Shujun Cheng

Chinese Academy of Medical Sciences, Peping, Beijing, China

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Publications (49)167.19 Total impact

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    ABSTRACT: Accumulating evidence suggests that interferon (IFN) alpha/beta are involved in antitumor immunity and cancer immunoediting, but information on the antitumor effects of IFN alpha/beta in lung cancer is limited. In our study, we elucidated the IFN alpha/beta signature during both human fetal lung development and lung tumorigenesis. Our findings indicated gradual upregulation in the IFN alpha/beta signature during human fetal lung development. In addition, this signature was progressively downregulated in normal human airway epithelial cells from lung cancer patients, in immortalized human bronchial epithelial cell lines from later passages, in late-stage lung squamous cell carcinoma (LSCC) tissues, and in LSCC tissues exhibiting lymph node metastasis. Therefore, from its earliest stages, lung tumorigenesis may be associated with a decreased IFN alpha/beta signature. This association may provide insight to guide the detection of high-risk lung cancer patients.
    Journal of interferon & cytokine research: the official journal of the International Society for Interferon and Cytokine Research 08/2015; DOI:10.1089/jir.2015.0061 · 3.90 Impact Factor
  • Lei Zhang · Run Tong · Jianwei Wang · Meng Li · Shun He · Shujun Cheng · Guiqi Wang
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    ABSTRACT: Background Conventional bronchoscopy with brushing alone for diagnosing peripheral pulmonary lesions (PPLs) is of low sensitivity. A manual mapping method was introduced and evaluated in this study, which could be routinely applied with bronchoscopic brushing to improve the sensitivity for malignant PPLs.Methods This mapping method involves the bronchoscopist drawing the route with a series of bronchial opening sketches and marking the leading bronchus at every bifurcation point based on thin-section computed tomography. This map is then used to guide bronchoscope insertion for brushing. A cross-sectional study on the evaluation of this method for the diagnosis of malignant PPLs was conducted on patients from July 2010 to June 2013.ResultsThe sensitivity for malignant PPLs of conventional brushing, conventional brushing with mapping on a portion of patients, and conventional brushing with mapping method increased from 17.0% to 25.8% to 31.5% (P < 0.001), respectively. For lesion sizes over 3 cm, the rate of these three groups increased from 25.1% to 38.6% to 50.9% (P < 0.001), respectively. The sensitivity of this mapping method for malignant PPLs was statistically associated with lesion size, lesion character, relationship between the lesion and the leading bronchus, linear distance between the targeted bronchus and the opening of the lobe bronchus, and accessibility (P < 0.001, P = 0.039, P < 0.001, P = 0.031, and P = 0.020, respectively).Conclusions The manual mapping method greatly increased the bronchoscopic brushing sensitivity for malignant PPLs compared to the conventional brushing method. During routine clinical work, it is economical and convenient for guiding bronchoscope insertion.
    Thoracic Cancer 07/2015; DOI:10.1111/1759-7714.12279 · 0.65 Impact Factor
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    ABSTRACT: A tumor can be viewed as a special "organ" that undergoes aberrant and poorly regulated organogenesis. Progress in cancer prognosis and therapy might be facilitated by re-examining distinctive processes that operate during normal development, to elucidate the intrinsic features of cancer that are significantly obscured by its heterogeneity. The global gene expression signatures of 44 human lung tissues at four development stages from Asian descent and 69 lung adenocarcinoma (ADC) tissue samples from ethnic Chinese patients were profiled using microarrays. All of the genes were classified into 27 distinct groups based on their expression patterns (named as PTN1 to PTN27) during the developmental process. In lung ADC, genes whose expression levels decreased steadily during lung development (genes in PTN1) generally had their expression reactivated, while those with uniformly increasing expression levels (genes in PTN27) had their expression suppressed. The genes in PTN1 contain many n-gene signatures that are of prognostic value for lung ADC. The prognostic relevance of a 12-gene demonstrator for patient survival was characterized in five cohorts of healthy and ADC patients [ADC_CICAMS (n = 69, p = 0.007), ADC_PNAS (n = 125, p = 0.0063), ADC_GSE13213 (n = 117, p = 0.0027), ADC_GSE8894 (n = 62, p = 0.01), and ADC_NCI (n = 282, p = 0.045)] and in four groups of stage I patients [ADC_CICAMS (n = 22, p = 0.017), ADC_PNAS (n = 76, p = 0.018), ADC_GSE13213 (n = 79, p = 0.02), and ADC_qPCR (n = 62, p = 0.006)]. In conclusion, by comparison of gene expression profiles during human lung developmental process and lung ADC progression, we revealed that the genes with a uniformly decreasing expression pattern during lung development are of enormous prognostic value for lung ADC.
