Tao Jiang

Beijing Neurosurgical Institute, Peping, Beijing, China

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Publications (318)1289.81 Total impact

  • Hui Luo · Zhengxin Chen · Shuai Wang · Rui Zhang · Wenjin Qiu · Lin Zhao · Chenghao Peng · Ran Xu · Wanghao Chen · Hong-Wei Wang · [...] · Shuyu Zhang · Dan Chen · Wenting Wu · Chunsheng Zhao · Gang Cheng · Tao Jiang · Daru Lu · Yongping You · Ning Liu · Huibo Wang
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    ABSTRACT: Resistance to temozolomide poses a major clinical challenge in glioblastoma multiforme treatment, and the mechanisms underlying the development of temozolomide resistance remain poorly understood. Enhanced DNA repair and mutagenesis can allow tumour cells to survive, contributing to resistance and tumour recurrence. Here, using recurrent temozolomide-refractory glioblastoma specimens, temozolomide-resistant cells, and resistant-xenograft models, we report that loss of miR-29c via c-Myc drives the acquisition of temozolomide resistance through enhancement of REV3L-mediated DNA repair and mutagenesis in glioblastoma. Importantly, disruption of c-Myc/miR-29c/REV3L signalling may have dual anticancer effects, sensitizing the resistant tumours to therapy as well as preventing the emergence of acquired temozolomide resistance. Our findings suggest a rationale for targeting the c-Myc/miR-29c/REV3L signalling pathway as a promising therapeutic approach for glioblastoma, even in recurrent, treatment-refractory settings.
    Brain 10/2015; DOI:10.1093/brain/awv287 · 9.20 Impact Factor
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    ABSTRACT: The dengue virus (DENV) envelope protein domain III (ED3) has been suggested to contain receptor recognition sites and the critical neutralizing epitopes. Up to date, relatively little work has been done on fine mapping of neutralizing epitopes on ED3 for DENV4. In this study, a novel mouse type-specific neutralizing antibody 1G6 against DENV4 was obtained with both prophylactic and therapeutic effects. The epitope was mapped to residues 387-390 of DENV4 envelope protein. Furthermore, site-directed mutagenesis assay identified two critical residues (T388 and H390). The epitope is variable among different DENV serotypes but is highly conserved among four DENV4 genotypes. Affinity measurement showed that naturally occurring variations in ED3 outside the epitope region did not alter the binding of mAb 1G6. These findings expand our understanding of the interactions between neutralizing antibodies and the DENV4 and may be valuable for rational design of DENV vaccines and antiviral drugs.
    PLoS ONE 10/2015; 10(10):e0139741. DOI:10.1371/journal.pone.0139741 · 3.23 Impact Factor
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    ABSTRACT: We recorded motor cortical activity using high- density electrocorticogram (ECoG) from three patients during awake craniotomy. Subjects repeatedly executed hand flexion/extension tasks according to auditory instructions. Clear event-related desynchronization (ERD) in beta band (8-32) Hz and event-related synchronization (ERS) in gamma band (60-200) Hz were observed. High frequency band (HFB: 60-200 Hz) activation was found to be more localized compared to low frequency band (LFB: 8-32 Hz) activation in all subjects. Local spatial correlation maps in LFB and HFB were constructed by computing the correlation between channels. Local spatial correlation dropped more in the ERD/ERS areas consistently in two subjects. The results indicate that ERD/ERS patterns are more spatially uncorrelated and denser ECoG electrode is necessary within these areas to map uncorrelated ‘sources’. High resolution electrodes might improve both clinical functional mapping and brain machine interface outcomes in the near future.
    37TH ANNUAL INTERNATIONAL CONFERENCE OF THE IEEE Engineering in Medicine and Biology Society; 08/2015
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    ABSTRACT: The goal of this work was to explore the most effective miRNAs affecting glioblastoma multiforme (GBM) phenotype transition and malignant progression. We annotated 491 TCGA samples' miRNA expression profiles according to their mRNA-based subtypes and found that the mesenchymal tumors had significantly decreased miR-181 family expression compared with the other three subtypes while the proneural subtype harbored extremely high miR-181 family expression. Patients with high miR-181 family expression had longer overall survival (p = 0.0031). We also confirmed that NF-κB-targeting genes and the EMT (epithelial-mesenchymal transition) pathway were inversely correlated with miR-181 family expression and that the entire miR-181 family inhibited glioma cell invasion and proliferation; of these, miR-181b was the most effective suppressor. Furthermore, miR-181b was validated to suppress EMT by targeting KPNA4 and was associated with survival outcome in the TCGA and CGGA datasets and in another independent cohort. The EMT-inhibitory effect of miR-181b was lost after KPNA4 expression was restored. We also identified the antitumorigenic activity of miR-181b in vitro and in vivo. Our results showed that miR-181 family expression was closely correlated with TCGA subtypes and patients' overall survival, indicating that miR-181b, a tumor-suppressive miRNA, could be a novel therapeutic candidate for treating gliomas.
