal and cancer cells with stem cell properties. Moreover, CSCs often exhibit EMT properties. This reciprocal relationship between EMT and CSCs might have many implications in tumor progression. In this paper, we review current studies related to EMT and CSCs in tumor progression and therapeutic resistance, with a special focus on the common characteristics and links between these processes, and explore the importance of these links in the development of improved antitumor therapies.
    Current pharmaceutical design. 12/2014;
  • Xingshun Qi, Xiaozhong Guo, Daiming Fan
    Hepatology 12/2014; · 11.19 Impact Factor
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    ABSTRACT: The risk of venous thromboembolism (VTE) may be increased in patients with liver diseases. A systematic review and meta-analysis were conducted to analyze the epidemiology of VTE in such patients. All relevant studies were searched via the PubMed, EMBASE, and Cochrane Library databases. The incidence and prevalence of VTE were pooled using random-effect models. Subgroup analyses were conducted according to the type of VTE [deep vein thrombosis (DVT), pulmonary embolism (PE)], type of liver disease (liver cirrhosis alone/unclassified liver diseases or non-cirrhotics), region in which the study was performed (USA/Europe/Asia), number of total observed patients with liver diseases (>1,000/<1,000 patients), study quality (high/low), and methods for identifying the cases (ICD codes/clinical charts). Of 4,843 papers initially identified, 20 were included. The incidence of VTE varied from 0.33 to 6.32 % in 14 studies with a pooled value of 1 % (95 % confidence interval (CI) 0.7-1.3 %). The pooled incidence of DVT and PE was 0.6 % (95 % CI 0.4-0.8 %) and 0.28 % (95 % CI 0.13-0.49 %), respectively. The prevalence of VTE varied from 0.6 to 4.69 % in six studies with a pooled value of 1.0 % (95 % CI 0.7-1.2 %). The pooled prevalence of DVT and PE was 0.7 % (95 % CI 0.6-0.9 %) and 0.36 % (95 % CI 0.13-0.7 %), respectively. The heterogeneity was statistically significant in the main and subgroup meta-analyses. In conclusion, about 1 % of patients with liver diseases develop or are diagnosed with VTE during their hospitalizations. However, the epidemiological data are very heterogeneous among studies.
    Internal and Emergency Medicine 12/2014; · 2.41 Impact Factor
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    ABSTRACT: Hypoxia has been implicated as a crucial microenvironmental factor that induces cancer metastasis. We previously reported that hypoxia could promote gastric cancer (GC) metastasis, but the underlying mechanisms are not clear. Long noncoding RNAs (lncRNAs) have recently emerged as important regulators of carcinogenesis that act on multiple pathways. However, whether lncRNAs are involved in hypoxia-induced GC metastasis remains unknown. In this study, we investigated the differentially expressed lncRNAs resulting from hypoxia-induced GC and normoxia conditions using microarrays and validated our results through real-time quantitative polymerase chain reaction. We found an lncRNA, AK058003, that is upregulated by hypoxia. AK058003 is frequently upregulated in GC samples and promotes GC migration and invasion in vivo and in vitro. Furthermore, AK058003 can mediate the metastasis of hypoxia-induced GC cells. Next, we identified γ-synuclein (SNCG), which is a metastasis-related gene regulated by AK058003. In addition, we found that the expression of SNCG is positively correlated with that of AK058003 in the clinical GC samples used in our study. Furthermore, we found that the SNCG gene CpG island methylation was significantly increased in GC cells depleted of AK058003. Intriguingly, SNCG expression is also increased by hypoxia, and SNCG upregulation by AK058003 mediates hypoxia-induced GC cell metastasis. These results advance our understanding of the role of lncRNA-AK058003 as a regulator of hypoxia signaling, and this newly identified hypoxia/lncRNA-AK058003/SNCG pathway may help in the development of new therapeutics. Copyright © 2014 Neoplasia Press, Inc. Published by Elsevier Inc. All rights reserved.