    PLoS ONE 08/2014; 9(8):e105639. DOI:10.1371/journal.pone.0105639 · 3.23 Impact Factor
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    ABSTRACT: The aim of this study was to detect the plasma concentration of OLC1 (overexpressed in lung cancer 1) protein as a potential cancer biomarker, and evaluating its clinical application value in the diagnosis of non-small cell lung cancer (NSCLC).
    Zhonghua zhong liu za zhi [Chinese journal of oncology] 05/2014; 36(5):362-5.
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    ABSTRACT: Advances in three-dimensional (3D) printing have enabled the direct assembly of cells and extracellular matrix materials to form in vitro cellular models for 3D biology, the study of disease pathogenesis and new drug discovery. In this study, we report a method of 3D printing for Hela cells and gelatin/alginate/fibrinogen hydrogels to construct in vitro cervical tumor models. Cell proliferation, matrix metalloproteinase (MMP) protein expression and chemoresistance were measured in the printed 3D cervical tumor models and compared with conventional 2D planar culture models. Over 90% cell viability was observed using the defined printing process. Comparisons of 3D and 2D results revealed that Hela cells showed a higher proliferation rate in the printed 3D environment and tended to form cellular spheroids, but formed monolayer cell sheets in 2D culture. Hela cells in 3D printed models also showed higher MMP protein expression and higher chemoresistance than those in 2D culture. These new biological characteristics from the printed 3D tumor models in vitro as well as the novel 3D cell printing technology may help the evolution of 3D cancer study.
    Biofabrication 04/2014; 6(3):035001. DOI:10.1088/1758-5082/6/3/035001 · 4.30 Impact Factor
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    ABSTRACT: Following a previous study reporting that BRK1 is upregulated in non-small cell lung cancer (NSCLC), the present study sought to clarify the role of specificity protein 1 (Sp1) in the transcriptional regulation of the BRK1 gene. Therefore, a construct, named F8, consisting of the -1341 to -1nt sequence upstream of the start codon of the BRK1 gene inserted into pGL4.26 was made. A series of truncated fragments was then constructed based on F8. Segment S831, which contained the -84 to -1nt region, displayed the highest transcriptional activity in the A549, H1299 and H520 NSCLC cell lines. Bioinformatic analysis showed a potential Sp1-binding element at -73 to -64nt, and a mutation in this region suppressed the transcriptional activity of S831. Then the RNAi assays of Sp1 and its coworkers Sp3 and Sp4 were performed, and suppression of Sp1 by siRNA inhibited the mRNA expression of BRK1. Both an electrophoretic mobility shift assay (EMSA) and a chromatin immunoprecipitation (ChIP) assay demonstrated that Sp1 bound to the promoter area of the BRK1 gene. Our data identified a functional and positive Sp1 regulatory element from -73 to -64nt in the BRK1 promoter, which may likely explain the overexpression of BRK1 in NSCLC.
    Gene 03/2014; DOI:10.1016/j.gene.2014.03.043 · 2.08 Impact Factor
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    ABSTRACT: The transmembrane and secreted protein delta-like 1 homolog (DLK1) belongs to the EGF-like family. It is widely accepted that DLK1 plays important roles in regulating cell differentiation, such as adipogenesis and osteogenesis. Aberrant expression of DLK1 has been found in various types of human cancers, including lung cancer. A previous study in this lab has revealed that DLK1 is associated with tumor invasion, although the mechanism is still unknown. To explore the potential effects that DLK1 might have on invasion, DLK1 was overexpressed or knocked down in the human lung cancer cell lines. The protein's influences on cell invasion were subsequently evaluated. A transwell assay showed that DLK1 overexpression significantly promoted cancer cell invasion. Western blotting and gelatin zymography analysis indicated that DLK1 could affect both matrix metalloproteinase-9 (MMP9) expression and its extracellular activity. An analysis of NOTCH1 and HES1 gene expression and Notch intracellular domain (NICD) nuclear translocation during DLK1 stimulation or depletion demonstrated that DLK1 could activate Notch signaling in lung cancer cells. Additionally, the elevated expression of MMP9 induced by DLK1 stimulation could be significantly decreased by inhibiting Notch signaling using γ-secretase inhibitor (GSI). The data presented in this study suggest that DLK1 can promote the invasion of lung cancer cells by upregulating MMP9 expression, which depends on Notch signaling.