    Scientific Reports 08/2015; 5:13072. DOI:10.1038/srep13072 · 5.58 Impact Factor
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    ABSTRACT: Isorhamnetin has been reported to have anti-inflammatory, anti-oxidative, and anti-proliferative effects. The aim of this study was to investigate the protective effect of isorhamnetin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice by inhibiting the expression of cyclooxygenase-2 (COX-2). The effects of isorhamnetin on LPS-induced lung pathological damage, wet/dry ratios and the total protein level in bronchoalveolar lavage fluid (BALF), inflammatory cytokine release, myeloperoxidase (MPO) and superoxide dismutase (SOD) activities, and malondialdehyde (MDA) level were examined. In addition, the COX-2 activation in lung tissues was detected by Western blot. Isorhamnetin pretreatment improved the mice survival rates. Moreover, isorhamnetin pretreatment significantly attenuated edema and the pathological changes in the lung and inhibited protein extravasation in BALF. Isorhamnetin also significantly decreased the levels of inflammatory cytokines in BALF. In addition, isorhamnetin markedly prevented LPS-induced oxidative stress. Furthermore, isorhamnetin pretreatment significantly suppressed LPS-induced activation of COX-2. Isorhamnetin has been demonstrated to protect mice from LPS-induced ALI by inhibiting the expression of COX-2.
    Inflammation 08/2015; DOI:10.1007/s10753-015-0231-0 · 2.21 Impact Factor
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    ABSTRACT: Glioma is a most common type of primary brain tumors. Extracellular vesicles, in the form of exosomes, are known to mediate cell-cell communication by transporting cell-derived proteins and nucleic acids, including various microRNAs (miRNAs). Here we examined the cerebrospinal fluid (CSF) from patients with recurrent glioma for the levels of cancer-related miRNAs, and evaluated the values for prognosis by comparing the measures of CSF-, serum-, and exosome-contained miR-21 levels. Samples from seventy glioma patients following surgery were compared with those from brain trauma patients as a non-tumor control group. Exosomal miR-21 levels in the CSF of glioma patients were found significantly higher than in the controls; whereas no difference was detected in serum-derived exosomal miR-21 expression. The CSF-derived exosomal miR-21 levels correlated with tumor spinal/ventricle metastasis and the recurrence with anatomical site preference. From additional 198 glioma tissue samples, we verified that miR-21 levels associated with tumor grade of diagnosis and negatively correlated with the median values of patient overall survival time. We further used a lentiviral inhibitor to suppress miR-21 expression in U251 cells. The results showed that the levels of miR-21 target genes of PTEN, RECK and PDCD4 were up-regulated at protein levels. Therefore, we concluded that the exosomal miR-21 levels could be demonstrated as a promising indicator for glioma diagnosis and prognosis, particularly with values to predict tumor recurrence or metastasis.
    Oncotarget 08/2015; 6(29). DOI:10.18632/oncotarget.4699 · 6.36 Impact Factor
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    ABSTRACT: Mitochondrial dysfunction contributes to cell death after cerebral ischemia/reperfusion (I/R) injury. Cannabinoid CB1 receptor is expressed in neuronal mitochondrial membranes (mtCB1R) and involved in regulating mitochondrial functions under physiological conditions. However, whether mtCB1R affords neuroprotection against I/R injury remains unknown. We used mouse models of cerebral I/R, primary cultured hippocampal neurons exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) and Ca(2+)-induced injury in purified neuronal mitochondria to investigate the role of mtCB1R in neuroprotection. Our results showed selective cell-permeant CB1 receptor agonist, arachidonyl-2-chloroethylamide (ACEA), significantly up-regulated the expression of mtCB1R protein in hippocampal neurons and tissue. In vitro, ACEA restored cell viability, inhibited generation of reactive oxygen species (ROS), decreased lactate dehydrogenase (LDH) release and reduced apoptosis, improved mitochondrial function. In vivo, ACEA ameliorated neurological scores, diminished the number of TUNEL-positive neurons and decreased the expression of cleaved caspase-3. However, ACEA-induced benefits were blocked by the selective cell-permeant CB1 receptor antagonist AM251, but just partially by the selective cell-impermeant CB1 receptor antagonist hemopressin. In purified neuronal mitochondria, mtCB1R activation attenuated Ca(2+)-induced mitochondrial injury. In conclusion, mtCB1R is involved in ACEA-induced protective effects on neurons and mitochondrial functions, suggesting mtCB1R may be a potential novel target for the treatment of brain ischemic injury.
