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| 1 | Quantitative analysis of vascular endothelial growth factor, microvascular density and their clinicopathologic features in human hepatocellular carcinoma显示文摘BACKGROUND: Angiogenesis is known to be essential to the survival, growth, invasion, and metastasis of tumor cells. Vascular endothelial growth factor (VEGF) are an important angiogenic factor regulating tumor angiogenesis, but its significance and tumor pathologic features are un- clear in hepatocellular carcinoma (HCC). In the present study, we analyzed expression of tissue VEGF, alteration of microvascular density (MVD) in microvessel angiogenesis, development and metastasis of HCC, and level of serum VEGF in differential diagnosis of benign and malignant liv- er diseases. METHODS: Tumor specimens were prospectively collected from HCC patients undergoing resection. Total RNAs were extracted and the expression levels were detected from different parts of HCC tissues. The cellular distributions of VEGF and MVD of liver tumors and their paracancerous and distal cancerous tissues were investigated by streptavi- din peroxidase (S-P) immunohistochemistry, respectively. The VEGF levels of circulating blood and hepatoma tissues were measured by enzyme-linked immunosorbent assay. RESULTS: The incidence of VEGF expression was 63.9% in HCCs (23/36 cases), 78.3% in non-encapsulated HCCs (18/23), and 90.9% in HCCs with extrahepatic metastasis (10/11), respectively. The VEGF expression was tightly correlated with MVD (P <0.01). The MVD in HCC with metastasis, low differentiation or non-encapsulation was significantly higher than that in HCC with intact capsule, high differentiation, or no metastasis. No significant diffe- rence was found between VEGF, MVD, tumor size, and hepatitis virus infection. The level of total RNA in HCC tis- sues was significantly lower but the VEGF level significantly higher than those in paracancerous or distal cancerous ones (P<0.01). The abnormal expression levels of VEGF in sera of HCC patients were directly correlated with the me- tastasis and recurrence of tumors. CONCLUSION: The high expression of VEGF and abnor- mality of tissue MVD are useful predictors for vascular inva- sion and metastasis of liver tumors. | Deng-Fu Yao, Xin-Hua Wu, Yong Zhu, Gong-Sheng Shi, Zhi-Zhen Dong, Deng-Bing Yao, Wei Wu, Li-Wei Qiu and Xian-Yong Meng Nantong, China Research Center of Clinical Molecular Biology , Department of Pathology and Department of Gastroenterology , Affiliated Hos- pital of Nantong University Department of Diagnostics , and Institute of Neurosciences , Nantong University Nantong 226001, China | 2005 | Hepatobiliary & Pancreatic Diseases International2005，4，2： | 81 |
| 2 | Dynamic changes of typeⅠ,Ⅲand N collagen synthesis and distribution of collagen-producing cells in carbon tetrachloride-induced rat liver fibrosis显示文摘AIM To find out the relationship between the gene transcription of different types ofprocollagen and the deposition of the relevant collagens in the liver tissue and to confirm the types of collagen producing cells in liverfibrogenesis.METHODS Dynamic changes of the expression of α1(Ⅰ ), α1 (Ⅲ ) and α1 (Ⅳ) procollagen mRNAand relevant collagens and the distribution ofcollagen producing cells during liver fibrogenesis of rat induced by CCl4 (20 weeks)were investigated with Northern blot analysis,in situ hybridization and immunohistochemicaltechniques.RESULTS The increased expression of α1 (Ⅲ)procollagen mRNA by Northern blot analysis was the most predominant one among the threemRNAs during fibrogenesis. However, theenhanced expression of al (Ⅳ) procollagenmRNA occurred very early while the expressionof α1 (Ⅰ) mRNA was not enhanced much until themiddle stage of the exPeriment. D6smin (Dm)positive hepatic stellate cells (HSCs) and fewmyofibroblasts (MFs) in and around the necrotic areas expressed α1 (Ⅰ), α1 (Ⅲ) and α1 (Ⅳ)procollagen mRNA signals detected by in situhybridization at the early stage of theexperiment. All