    PLoS ONE 03/2014; 9(3):e91509. DOI:10.1371/journal.pone.0091509 · 3.23 Impact Factor
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    ABSTRACT: Objective. This study was aimed to create a large-scale laryngeal cancer relevant secretory/releasing protein database and further discover candidate biomarkers. Methods. Primary tissue cultures were established using tumor tissues and matched normal mucosal tissues collected from four laryngeal cancer patients. Serum-free conditioned medium (CM) samples were collected. These samples were then sequentially processed by SDS-PAGE separation, trypsin digestion, and LC-MS/MS analysis. The candidates in the database were validated by ELISA using plasma samples from laryngeal cancer patients, benign patients, and healthy individuals. Results. Combining MS data from the tumor tissues and normal tissues, 982 proteins were identified in total; extracellular proteins and cell surface proteins accounted for 15.0% and 4.3%, respectively. According to stringent criteria, 49 proteins were selected as candidates worthy of further validation. Of these, human tissue kallikrein 6 (KLK6) was verified. The level of KLK6 was significantly increased in the plasma samples from the cancer cohort compared to the benign and healthy cohorts and moreover showed a slight decrease in the postoperative plasma samples in comparison to the preoperative plasma samples. Conclusions. This laryngeal cancer-derived protein database provides a promising repository of candidate blood biomarkers for laryngeal cancer. The diagnostic potential of KLK6 deserves further investigation.
    Disease markers 02/2014; 2014:594093. DOI:10.1155/2014/594093 · 2.17 Impact Factor
  • Henglei Dong · Hui Li · Ningzhi Xu · Weicheng You · Shujun Cheng · Yan Sun · Xishan Hao
    Zhonghua yi xue za zhi 01/2014; 94(2):83-5.
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    ABSTRACT: For successful therapy, hepatocellular carcinoma (HCC) must be detected at an early stage. Herein, we used a proteomic approach to analyze the secretory/releasing proteome of HCC tissues to identify plasma biomarkers. Serum-free conditioned media (CM) were collected from primary cultures of cancerous tissues and surrounding noncancerous tissues. Proteomic analysis of the CM proteins permitted the identification of 1365 proteins. The enriched molecular functions and biological processes of the CM proteins, such as hydrolase activity and catabolic processes, were consistent with the liver being the most important metabolic organ. Moreover, 19% of the proteins were characterized as extracellular or membrane-bound. For validation, secretory proteins involved in transforming growth factor-β signaling pathways were validated in plasma samples. Alpha-fetoprotein (AFP), metalloproteinase (MMP)1, osteopontin (OPN), and pregnancy-specific beta-1-glycoprotein (PSG)9 were significantly increased in HCC patients. The overall performance of MMP1 and OPN in the diagnosis of HCC remained greater than that of AFP. In addition, this study represents the first report of MMP1 as a biomarker with a higher sensitivity and specificity than AFP. Thus, this study provides a valuable resource of the HCC secretome with the potential to investigate serological biomarkers. MMP1 and OPN could be used as novel biomarkers for the early detection of HCC and to improve the sensitivity of biomarkers compared with AFP.