    Scientific Reports 07/2015; 5:12440. DOI:10.1038/srep12440 · 5.58 Impact Factor
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    ABSTRACT: Effective annual influenza vaccination requires frequent changes in vaccine composition due to both antigenic shift for different subtype hemagglutinins (HAs) and antigenic drift in a particular HA. Here we present a broadly neutralizing human monoclonal antibody with an unusual binding modality. The antibody, designated CT149, was isolated from convalescent patients infected with pandemic H1N1 in 2009. CT149 is found to neutralize all tested group 2 and some group 1 influenza A viruses by inhibiting low pH-induced, HA-mediated membrane fusion. It promotes killing of infected cells by Fc-mediated antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity. X-ray crystallographic data reveal that CT149 binds primarily to the fusion domain in HA2, and the light chain is also largely involved in binding. The epitope recognized by this antibody comprises amino-acid residues from two adjacent protomers of HA. This binding characteristic of CT149 will provide more information to support the design of more potent influenza vaccines.
    Nature Communications 07/2015; 6:7708. DOI:10.1038/ncomms8708 · 11.47 Impact Factor
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    ABSTRACT: Anaplastic gliomas are characterized by variable clinical and genetic features, but there are few studies focusing on the substratification of anaplastic gliomas. To identify a more objective and applicable classification of anaplastic gliomas, we analyzed whole genome mRNA expression profiling of four independent datasets. Univariate Cox regression, linear risk score formula and receiver operating characteristic (ROC) curve were applied to derive a gene signature with best prognostic performance. The corresponding clinical and molecular information were further analyzed for interpretation of the different prognosis and the independence of the signature. Gene ontology (GO), Gene Set Variation Analysis (GSVA) and Gene Set Enrichment Analysis (GSEA) were performed for functional annotation of the differences. We found a three-gene signature, by applying which, the anaplastic gliomas could be divided into low risk and high risk groups. The two groups showed a high concordance with grade II and grade IV gliomas, respectively. The high risk group was more aggressive and complex. The three-gene signature showed diagnostic and prognostic value in anaplastic gliomas.
    Oncotarget 07/2015; DOI:10.18632/oncotarget.5421 · 6.36 Impact Factor
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    ABSTRACT: CHARGE syndrome is an autosomal-dominant disorder involved in multiple organs. Loss-of-function mutations in CHD7, a member of the chromodomain helicase DNA-binding (CHD) protein family, are known to cause the CHARGE syndrome. The purposes of this paper were to affirm the diagnosis and to identify the molecular basis of one atypical CHARGE syndrome patient from China, where only one CHARGE case was reported before. We employed the Verloes criteria to make a preliminary clinical diagnosis, and performed mutation screening of CHD7 via Ion Torrent semiconductor sequencing. The patient was preliminary diagnosed as atypical CHARGE syndrome according to Verloes criteria with a novel heterozygous small deletion of CHD7 (CHD7: c.3462_3471delTCGCTTCCCT). As the second reported case of CHARGE syndrome in China, it was caused by one novel heterozygous mutation of the CHD7 gene. Our findings further reveal the relationship between CHD7 and CHARGE syndrome and provide a potential clinical diagnosis for CHARGE syndrome. Copyright © 2015. Published by Elsevier B.V.