the three procollagen mRNAsignals thereafter mainly localized in fibroblasts (Fbs) and MFs in fibrotic septa during the middle and late stages of fibrosis, which distributedparallel to the corresponding collagens detected by immunohistochemical study. ln addition, the endothelial cells of sinusoids and the small blood vessels within the septa also showed α1(Ⅳ) procollagen mRNA and type Ⅳ collagen expressionCONCLUSION It is considered that 'HSC-MF-Fb' effect cell system is the major cellularsource of collagen production in liver fibrosis, in which HSCs are collagen producing precursor cells in the early liver fibrogenesis, thereafter the synthesis of type Ⅰ, Ⅲ and Ⅳ collagens (Col Ⅰ, Col Ⅲ and Col Ⅳ) mainly derives fromMFs and Fbs, which play a very important role in the progress of liver fibrosis. The endothelialcells along sinusoids, as another source of Col Ⅳ production, might participate in the capillization of liver sinusoids. | DU Wei-Dong ZHANG Yue-E ZHAl Wei-Rong and ZHOU Xiao-Mei(Department of Pathology, Shanghai Medical University, Shanghai200032, China)(National Laboratory for Oncogenes and Related Genes, ShanghaiCencer Institute)See invited commentary on page 388 | 1999 | World Journal of Gastroenterology1999，5，5： | 47 |
| 3 | Morphological and functional changes of mitochondria in apoptotic esophageal carcinoma cells induced by arsenic trioxide显示文摘AIM:To demonstrate that mitochondrial morphological andfunctional changes are an important intermediate link in thecourse of apoptosis in esophageal carcinoma calls inducedby As_2O_3.METHODS:The esophageal carcinoma call line SHEEC1,established in our laboratory,was cultured in 199 growthmedium,supplemented with 100mL·L^(-1)calf serum and3 mol·L^(-1)As_2O_3(the same below).After 2,4,6,12,24 hof drug adding,the SHEECl calls were collected for light-and electron-microscopic examination.The mitochondriawere labeled by Rhodamine fluorescence probe and thefluorescence intensity of the mitochondria was measured byflow cytorneter and cytofluorimetric analysis.Further,themitochondrial transmembrane potential(MTP,ΔΨm)change was also calculated.RESULTS:The mitochondrial morphological change afteradding As_2O_3 could be divided into three stages.In theearly-stage(2-6h)after adding As203,an adaptiveproliferation of mitochondria appeared;in the mid-stage(6-12 h)a degenerative change was observed;and in the late-stage(12-24 h)the mitochondria swelled with outermembrane broken down and then calls death with apoptoticchanges of nucleus.The functional change of themitochondria indicated by fluorescent intensity,whichreflected the MTP status of mitochondria,was in accordancewith morphological change of the mitochondria.Thefluorescent intensity increased at early-stage,decUned inmid-stage and decreased to the lowest in the late-stage.24h after As_2O_3 adding,the cell nucleus showed typicalapoptotic changes.CONCLUSION:Under the inducement of As_2O_3,the earlyapoptotic changes of SHEEC1 cells ware the apparentmorphological and functional changes of mitochondria,afterwards the nucleus changes followed.It is consideredthat changes of mitochondria are an important intermediatelink in the course of apoptosis of esophageal carcinoma cells induced by As_2O_3. | Zhong-Ying Shen Jian Shen Qiao-Shan Li Department of Pathology,Medical College of Shantou University,Shantou 515031,Guandong Province,China Cai-Yun Chen Central Lab.Medical College of Shantou University Jiong-Yu Chen Central Lab.of Tumor Hospital,Medical College of Shantou University Yi Zeng Institute of Virology,Chinese Academy of Preventive Medicine,Beijing 100052,China | 2002 | World Journal of Gastroenterology2002，8，1： | 35 |