    Neoplasia (New York, N.Y.) 12/2014; 16(12):1094-106. · 5.40 Impact Factor
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    ABSTRACT: Mesenchymal stem cells (MSCs) have been shown to integrate into the tumor stroma; however, the precise mechanisms of this process are still elusive. In this study, the EMT phenotype and the enhanced metastatic ability of tumor cells were observed using transwell and trans-endothelial migration assays, respectively, as well as by using electron and laser confocal microscopy. Critical genes were screened and validated using gene arrays and clinical samples, and the changes at the protein level were examined both in vitro and in vivo. Cancer cells acquired an “activated” carcinoma-associated fibroblasts (CAFs) phenotype after being in close contact with MSCs and enhancing tumor metastasis and growth in vivo. Paracrine signals also induced EMT and promoted transwell and trans-endothelial migration, the changes were dependent on β-catenin, MMP-16, snail and twist. Notably, the higher expression levels of β-catenin and MMP-16 were correlated with tumor invasion and distant organ and lymph node metastases in intestinal type gastric cancer. MSCs within the tumor niche significantly facilitated tumor growth and metastasis by paracrine cues and close physical connection. This occurred partly through snail, twist and its downstream targets, specifically β-catenin/MMP-16. This article is protected by copyright. All rights reserved
    Journal of Cellular Biochemistry 11/2014; · 3.37 Impact Factor
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    ABSTRACT: Uncontrolled proliferation is a key characteristic of gastric carcinogenesis and the precise mechanisms underlying the altered proliferation behaviors of GC cells have not been clearly elucidated. miRNAs has been suggested to play a crucial role in the pathogenesis and development of various cancers. In the present study, we employed an impedance-based real-time cell electronic sensing (RT-CES) system to detect the effects of ectopically expressed miRNAs on GC cell proliferation.
    Journal of Cancer Research and Clinical Oncology 10/2014; · 3.01 Impact Factor
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    ABSTRACT: To investigate and compare the efficacy and safety of percutaneous transhepatic biliary stenting (PTBS) using a one- or two-stage procedure and determine the predictive factors for the efficacious treatment of malignant hilar obstruction (MHO).
    CardioVascular and Interventional Radiology 10/2014; · 1.97 Impact Factor
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    ABSTRACT: Recent studies have reported that hyper-methylation in the promoter region of miRNAs could silence the expression of tumor suppressive miRNAs and might play significant roles in the process of tumor development. However, the potential mechanisms regarding how methylation of miRNA CpG Island could regulate cancer cell chemo-resistance have not yet been studied. Using microarray and BSP (Bisulfate Sequencing PCR) assays, we found that compared with the parent SGC7901/VCR cells, expression of miR-129-5p was restored in SGC7901/VCR gastric cancer multi-drug resistant cell line treated by de-methylation reagent (5-AZA-dC). Using gain or loss of function assays, we found the over-expressed miR-129-5p reduced the chemo-resistance of SGC7901/VCR and SGC7901/ADR cells, while down-regulation of miR-129-5p had an opposite effect. Furthermore, three members of multi-drug resistance (MDR) related ABC transporters (ABCB1, ABCC5 and ABCG1) were found to be direct targets of miR-129-5p using bioinformatics analysis and report gene assays. The present study indicated that hyper-methylation of miR-129-5p CpG island might play important roles in the development of gastric cancer chemo-resistance by targeting MDR related ABC transporters and might be used as a potential therapeutic target in preventing the chemo-resistance of gastric cancer.
    Oncotarget 10/2014; · 6.63 Impact Factor
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    ABSTRACT: A growing amount of evidence indicates that miRNAs are important regulators of multiple cellular processes and, when expressed aberrantly in different types of cancer such as hepatocellular carcinoma (HCC), play significant roles in tumorigenesis and progression. Aberrant expression of miR-199a-5p (also called miR-199a) was found to contribute to carcinogenesis in different types of cancer, including HCC. However, the precise molecular mechanism is not yet fully understood. The present study showed that miR-199a is frequently down-regulated in HCC tissues and cells. Importantly, lower expression of miR-199a was significantly correlated with the malignant potential and poor prognosis of HCC, and restoration of miR-199a in HCC cells led to inhibition of the cell proliferation and cell cycle in vitro and in vivo. Furthermore, Frizzled type 7 receptor (FZD7), the most important Wnt receptor involved in cancer development and progression, was identified as a functional target of miR-199a. In addition, these findings were further strengthened by results showing that expression of FZD7 was inversely correlated with miR-199a in both HCC tissues and cells and that over-expression of miR-199a could significantly down-regulate the expression of genes downstream of FZD7, including β-catenin, Jun, Cyclin D1 and Myc. In conclusion, these findings not only help us to better elucidate the molecular mechanisms of hepatocarcinogenesis from a fresh perspective but also provide a new theoretical basis to further investigate miR-199a as a potential biomarker and a promising approach for HCC treatment.