    Gene 07/2015; 571(2). DOI:10.1016/j.gene.2015.07.042 · 2.14 Impact Factor
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    ABSTRACT: Isocitrate dehydrogenase 1 gene mutations are found in most World Health Organization grade II and III gliomas and secondary glioblastomas. Isocitrate dehydrogenase 1 mutations are known to have prognostic value in high-grade gliomas. However, their prognostic significance in low-grade gliomas remains controversial. We determined the predictive and prognostic value of isocitrate dehydrogenase 1 status in low-grade gliomas. The association of isocitrate dehydrogenase 1 status with clinicopathological and genetic factors was also evaluated. Clinical information and genetic data including isocitrate dehydrogenase 1 mutation, O 6-methylguanine DNA methyltransferase promoter methylation, 1p/19q chromosome loss, and TP53 mutation of 417 low-grade gliomas were collected from the Chinese Glioma Genome Atlas database. Kaplan-Meier and Cox proportional hazards regression analyses were performed to evaluate the prognostic effect of clinical characteristics and molecular biomarkers. Isocitrate dehydrogenase 1 mutation was identified as an independent prognostic factor for overall, but not progression-free, survival. Notably, isocitrate dehydrogenase 1 mutation was found to be a significant prognostic factor in patients with oligodendrogliomas, but not in patients with astrocytomas. Furthermore, O 6-methylguanine DNA methyltransferase promoter methylation (p = 0.017) and TP53 mutation (p < 0.001), but not 1p/19q loss (p = 0.834), occurred at a higher frequency in isocitrate dehydrogenase 1-mutated tumors than in isocitrate dehydrogenase 1 wild-type tumors. Younger patient age (p = 0.041) and frontal lobe location (p = 0.010) were significantly correlated with isocitrate dehydrogenase 1 mutation. Chemotherapy did not provide a survival benefit in patients with isocitrate dehydrogenase 1-mutated tumors. Isocitrate dehydrogenase 1 mutation was an independent prognostic factor in low-grade gliomas, whereas it showed no predictive value for chemotherapy response. Isocitrate dehydrogenase 1 mutation was highly associated with O 6-methylguanine DNA methyltransferase promoter methylation and TP53 mutation.
    PLoS ONE 06/2015; 10(6):e0130872. DOI:10.1371/journal.pone.0130872 · 3.23 Impact Factor
  • Zheng Wang · Zhong Zhang · Yinyan Wang · Gan You · Tao Jiang
    Epilepsy research 06/2015; 115. DOI:10.1016/j.eplepsyres.2015.06.004 · 2.02 Impact Factor
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    ABSTRACT: The highly pathogenic H5N1 avian influenza virus is one of the greatest influenza pandemic threats since 2003. The association of the receptor binding domain (RBD) with the virulence of influenza virus is rarely addressed, particularly of H5N1 influenza viruses. In this study, BALB/c mice were intranasally infected with A/Vietnam/1194/2004 (VN1194, H5N1). The mouse lung-adapted variants were isolated and the mutation of E190G (H3 numbering) in the RBD was recognized. The recombinant virus, rVN-E190G carrying E190G in hemagglutinin (HA) was designed and rescued using reverse genetics techniques. The receptor binding activity, growth curve and pathogenicity in mice of the rVN-E190G were investigated. Results demonstrated that rVN-E190G virus increased the binding avidity to α2,6 SA (sialic acid) and reduced the affinity to α2,3 SA, meanwhile weakened the viral replication in vitro. Moreover, the virulence assessment demonstrated that rVN-E190G was attenuated in mice. These results indicated that the mutation E190G in HA decreases H5N1 viral replication in vitro and significantly attenuates virulence in vivo. These findings identify one of the determinants in RBD which can be associated with H5N1 virulence in mice. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Medical Virology 06/2015; 87(11). DOI:10.1002/jmv.24257 · 2.35 Impact Factor
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    ABSTRACT: Therapeutics targeting the Nogo-A signal pathway hold promise to promote recovery following brain injury. Based on the temporal characteristics of Nogo-A expression in the process of cerebral ischemia and reperfusion, we tested a novel asynchronous treatment, in which TAT-M9 was used in the early stage to decrease neuronal loss, and TAT-NEP1-40 was used in the delayed stage to promote neurite outgrowth after bilateral common carotid artery occlusion (BCCAO) in mice. Both TAT-M9 and TAT-NEP1-40 were efficiently delivered into the brains of mice by intraperitoneal injection. TAT-M9 treatment promoted neuron survival and inhibited neuronal apoptosis. Asynchronous therapy with TAT-M9 and TAT-NEP1-40 increased the expression of Tau, GAP43 and MAP-2 proteins, and enhanced short-term and long-term cognitive functions. In conclusion, the asynchronous treatment had a long-term neuroprotective effect, which reduced neurologic injury and apoptosis, promoted neurite outgrowth and enhanced functional recovery after ischemia. It suggests that this asynchronous treatment could be a promising therapy for cerebral ischemia in humans.