| 4 | Polymorphism of p16INK4a gene and rare mutation of p15INK4b gene exon2 in primary hepatocarcinoma显示文摘INTRODUCTION Hepatocellular carcinoma(HCC)is the mostcommon cause of death from cancer in China.Themechanisms of hepatocarcinogenesis are not yetknown clearly,p16INK4a gene,the multiple tumorsuppressor gene 1(MTS1),encodes P16 protein,which acts as an inhibitor by binding directly toCDK4 and CDK6 and preventing its association | Yang Qin Bo Li Yong Shu Tan Zhi Lin Sun Feng Qiong Zuo Ze Fang Sun Institute of Biochemistry and Molecular Biology,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China Department of General Surgery,The First Affiliated Hospital,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China Department of Pathology,The First Affiliated Hospital,West China University of Medical Sciences,Chengdu 610041,Sichuan Province,China | 2000 | World Journal of Gastroenterology2000，6，3： | 30 |
| 5 | Expression of p53 and C-myc genes and its clinical relevance in the hepatocellular carcinomatous and pericarcinomatous tissues显示文摘AIM: To investigate the possible roles of p53 and C-mycgenes in the primary hepatocellular carcinogenesis and therelationship between the liver hyperplastic nodule(LHN) andhepatocellular carcinoma(HCC).METHODS: The expression of p53 and C-myc genes wasdetected immunohist-ochemically in 73 and 60 cases of HCCand pericarcinomatous tissues, respectively .RESULTS: The positive expression of p53 in HCC wassignificantly higher than that in pericarcinomatous tissues(P<0.05). In pericarcinomatous tissues, the p53 expressionwas observed only in LHN, but not in liver cirrhosis (LC) andnormal liver tissues. The positive expression rate of C-mycin HCC or LHN was significantly higher than that in LC ornormal liver tissues (P<0.05 and P<0.01), however, nosignificant difference was found between HCC and LHN(P>0.05). The positive expression rate of p53 and C-myc inHCC was correlated with the histological differentiation, thatin the poorly differentiated was significantly higher than thatin well differentiated samples (P<0.05).CONCLUSION: The overexpression of p53 and C-myc genesmight play a role in the carcinogenesis of HCC; And LHNseems a preneoplastic lesion related to hepatocarcinogenesis;No evidence supports that LC contribute directly to thehepatocarcinogenesis. | Zhao-Shan Niu Bo-Kian Li Department of Pathology,Medical College of Qingdao University,Qingdao 266021,Shandong Province,China Mei Wang Department of Foreign languages,Qingdao institute of Architecture and Engineering,Qingdao 266033,Shandong Province,China | 2002 | World Journal of Gastroenterology2002，8，5： | 30 |
| 6 | Glutamine synthetase as an early marker for hepatocellular carcinoma based on proteomic analysis of resected smal hepatocel ular carcinomas显示文摘BACKGROUND:Hepatocellular carcinoma(HCC)is a highly malignant tumor with a poor prognosis.Because small HCCs possess most of the characteristics of early HCC,we investigated small HCCs to screen potential biomarkers for early diagnosis.METHODS:Proteins were extracted from 10 sets of paired tissue samples from HBV-infected small-HCC patients.The extracted proteins were well resolved by two-dimensional electrophoresis.These HCC-associated proteins were then identified by MALDI-TOF/TOF MS following image analysis.Western blotting and immunohistochemistry were used to assess glutamine synthetase(GS)and phenazine biosynthesislike domain-containing protein(PBLD)expression in liver tissue.Enzyme-linked immunosorbent assays in 152 serum samples(from 49 healthy donors,24 patients with liver cirrhosis,and 79 with HCC)were used to further assess the significance of GS clinically.RESULTS:Fifteen up-regulated and three down-regulated proteins were identified.Western blotting confirmed GS overexpression and decreased PBLD expression in liver tissue.Immunohistochemistry showed that GS was expressed in 70.0%(84/120)of HCCs and 35.8%(43/120)of nontumor tissues;PBLD was expressed in 74.2%(89/120) of nontumor tissues and 40.8%(49/120)of HCCs.The Chi-square test showed significant expression differences between HCCs and adjacent tissues.Consistent with this,serum GS levels in HCC patients were significantly higher than those in liver cirrhosis patients and healthy donors,while the latter two groups were also significantly different.In addition, a diagnostic cutoff value