    PLoS ONE 10/2014; 9(10):e110074. · 3.53 Impact Factor
  • Xingshun Qi, Xiaozhong Guo, Daiming Fan
    CardioVascular and Interventional Radiology 10/2014; · 1.97 Impact Factor
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    Xingshun Qi, Zhiping Yang, Daiming Fan
    Saudi Journal of Gastroenterology 09/2014; 20(5):265-266. · 1.22 Impact Factor
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    ABSTRACT: An increasing body of evidence indicates that miRNAs have a critical role in carcinogenesis and cancer progression; however, the role of miRNAs in the tumorigenesis of adencarcinoma of gastric esophageal junction (AGEJ) remains largely unclear.
    BMC Cancer 08/2014; 14(1):633. · 3.32 Impact Factor
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    ABSTRACT: Acute variceal bleeding is the most common lethal complication of liver cirrhosis. A meta-analysis was conducted to compare the outcomes of transjugular intrahepatic portosystemic shunt (TIPS) to those of medical/endoscopic therapy for acute variceal bleeding in cirrhotic patients.
    Journal of Clinical Gastroenterology 08/2014; · 3.19 Impact Factor
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    ABSTRACT: AbstactBackground and AimThe gut microbiota plays a pivotal role in the intestinal diseases. Fecal microbiota transplantation (FMT) might be a rescue therapy for refractory inflammatory bowel disease. This study aimed to evaluate the safety, feasibility and efficacy of FMT through mid-gut for refractory Crohn's disease (CD).Methods We established standardized laboratory protocol and clinical work flow for FMT. Only refractory CD patients with Harvey-Bradshaw Index (HBI) score ≥ 7 were enrolled for this study. All included patients were treated with single FMT through mid-gut and assessed during follow-up.ResultsMetagenomics analysis showed a high concordance between feces sample and purified fecal microbiota from same donors. Standardized fecal microbiota preparation and clinical flow significantly simplified the practical aspects of FMT. Totally 30 patients were qualified for the present analysis. The rate of clinical improvement and remission based on clinical activity at the first month was 86.7 % (26/30) and 76.7 % (23/30) respectively, which was higher than other assessment points within 15-month follow-up. Patients’ body weight increased after FMT, and the lipid profile improved as well. FMT also showed a fast and continuous significant effect in relieving the sustaining abdominal pain associated with sustaining CD.Conclusions This is a pilot study with the largest sample of patients with refractory CD underwent single FMT. The results demonstrated that FMT through mid-gut might be a safe, feasible, and efficient rescue therapy for refractory CD.
    Journal of Gastroenterology and Hepatology 08/2014; · 3.33 Impact Factor

Publication Stats

5k Citations
1,900.97 Total Impact Points

Institutions

  • 2000–2014
    • Fourth Military Medical University
      • • State Key Laboratory of Cancer Biology
      • • Department of Gastroenterology
      Xi’an, Liaoning, China
    • Virginia Commonwealth University
      • School of Medicine
      Richmond, VA, United States
  • 2012
    • Chinese Academy of Engineering Physics
      Peping, Beijing, China
  • 2009–2011
    • State Key Laboratory of Medical Genetics of China
      Ch’ang-sha-shih, Hunan, China
  • 1998–2010
    • Xi'an Jiaotong University
      • • School of Science
      • • Department of Gastroenterology
      Xi’an, Shaanxi Sheng, China
  • 2008
    • Logistical College of Chinese People's Armed Police Force
      T’ien-ching-shih, Tianjin Shi, China
  • 2004
    • Huazhong University of Science and Technology
      Wu-han-shih, Hubei, China
  • 2002
    • General Hospital of Jinan Military Region
      Chi-nan-shih, Shandong Sheng, China
  • 2001–2002
    • Southern Medical University
      Shengcheng, Guangdong, China
  • 1997–2001
    • Emory University
      • Department of Internal Medicine
      Atlanta, GA, United States