    Science China. Life sciences 06/2013; 56(7). DOI:10.1007/s11427-013-4497-x · 1.51 Impact Factor
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    ABSTRACT: It has been proven that epithelial-mesenchymal transition (EMT) is a critical process which is precisely regulated by multiple signaling pathways during the progression and metastasis of non-small cell lung cancer (NSCLC). Canonical MAPK signaling is essential to transforming growth factor β (TGFβ)-induced EMT. Using the NSCLC cell line A549 as a model, the aim of this study is to explore the molecular mechanism of ENO1 affecting EMT. We established an A549 strain stably overexpressing ENO1. Cell mobility was measured by the wound-healing assay. EMT-related molecular alterations were detected by Western blot analysis. The effect of ENO1 on EMT was also detected by TGFβ-1-inducing assay. EGF-stimulating assay was performed to illustrate ERK1/2 phosphorylation changes resulting from ENO1 overexpression. Overexpressed ENO1 inhibited the mobility of A549 (P<0.05), as well as the expression of the mesenchymal markers N-cadherin and vimentin, but upregulated the epithelial marker E-cadherin. TGFβ-inducing assay also showed that the negative effect of ENO1 on EMT. ERK1/2 phosphorylation was also obviously suppressed by ENO1 in the EGF-stimulating assay. In NSCLC cells, ENO1 overexpression can inhibit EMT in vitro by suppressing ERK1/2 phosphorylation.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 05/2013; 16(5):221-6. DOI:10.3779/j.issn.1009-3419.2013.05.01
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    ABSTRACT: Whether the heterogeneity in tumor cell morphology and behavior is the consequence of a progressive accumulation of genetic alterations or an intrinsic property of cancer-initiating cells established at initiation remains controversial. The hypothesis of biological predetermination in human cancer was proposed many years ago and states that the biological potency of cancer cells is predestinated in the precancerous stage. The present study aimed to investigate whether the aberrant molecular events occurring in initial cancer stages could eventually influence colorectal cancer (CRC) progression. We analyzed the mRNA and miRNA expression profiles of colorectal normal mucosa, low-grade intraepithelial neoplasia (LIN), high-grade intraepithelial neoplasia (HIN), and adenocarcinoma tissues. Compared with the transitions from LIN to HIN to invasive carcinoma, the transition from normal epithelium to LIN appeared to be associated with greater changes in the number and expression levels of mRNAs and miRNAs, with a differential expression of 2,322 mRNAs and 71 miRNAs detected. Utilizing these early molecular changes, a miRNA-hub network analysis showed that 166 genes were identified as targets regulated by 30 miRNAs. Among these genes, a 55-gene signature regulated by 5 miRNAs was shown to be associated with overall survival or disease-free survival in three independent sample sets. Thus, the molecular changes in the transcriptome associated with the transition from normal to intraepithelial neoplasm may influence CRC progression.
    Biochemical and Biophysical Research Communications 04/2013; DOI:10.1016/j.bbrc.2013.04.063 · 2.28 Impact Factor
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    ABSTRACT: DENND2D was identified as being down-regulated in lung cancer using a lung cancer low-expression suppression subtractive hybridization (SSH) library. In this study, DENND2D down-regulation has been observed not only in non-small cell lung cancer (NSCLC) cell lines and lung squamous cell carcinoma (SCC) tissues, but also in immortalized human bronchial epithelial (IHBE) cell lines and precancerous lesions, indicating that the down-regulation of DENND2D may be an early event in lung cancer. The relative DNA copy number and mRNA and protein expression levels of DENND2D were determined in vitro, and they revealed a complicated regulatory network at the genomic, transcriptional and translational levels. Over-expression of DENND2D significantly suppressed the proliferation of NSCLC cells in vitro and in vivo by inducing apoptosis. These results indicate that DENND2D might function as a tumor suppressor-like gene to prevent the survival and expansion of cells with genetic damage through apoptosis mechanism, and absence of DENND2D might play a permissive role, as an early event, in tumorigenesis.
    Lung cancer (Amsterdam, Netherlands) 11/2012; 79(2). DOI:10.1016/j.lungcan.2012.10.012 · 3.74 Impact Factor
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    ABSTRACT: Cancer/testis antigens (CTAs) are highly immunogenic in many tumors, especially in non-small cell lung cancer (NSCLC). A low-density protein microarray, which consisted of 72 CTAs and six non-CTAs, was used to screen for lung cancer-related autoantibodies. The CTA panel of NY-ESO-1, XAGE-1, ADAM29 and MAGEC1, had sensitivity and specificity values of 33% and 96%, respectively. When examined in a test set, this panel of markers had sensitivity and specificity values of 36% and 89%, respectively. This array of markers preferentially detected NSCLC, but did not detect breast cancer, and non-cancer lung disease.