of 2.6 mg/ml was used for GS;it was elevated in 19(76.0%)of 25 HCC patients with AFP≤20 ng/ml and 47(88.7%)of 53 HCC patients with AFP≤200 ng/ml.CONCLUSION:GS and PBLD are abnormally expressed in most HCCs.GS may be a novel serum marker for early HCC, especially for those patients with low AFP levels(≤200 ng/ml). | Jiang Long,Zhen-Wei Lang,Hua-Guang Wang,Tai-Ling Wang,Bao-En Wang and Si-Qi Liu Liver Research Center,Beijing Friendship Hospital, Capital Medical University,Beijing 100050,China Department of Hepatology,Department of Pathology, Beijing Youan Hospital,Capital Medical University,Beijing 100069,China Department of Pharmaceutical Affairs,Beijing Chaoyang Hospital,Capital Medical University,Beijing 100020,China Department of Pathology,China-Japan Friendship Hospital,Beijing 100029,China Beijing Genomics Institute,Chinese Academy of Science,Beijing Airport Industrial Zone B-6,Shunyi,Beijing 101300,China | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，3： | 21 |
| 7 | Telomere and telomerase in the initial stage of immortalization of esophageal epithelial cell显示文摘AIM: To search for the biomarker of cellular immortalization,the telomere length, telomerase activity and its subunits incultured epithelial cells of human fetal esophagus in theprocess of immortalization.METHODS: The transgenic cell line of human fetalesophageal epithelium (SHEE) was established with E6 E7genes of bt man papillomavirus (HPV) type 18 in ourlaboratory. Morphological phenotype of cultured SHEE cellsfrom the 6th to 30th passages, was examined by phasecontrast microscopy, the telomere length was assayed bySouthern blot method, and the activity of telomerase wasanalyzed by telomeric repeat amplification protocol (TRAP).Expressions of subunits of telomerase, hTR and hTERT,were assessed by RT-PCR. DNA content in cell cycle wasdetected by flow cytometry. The cell apoptosis wasexamined by electron microscopy (EM) and TUNEL label.RESULTS: SHEE cells from the 6 th to 10 th passagesshowed cellular proliferation with a good differentiation.From the 12 th to the 16 th passages, many senescent andapoptotic cells appeared, and the telomere length sharplyshortened from 23 kb to 17 kb without expression of hTERTand telornerase activity. At the 20 th passage, SHEE cellsovercame the senescence and apoptosis and restored theirproliferative activity with expression of telomerase andhTERT at low levels, but the telomere length shortenedcontinuously to the lowest of 3 kb. After the 30 th passagecells proliferation was restored by increment of cells at S andG2M phase in the cell cycle end telomerase activity expressedat high levels and with maintenance of telomere length.CONCLUSION: At the early stage of SHEE cells, telomeresare shortened without expression of telomerase and hTERTcausing cellular senescence and cell death. From the 20 thto the 30 th passages, the activation of telomerase andmaintenance of telomere length show a progressive processfor immortalization of esophageal epithelial cells. Theexpression of telomerase may constitute a biomarker fordetection of immortalization of cells. | Zhong-Ying Shen Li-Yan Xu Wei-Jia Cai Min-Hua Chen Jian Shen,Department of Tumor Pathology,Medical College of Shantou University,Shantou 515031,Guangdong Province,China En-Min Li,Department of Biochemistry and Molecular Biology,Medical College of Shantou University,Shantou 515031,Guangdong Province,China Yi Zeng,Institute of Virology,Chinese Academy of Preventive Medicine,Beijing 100052,China | 2002 | World Journal of Gastroenterology2002，8，2： | 21 |