    Journal of Drug Targeting 06/2015; DOI:10.3109/1061186X.2015.1052070 · 2.74 Impact Factor
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    ABSTRACT: Infection in airspaces and lung parenchyma may cause acute lung injury and multiple organ dysfunction syndrome due to acute inflammatory response, leading to organ failure and high mortality. ZC3H12D has been shown to modulate Toll-like receptor signaling. This study aimed to investigate the change of ZC3H12D during acute lung injury and its role in inflammation processes. Mice were challenged with lipopolysaccharides (LPS) intratracheally. The expression levels of Zc3h12d, NF-κB, and cytokines were analyzed by quantitative real-time PCR (qPCR), ELISA, and Western blot. The mRNA stability was assessed by qPCR after cells were treated with actinomycin D for specified times. The 3' untranslated region (3'-UTR) of c-fos was cloned immediately downstream of the luciferase coding sequence driven by CMV promoter and luciferase activity was measured with a Luciferase Assay kit. Upon LPS treatment, ZC3H12D levels were reduced in mouse immune cells, whereas levels of NF-κB, IL-6, and TNF-α were significantly increased. Knockdown Zc3h12d in THP1 cells resulted in the upregulation of NF-κB while overexpression of Zc3h12d inhibited NF-κB expression. Ectopic Zc3h12d significantly reduced the mRNA stability of c-fos, NF-κB, TNF-α, IL-1β, and IL-6. Attachment of the c-fos 3'-UTR made luciferase expression levels sensitive to levels of ZC3H12D. The data indicated that ZC3H12D could suppress both the initial inflammation storm and chronic inflammation by targeting the mRNA of cytokines as well as NF-κB and c-fos. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Molecular Immunology 06/2015; 67(2 Pt B). DOI:10.1016/j.molimm.2015.05.018 · 2.97 Impact Factor
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    ABSTRACT: Internal ribosomal entry site (IRES)-mediated translation initiation is constitutively activated during stress conditions such as tumorigenesis and hypoxia. The RNA editing enzyme ADAR1 plays an important role in physiology and pathology. Initially, we found that the ADAR1 p150 or p110 transcript levels were decreased in glioma cells compared with normal astrocyte cells. In contrast, protein levels of ADAR1 p110 were significantly upregulated in glioma tissues and cells. This expression pattern indicated translationally controlled regulation. We identified an 885-nt sequence that was located between AUG1 and AUG2 within the ADAR1 mRNA that exhibited IRES-like activity. Furthermore, we confirmed that the translational mode of ADAR1 p110 was mediated by PTBP1 in glioma cells. The protein levels of PTBP1 and ADAR1 were cooperatively expressed in glioma tissues and cells. Knocking down ADAR1 p110 significantly decreased cell proliferation in three types of glioma cells (T98G, U87MG and A172). The removal of a minimal IRES-like sequence in a p150-overexpression construct could effectively abolish p110 induction and resulted in the slight suppression of cell proliferation compared with ADAR1-p150 overexpression in siPTBP1-treated T98G cells. In summary, our study revealed a mechanism whereby ADAR1 p110 can be activated by PTBP1 through an IRES-like element in glioma cells, and ADAR1 is essential for the maintenance of gliomagenesis.