    Cancer letters 08/2012; 328(1). DOI:10.1016/j.canlet.2012.08.019 · 5.62 Impact Factor
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    ABSTRACT: Ovarian cancer is the most lethal gynecological malignancy worldwide, and early detection of this disease using serum or plasma biomarkers may improve its clinical outcome. In the present study, a large scale protein database derived from ovarian cancer was created to enable tumor marker discovery. First, primary organ cultures were established with the tumor tissues and corresponding normal tissues obtained from six ovarian cancer patients, and the serum-free conditioned medium (CM) samples were collected for proteomic analysis. The total proteins from the CM sample were separated by SDS-PAGE, digested with trypsin and then analyzed by LC-MS/MS. Combining data from the tumor tissues and the normal tissues, 1129 proteins were identified in total, of which those categorized as "extracellular proteins" and "plasma membrane proteins" accounted for 21.4% and 16.9%, respectively. For validation, three secretory proteins (NID1, TIMP2, and VCAN) involved in "organ development"-associated subnetwork, showed significant differences between their levels in the circulating plasma samples from ovarian cancer patients and healthy women. In conclusion, this ovarian cancer-derived protein database provides a credible repertoire of potential biomarkers in blood for this malignant disease, and deserves mining further.
    Proteomics 06/2012; 12(11):1883-91. DOI:10.1002/pmic.201100654 · 3.97 Impact Factor
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    ABSTRACT: Lung cancer patients within the pN0 category have a significantly different outcome. The aim of this study was to develop a mathematical model to assist in predicting the prognosis of pN0 lung squamous cell carcinoma (SCC). Twenty-three proteins were examined by immunohistochemical (IHC) analysis on primary tumour tissues from 319 lung SCC patients. In a training group, using IHC data, a recursive partitioning decision tree (RP-DT) was used to build a model for estimating the risk for lymphatic metastasis. This model was then validated in a test cohort. Of 23 proteins, 8 (matrix metallopeptidase 1, metalloproteinase inhibitor 1, Ras GTPase-activating-like protein IQGAP1, targeting protein for Xklp2, urokinase-type plasminogen activator, cathepsin D, fascin, polymeric immunoglobulin receptor/secretory component) were selected, and generated a tree model in a training group of 255 patients to classify them as at high or low risk of lymphatic invasion, with accuracy of 78.0% (compared to histopathological diagnosis), sensitivity of 83.0% and specificity of 70.3%. When the tree model was applied to the test group, the accuracy, sensitivity and specificity were 76.6%, 76.0% and 76.9%, respectively. The performance of this mathematical model was substantiated further in 34 'problematic' stage I/pN0 patients by survival analysis. The RP-DT model, constructed with eight protein markers for estimating lymphatic metastasis risk in pN0 lung SCC, is clinically feasible and practical, using IHC data from the primary tumour.
    Histopathology 11/2011; 59(5):882-91. DOI:10.1111/j.1365-2559.2011.04013.x · 3.30 Impact Factor
  • Xiaojing Zhang · Ting Xiao · Shujun Cheng · Tong Tong · Yanning Gao
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    ABSTRACT: The newly identified gene, overexpressed in lung cancer 1 (OLC1), is highly expressed as OLC1 protein in the tumor tissues of lung cancer patients with histories of cigarette smoking. However, the underlying mechanisms of how the gene is affected by cigarette smoke have been poorly characterized. In this study, we investigated how OLC1 is regulated in lung cancer cells by cigarette smoke condensate (CSC). Compared to the controls, CSC treatment increased OLC1 protein levels in a dose- and time-dependent manner without affecting OLC1 mRNA levels in lung cancer cells. Ubiquitination of OLC1 protein was blocked upon CSC treatment. Biochemical analysis revealed that the ubiquitin E3 ligase anaphase promoting complex (APC) and its activators cell-division cycle protein 20 (CDC20) and cadherin-1 (CDH1) are responsible for the degradation of OLC1. However, upon introducing CSC the binding of OLC1 to the proteins CDC20, CDH1, and APC2 was impaired. These results demonstrate that CSC regulates OLC1 expression in lung cancer cells by compromising its ubiquitination and subsequent degradation through the ubiquitin E3 ligase APC.