| 8 | APC and K-ras gene mutation in aberrant crypt foci of human colon显示文摘AIM To study the genetic alteration in ACF andto define the possibility that ACF may be a veryearly morphological lesion with molecularchanges, and to explore the relationshipbetween ACF and colorectal adenoma evencarcinoma.METHODS DNA from 35 CRC, 15 adenomas, 34ACF and 10 normal mucus was isolated by meansof microdissection. Direct gene sequencing of K-ras gene including codon 12, 13 and 61 as well asthe mutation cluster region (MCR) of APC genewas performed.RESULTS K-ras gene mutation frequency inACF, adenoma and carcinoma was 17.6% (6/34), 13.3% (2/ 15), and 14.3% (5/ 35)respectively, showing no difference ( P > 0.05)in K-fas gene mutation among three pathologicprocedures. The K-ras gene mutation inadenoma, carcinoma and 4 ACF restricted incodon 12 (GGT→GAT), but the other 2 mutationsfrom ACF located in codon 13 (GGC→GAC). K-res gene mutation was found more frequently inolder patients and patients with polypoidcancer. No mutation in codon 61 was found in thethree tissue types. Mutation rate of APO gene inadenoma and carcinoma was 22.9% (8/35) and26.7% (4/ 15), which was higher than ACF(2.9%) (P < 0.05). APC gene mutation incarcinoma was not correlated with age ofpatients, location, size and differentiation oftumor.CONCLUSION ACF might be a very earlymorphological lesion in the tumorogenesis ofcolorectal tumor. The morphological feature andgene mutation status was different in ACF andadenoma. ACF is possibly putative'microadenoma' that might be the precursor ofadenoma. In addition, the development of asubgroup of colorectal carcinomas mightundergo a way of 'normal epithelium→ ACF→carcinomas'. | Ping Yuan~1 Meng Hong Sun~2 Jin Sheng Zhang~1 Xiong Zeng Zhu~2 Da Ren Shi~2 ~1Department of Pathology,Medical College of Fudan University,~2Department of Pathology,Cancer Hospital/Cancer Institute,Fudan University,Shanghai 200032,ChinaDr.Ping Yuan Studying Province.studying in Medical College of Fudan University,worked in Department of Pathology,Wannan Medical College,having eighteen papers published. | 2001 | World Journal of Gastroenterology2001，7，3： | 20 |
| 9 | Overexpression of p27^(KIP1)induced cell cycle arrest in G_1 phase and subsequent apoptosis in HCC-9204 cell line显示文摘AIM We have previously reported that inducibleover-expression of Bak may prolong cell cycle inG1 phase and lead to apoptosis in HCC-9204 cells.This study is to investigate whether p27KIP1playsan important role in this process.METHODS In order to elucidate the exactfunction of p27KIP1in this process,a zinc induciblep27KIP1stable transfectant and transient p27KIP1-GFP fusion transfectant were constructed.Theeffects of inducible,p27KIP1on cell growth,cellcycle arrest and apoptosis were examined in themock,control pMD vector,and pMD-KIP1transfected HCC-9204 cells.RESULTS This p27KIP1-GFP transfectant maytransiently express the fusion gene.The cellgrowth was reduced by 35% at 48 h of p27KIP1induction with zinc treatment as determined bytrypan blue exclusion assay.These differencesremained the same after 72 h of p27KIP1expression,p27KIP1caused cell cycle arrest after24 h of induction,with 40% increase in G1population.Prolonged p27KIP1expression in thiscell line induced apoptotic cell death reflected byTUNEL assay.Fourty-eight h and 72 h of p27KIP1expression showed a characteristic DNA ladder onagarose gel electrophoresis. CONCLUSION Bak may induce cell cycle arrest inG1 phase through upregulating expression ofp27KIP1and subsequently lead to apoptosis inHCC-9204 cells.The p27KIP1-GFP fusion proteincan be transiently expressed in HCC-9204 cells.The inducible p27KIP1-expressing cell line providesa model to assess p27KIP1function. | Jiang Li Xin Ke Yang Xin Xin Yu Meng Liang Ge Wen Liang Wang Jie Zhang Yun De Hou Department of Pathology,Fourth Military Medical University,Xi’an 710033,Shaanxi Province,China State Key Laboratory for Molecular Virology and Genetic Engineering,Beijing 100052,China Department of Dermatology,Beijing Hospital,Beijing 100016,China Institute of Radiation Medicine,Beijing 100085,China | 2000 | World Journal of Gastroenterology2000，6，4： | 20 |