    Cellular and Molecular Life Sciences CMLS 06/2015; DOI:10.1007/s00018-015-1938-7 · 5.81 Impact Factor
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    ABSTRACT: Live attenuated influenza vaccines (LAIV) are now available for the prevention of influenza, with LAIV strains generally derived from serial passaging in cultures or by reverse genetics. The receptor binding domain (RBD) in the hemagglutinin (HA) of influenza virus is responsible for viral binding to avian type, α2,3-linked or human type α2,6-linked sialic acid receptor; however the virulence determinants in the RBD of H5N1 virus remain largely unknown. In the present study, serial passaging of H5N1 virus A/Vietnam/1194/2004 (VN1194) in MDCK cells resulted in the generation of adapted variants with large-plaque morphology, and genomic sequencing of selected variants revealed two specific amino acid substitutions (K193E and G225E) in the RBD. Reverse genetics (RG) was used to generate H5N1 viruses containing either single or double substitutions in the HA. The RG virus containing K193E and G225E mutations (rVN-K193E/G225E) demonstrated large plaque morphology, enhanced replication, and genetic stability after serial passaging, without changing the receptor binding preference. Importantly, in vivo virulence assessment demonstrated that rVN-K193E/G225E was significantly attenuated in mice. Microneutralization and hemagglutination inhibition assays demonstrated that immunization with rVN-K193E/G225E efficiently induced a robust antibody response against wild type H5N1 virus in mice. Taken together, our experiments demonstrate that K193E and G225E mutations synergistically attenuated H5N1 virus without enhancing the receptor binding avidity, and that the RG virus rVN-K193E/G225E represents a potential H5N1 LAIV strategy that deserves further development. These findings identify the RBD as novel attenuation target for live vaccine development and highlight the complexity of RBD interactions.
    Journal of General Virology 05/2015; 96(9). DOI:10.1099/vir.0.000193 · 3.18 Impact Factor
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    ABSTRACT: Both age of patients and tumor location are associated with tumor origin, genetic characteristics, and prognosis. The objective of this study was to investigate the relationship between tumor location and age at diagnosis in a large cohort of patients with a primary diagnosis of glioma. We consecutively enrolled a cohort of 200 adults with glioblastoma and another cohort of 200 adults with diffuse low-grade gliomas. The magnetic resonance images of all tumors were manually segmented and then registered to a standard brain space. By using voxel-by-voxel regression analysis, specific brains regions associated with advanced age at tumor diagnosis were localized. In the low-grade gliomas cohort, the brain regions associated with advanced age at tumor diagnosis were mainly located in the right middle frontal region, while a region in the left temporal lobe, particularly at the subgranular zone, was associated with lower age at tumor diagnosis. In the glioblastoma cohort, the brain regions associated with advanced age at tumor diagnosis were mainly located in the temporal lobe, particularly at the posterior region of the subventricular zones. A region in the left inferior frontal region was associated with lower age at tumor diagnosis. Significant differences in the age of patients were found between tumors located in the identified regions and those located elsewhere in both cohorts. The current study demonstrated the correlation between tumor location and age at diagnosis, which implies differences in the origin of gliomas in young and older patients.
    Journal of Neuro-Oncology 05/2015; 123(2). DOI:10.1007/s11060-015-1798-x · 3.07 Impact Factor
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    ABSTRACT: Glioblastomas (GBM) are comprised of a heterogeneous population of tumor cells, immune cells, and extracellular matrix. Interactions among these different cell types and pro-/anti-inflammatory cytokines may promote tumor development and progression. The objective of this study was to develop a cytokine-related gene signature to improve outcome prediction for patients with primary GBM. Here, we used Cox regression and risk-score analysis to develop a cytokine-related gene signature in primary GBMs from the whole transcriptome sequencing profile of the Chinese Glioma Genome Atlas (CGGA) database (n=105). We also examined differences in immune cell phenotype and immune factor expression between the high-risk and low-risk groups. Cytokine-related genes were ranked based on their ability to predict survival in the CGGA database. The six genes showing the strongest predictive value were CXCL10, IL17R, CCR2, IL17B, IL10RB, and CCL2. Patients with a high-risk score had poor overall survival and progression-free survival. Additionally, the high-risk group was characterized by increased mRNA expression of M2 microglia/macrophage markers and elevated levels of IL10 and TGFβ1. The six cytokine-related gene signature is sufficient to predict survival and to identify a subgroup of primary GBM exhibiting the M2 cell phenotype.