    Biochemical and Biophysical Research Communications 03/2011; 407(4):753-7. DOI:10.1016/j.bbrc.2011.03.095 · 2.28 Impact Factor
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    ABSTRACT: proper tumor markers are useful to diagnosis, prognosis and treatment for lung cancer. The aim of this study is to examine the levels of alpha-enolase (ENO1) protein in the tumor tissues and peripheral plasma samples obtained from non-small cell lung cancer (NSCLC) patients, and evaluate its potential clinical significance. the ENO1 protein levels in the tumor tissues and corresponding normal tissues from 16 cases of lung squamous cell carcinoma were analyzed by Western blot. The ENO1 protein levels in the plasma samples from 42 healthy individuals, 34 patients with lung benign disease and 84 patients with NSCLC were measured by double antibody sandwich enzyme-linked immunosorbent assay. for 87.5% (14/16) of the patients with lung squamous cell carcinoma, the ENO1 protein level in the tumor tissues was higher than that in the corresponding normal lung tissues. The ENO1 protein level in the plasma of NSCLC patients was significantly higher than that in the plasma of healthy individuals (P=0.031) and patients with lung benign disease (P=0.019). Furthermore, the ENO1 protein level was significantly higher in the plasma of patients with lung adenocarcinoma than that of patients with lung squamous cell carcinoma. the elevated levels of ENO1 protein in the tumor tissues and the plasma samples from NSCLC patients indicate ENO1 may be a candidate biomarker of lung cancer.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 12/2010; 13(12):1089-93. DOI:10.3779/j.issn.1009-3419.2010.12.02
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    ABSTRACT: Matrix metalloproteinase-1 (MMP-1) participates in a variety of physiological and pathological processes. We previously found that MMP-1 was one of the lung cancer-related proteins detectable in peripheral blood. To validate our preliminary observations and explore the clinical significance of MMP-1 for lung cancer further, we carried out the present study. The concentrations of MMP-1 in circulating plasma specimens of 170 lung cancer patients and 70 healthy individuals were measured by an enzyme-linked immunosorbance assay. The expression status of the MMP-1 in archival tissue samples from 122 lung cancer patients was examined by immunohistochemical analysis. The correlation between the MMP-1 levels and prognosis of the lung cancer patients was then assessed statistically. Protein levels of MMP-1 were considerably raised in the plasma from lung cancer patients relative to those in healthy controls. The high plasma MMP-1 levels were associated with advanced-stage of the disease and significantly lower overall survival rate of the patients. Coincidently, MMP-1 protein extraordinarily overexpressed in the tumour tissues of lung cancer; and the up-regulated MMP-1 was associated with the progression (including tumour size, staging and lymphatic invasion), especially with decreased survival rate of the patients. Statistic analysis revealed that MMP-1 protein levels had an independent influence on survival. MMP-1 levels were elevated in both tumour tissue and blood; the latter may serve as an independent predictor for survival of lung cancer patients. MMP-1 protein levels in plasma/serum thus represent a potential and clinically relevant biomarker for the prognosis of patients with lung cancers.
    Lung cancer (Amsterdam, Netherlands) 09/2010; 69(3):341-7. DOI:10.1016/j.lungcan.2009.12.007 · 3.74 Impact Factor
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    ABSTRACT: To explore the effects on foci formation and wound-healing of NIH3T3 cells, and to provid the experimental evidence of its function. DNA from human lung cells was extracted and amplification of Rap2b gene was done by PCR. Eukaryotic expression vector pcDNA3. 1-Rap2b was constructed and was stable transfected into NIH3T3 cell followed with foci formation assay and wound-healing assay. The number of the foci formation of NIH3T3 cell transfected by eukaryotic expression vector pcDNA3. 1-Rap2b was increased remarkably in foci formation assay (P < 0.01) and NIH3T3 cells transfected by eukaryotic expression vector pcDNA3. 1-Rap2b were quickly heal up in wound-healing assay. The extrinsic expression of Rap2b could transform NIH3T3 cell using foci formation assay and wound-healing assay. Rap2b gene might play an oncogenic role in tumorigenesis.
    Wei sheng yan jiu = Journal of hygiene research 07/2010; 39(4):403-6.

Publication Stats

617 Citations
167.19 Total Impact Points

Institutions

  • 1997–2015
    • Chinese Academy of Medical Sciences
      Peping, Beijing, China
  • 2014
    • Tsinghua University
      • Department of Mechanical Engineering
      Peping, Beijing, China
  • 2002–2014
    • Peking Union Medical College Hospital
      Peping, Beijing, China
  • 2010
    • Zhengzhou University
      Cheng, Henan Sheng, China
  • 2004
    • Charité Universitätsmedizin Berlin
      • Institute of Pathology
      Berlin, Land Berlin, Germany
  • 2001
    • Chongqing Cancer Hospital and Institute
      Ch’ung-ch’ing-shih, Chongqing Shi, China