| 10 | Effects of hypoxia,hyperoxia on the regulation of expression and activity of matrix metalloproteinase-2 in hepatic stellate cells显示文摘AIM To study the effects of hypoxia, hyperoxia on the regulation of expression and activity of matrix metalloproteinase-2 (MMP-2) in hepatic stellate cells ( HSC).``METHODS The expressions of MMP-2, tissue inhibitor of mjatrix metalloproteinese-2 ( TIMP-2 ) and membrane type matrix metalloproteiness-l (MT1-MMP) in cultured rat HSC were detected by immunocytochemistry (ICC) and in situ hybridization (ISH). The contents of MMP-2 and TIMP-2 in culture supernatant were detected with ELISA and the activity of MMP-2 in supematant was revealed by zymography.``RESULTS In the situation of hypoxia for 12 h, the expression of MMP-2 protein wss enhenced (hypoxiagroup positive indexes: 5.7 ± 2.0, n = 10; control: 3.2 ±1 .0. n -- 7; P<0.05). while TIMP-2 protein wss decreased in HSC ( hypoxia group positive indexes: 2.5 ± 0.7, n =10: control: 3.6 ± 1.0, n = 7; P | Ping-Sheng Chen~(1,2) Wei-Rong Zhai~1 Xiao-Mei Zhou~3 Jin-Sheng Zhang~1 Yue-E Zhang~1 Yu-Qin Ling~1 Ying-Hong Gu~1 1 Department of Pathology,School of Basic Medical Sciences,Fudan University,Shanghai 200032,China2 Ping-Sheng Chen now works in the Department of Pathology,School of Basic Medical Sciences the (former Nanjing Railway Medical College),Southeast University,Nanjing 210009,China3 Institute of Cancer Research,Shanghai 200032,China | 2001 | World Journal of Gastroenterology2001，7，5： | 18 |
| 11 | VEGF-D expression correlates with colorectal cancer aggressiveness and is downregulated by cetuximab显示文摘AIM:To gain mechanistic insights into the role played by epidermal growth factor receptor (EGFR) in the regulation of vascular endothelial growth factors (VEGFs) in colorectal cancer (CRC). METHODS:The impact of high-level expression of the growth factor receptors EGFR and VEGF receptor (VEGFR)3 and the VEGFR3 ligands VEGF-C and VEGF-D on disease progression and prognosis in human CRC was investigated in 108 patients using immunohistochemistry. Furthermore, the expression of the lymphangiogenic factors in response to the modulation of EGFR signalling by the EGFR-targeted monoclonal antibody cetuximab was investigated at the mRNA and protein level in human SW480 and SW620 CRC cell lines and a mouse xenograft model. RESULTS: Human CRC specimens and cell lines displayed EGFR, VEGF-C and VEGF-D expression with varying intensities. VEGF-C expression was associated with histological grade. Strong expression of VEGF-D was significantly associated with lymph node metastases and linked to a trend for decreased survival in lymph node-positive patients. EGFR blockade with cetuximab resulted in a significant decrease of VEGF-D expression in vitro and in vivo. CONCLUSION:In conclusion, the expression of VEGF-D in colorectal tumours is significantly associated with lymphatic involvement in CRC patients and such expression might be blocked effectively by cetuximab. | Markus Moehler Christian Frings Annett Mueller Ines Gockel Carl C Schimanski Stefan Biesterfeld Institute of Pathology Johannes Gutenberg University Mainz 55101 Germany Peter R Galle Martin H Holtmann | 2008 | World Journal of Gastroenterology2008，14，26： | 15 |
| 12 | Population-based study of DNA image cytometry as screening method for esophageal cancer显示文摘AIM:To explore the DNA image cytometry (DNA-ICM) technique as a primary screening method for esopha-geal squamous precancerous lesions.METHODS:This study was designed as a population-based screening study.A total of 582 local residents aged 40 years-69 years were recruited from Linzhou in Henan and Feicheng in Shandong.However,only 452 subjects had results of liquid-based cytology,DNA-ICM and pathology.The sensitivity and specificity of DNA-ICM were calculated and compared with liquid-based cytology in moderate dysplasia or worse.RESULTS:Sensitivities of DNA-ICM ranging from at least 1 to 4 aneuploid cells were 90.91%,86.36%,79.55% and 77.27%,respectively,which were better than that of liquid-based cytology (75%).Specifici-ties of DNA-ICM were 70.83%,84.07%,92.65% and 96.81%,but the specificity of liquid-based cytology was 91.91%.The sensitivity and specificity of a combination of liquid-based cytology and DNA-ICM were 84.09% and 85.78%,respectively.CONCLUSION:It is possible to use DNA-ICM