    PLoS ONE 05/2015; 10(5):e0126022. DOI:10.1371/journal.pone.0126022 · 3.23 Impact Factor
  • Kun Yao · Xue-Ling Qi · Xi Mei · Tao Jiang
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    ABSTRACT: We describe a rare case of gliosarcoma with primitive neuroectodermal, osseous, cartilage and adipocyte differentiation. A 57-year-old man experienced a month history of headache, nausea and vomiting. Worse yet, the headache has become more severe for the past 6 days. Magnetic resonance (MR) images disclosed a lesion with operative indications located in the right frontal lobe. Then the tumor was macroscopically totally removed. Histologically, the tumor showed two kinds of components. One kind of the tumor cells appeared typical astrocytic tumor cells with anaplastic appearance. The other kind of the tumor cells appeared sheets of small round hyperchromatic cells, which presented a kind of pancreatic neuroendocrine tumor (PNET)-like structure. These sheets of small round cells were surrounded by a large number of relative-sparse-spindle cells. Multiple separate distinct areas of adipose tissue, osteoid matrix laid down and cartilage tissue were also identified. Immunohistochemically, a portion of typical astrocytic tumor cells and some small round hyperchromatic cells showed GFAP positivity. Small round hyperchromatic cells were positive for S-100, Fli-1, Nestin, MAP-2 and Syn. A large amount of relative sparse spindle cells (sarcomatous areas) were positive for vimentin. In addition, reticulin staining demonstrated expression of reticular fibers in relative-sparse-spindle cells areas but not in the astrocytic tumor cells and small round hyperchromatic cells areas. Molecular cytogenetic analyses demonstrated PTEN allele loss and no evidence of amplification of EGFR in both the astrocytic tumor cells, PNET-like structure and sparse spindle cells areas. These data suggest that this tumor was a gliosarcoma with primitive neuroectodermal, osseous, cartilage and adipocyte differentiation. To our knowledge, this is a rare gliosarcoma , reporting our additional new case would add to the better understanding of this tumor.
    International journal of clinical and experimental pathology 05/2015; 8(2):2079-84. · 1.89 Impact Factor

Publication Stats

5k Citations
1,289.81 Total Impact Points


  • 2010–2015
    • Beijing Neurosurgical Institute
      Peping, Beijing, China
    • Qingdao University of Science and Technology
      Tsingtao, Shandong Sheng, China
  • 2009–2015
    • Fourth Military Medical University
      • Department of Thoracic Surgery
      Xi’an, Liaoning, China
  • 2008–2015
    • Capital Medical University
      Peping, Beijing, China
  • 2007–2015
    • Beijing Tiantan Hospital
      Peping, Beijing, China
  • 2003–2015
    • Beijing Institute of Microbiology and Epidemiology
      Peping, Beijing, China
    • Beijing Centers for Disease Control and Prevention
      Peping, Beijing, China
  • 2014
    • Beijing Shijitan Hospital
      Peping, Beijing, China
    • University of Oklahoma Health Sciences Center
      • Department of Surgery
      Oklahoma City, Oklahoma, United States
    • Southern Medical University
      • Department of Anesthesiology
      Shengcheng, Guangdong, China
    • Chinese Academy of Sciences
      Peping, Beijing, China
    • Xinjiang Medical University
      Ouroumtchi, Xinjiang Uygur Zizhiqu, China
  • 2013–2014
    • Sichuan University
      • • State Key Laboratory of Biotherapy
      • • Department of Gastroenterology and Hepatology
      Hua-yang, Sichuan, China
    • Thomas Jefferson University
      • Department of Cancer Biology
      Filadelfia, Pennsylvania, United States
    • Guangzhou Medical University
      Shengcheng, Guangdong, China
  • 2012–2014
    • State Key Laboratory of Medical Genetics of China
      Ch’ang-sha-shih, Hunan, China
    • FAW Group Corporation
      Changchun, Fujian, China
  • 2011–2014
    • Harbin Medical University
      • Department of Neurosurgery
      Charbin, Heilongjiang Sheng, China
    • University of Utah
      • Department of Psychiatry
      Salt Lake City, Utah, United States
  • 2008–2014
    • Nanjing Medical University
      • • Key Laboratory of Reproductive Medicine
      • • Department of Pediatrics
      Nan-ching, Jiangsu Sheng, China
  • 2011–2013
    • Beijing Genomics Institute
      Bao'an, Guangdong, China
  • 2010–2012
    • National Human Genome Research Institute
      Maryland, United States
    • Shandong University of Science and Technology
      Tsingtao, Shandong Sheng, China
  • 2009–2011
    • Jilin University
      • • College of Material Science and Engineering
      • • State Key Lab of Superhard Materials
      • • Department of Material Science and Engineering
      Yung-chi, Jilin Sheng, China
  • 2006–2008
    • Academy of Military Medical Sciences
      T’ien-ching-shih, Tianjin Shi, China