tech-nique as a primary screening method for esophageal squamous precancerous lesions. | Lin Zhao,Wen-Qiang Wei,Xin-Qing Li,Guo-Qing Wang,Qi Shang,You-Lin Qiao,Department of Cancer Epidemiology,Cancer Institute/Hospital,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100021,China De-Li Zhao,Department of Epidemiology,Feicheng People’s Hospital,Feicheng 271600,Shandong Province,China Chang-Qing Hao,Department of Endoscopy,Linzhou Cancer Hospital,Linzhou 456500,Henan Province,China Dong-Mei Lin,Qin-Jing Pan,Department of Pathology,Cancer Institute/Hospital,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100021,China Fu-Hua Lei,Department of Pathology,Feicheng People’s Hospi-tal,Feicheng 271600,Shandong Province,China Jin-Wu Wang,Department of Pathology,Linzhou Cancer Hospi-tal,Linzhou 456500,Henan Province,China | 2012 | World Journal of Gastroenterology2012，18，4： | 15 |
| 13 | Extraction and purification of TGFβ and its effect on the induction of apoptosis of hepatocytes显示文摘AIM To extract and purify the transforming growth factor β (TGF β), and to demonstrate its biological activity in vivo and induction of apoptosis of hepatocytes in vitro.METHODS TGF β was isolated from fresh bovine platelets by acid/ethanol extraction method and purified with ion exchange and gel chromatography. The extracted TGF β was injected subcutaneously to mice, and its biological activity in vivo was observed 72 hfs post-injection by HE staining. The morphological changes were observed by HE staining and the occurrence of apoptosis was detected by TUNEL method after the human normal hepatic cell line QZG was treated with 8 μg@L 1 TGFβ for 12 hrs in vitro.RESULTS The molecular mass 25 ku TGF β protein was successfully extracted. It was able to induce localized granulation tissue formation in vivo. TGF β-treated hepatocytes showed obvious apoptotic morphological changes, including the pyknosis and dense-stained nuclei and cytoplasm, the fragmentary, annular or crescent nuclei, and the 'bubbling' cytoplasm. Moreover, its apoptotic rate was significantly higher than that of the control group (P<0.05).CONCLUSION Biological active TGF β protein is extracted and purified successfully from bovine platelets, and it is able to induce the apoptosis of hepatocytes. | Xiao-Hui Si Lian-Jun Yang Research Institute of Stomatology,the Ninth People’s Hospital,Shanghai Second Medical University,Shanghai 200011,ChinaDepartment of Pathology,Fourth Military Medical University,Xi’an 710033,Shaanxi Province,China | 2001 | World Journal of Gastroenterology2001，7，4： | 15 |
| 14 | Preparation of monoclonal antibody against apoptosis-associated antigens of hepatoma cells by subtractive immunization显示文摘AIM: To elucidate the expression of the apoptosis-associatedmolecules in human primary hepatocellular carcinoma (HCC)cells, and prepare the monoclonal antibodies (mAb) againstthe apoptosis-associated antigens of HCC cells.METHODS: Human HCC cell line HCC-9204 cells wereinduced apoptosis with 60 mL.L-1 ethanol for 6 h and theirmorphological changes were observed by transmissionelectron microscope. The cell DNA fragmentations weredetected by Terminal Deoxynucleotidyl transferase-mediateddUTP nick end labeling (TUNEL) assay, and the cell DNAcontents by flow cytometry. Ten mice were immunized withethanol-induced apoptotic HCC-9204 cells with the methodof subtractive immunization, while the other 10 mice usedas the control were immunized by the routine procedures.The tail blood of all the mice were prepared after the lastimmunization, and the produced antibodies were determinedby the immunocytochemical ABC staining. The splenic cellsof the mice whose tail blood sera-HCC-9204 cells serumreactions were most different between the apoptotic andthe non-apoptotic were prepared and fused with the mousemyeloma cell line SP2/0 cells. The positive antibodies wereselected by ELISA assay. The fusion rates of hybridoma cellsand the producing rates of antibodies were calculated. Thefused cells that secreted candidate objective antibody werecloned continually with the of limited dilution method, andthen selected and analyzed further by theimmunocytochemical ABC staining. The chromosomes of thecloned hybridoma cells that secreted objective mAb and themAb immunoglobulin (Ig) subtype of the prepared mAb werealso determined. The molecular mass of the mAb associatedantigen was analyzed by Western blot assay.RESULTS: HCC-9204 cells treated with 60 mL.L-1 ethanolfor 6 h, manifested obvious apoptotic morphological changes,the majority of the cells were TUNEL-positive, and the sub-G1 apoptotic peak was evident. There were 2 mice in theexperimental group whose tail blood serum reacted stronglywith the apoptotic HCC-9204 cells, but weakly with theirnon-apoptotic counterparts. In the fusion rates of hybridomacells as well as the producing rates of the antibody deseribedabove, there did not show significant difference betweenthe experimental and the control group, but weakly withnon-apoptotic HCC-9204. However, the total producing rateof antibodies in the experimental group was significantlylower compared with the control (P<0.01), and so was theproducing rate of the antibodies which reacted strongly withboth apoptotic and non-apoptotic HCC-9204 cells(P<0.01).After cloned continually for several times the cell that producemAb which reacted strongly with the nuclei of ethanol-induced apoptotic HCC-9204 cells, but very weakly with thatof non-apoptotic cells was selected out. Chromosome analysisrevealed that the selected cell was with the universalcharacteristics of the monoclonal hybridoma cells whichsecreted mAb, and the Ig subtype of the prepared mAb wasIgG1. The molecular mass of this mAb associated antigenof was about 75 ku.CONCLUSION: Subtractive immunization is a useful methodto prepare the mAb against the apoptosis-associated antigensof cells. The expression of some molecules increases to someextent in HCC-9204 cells in the process of apoptosis inducedby Iow-concentration ethanol. The mAb that may be againstethanol-induced apoptosis-associated antigens of HCC cellswas successfully prepared and primarily identified. | Lian-Jun Yang Wen-Liang Wang Department of Pathology,Institute of Cancer Research,The Fourth Military Medical University (FMMU),Xian 710032,Shaanxi Province,China | 2002 | World Journal of Gastroenterology2002，8，5： | 13 |
| 15 | Human papillomavirus DNA and P16~(INK4A) expression in concurrent esophageal and gastric cardia cancers显示文摘AIM:To investigate the relationship between human papillomavirus (HPV) infection and concurrent esophagus and gastric cardia cancer from the same patient (CC) and examine the significance of P16 INK4A protein expression.METHODS:Polymerase chain reaction was used to detect the presence of HPV type16 (HPV16).The expression of P16 INK4A protein was detected using immunohistochemistry.RESULTS:Among the CC specimens,HPV16-DNA was found in eight cases of esophageal squamous cell carcinoma (ESCC) and five cases of gastric cardia adenocarcinoma (GCA),respectively (47% vs 29%),and two of both ESCC and GCA.P16 INK4A was highly expressed in both ESCC and GCA.In the HPV-associated positive CC,higher P16 INK4A expression was observed in the GCA than in the ESCC (75% vs 25%,P < 0.05).CONCLUSION:HPV16 as a correlated risk factor may play an important role in the development of ESCC and GCA.P16 INK4A may be a screening index in the HPVassociated carcinoma of gastric cardia. | Guang-Cheng Ding,Tao Guo,Department of Gastroenterology,The First Affiliated Hospital and The Fifth Affiliated Hospital,Zhengzhou University,Zhengzhou 450052,Henan Province,China Jing-Li Ren,Xin Song,Sheng-Li Zhou,Zong-Min Fan,LiDong Wang,Henan Key Laboratory for Esophageal Cancer Research,Department of Gastroenterology,The First Affiliated Hospital,College of Basic Medicine,Zhengzhou University,Zhengzhou 450052,Henan Province,China Fu-Bao Chang,Department of Thoracic Surgery,Linzhou Center Hospital,Linzhou 456500,Henan Province,China Ji-Lin Li,Department of Pathology,Yaocun Esophageal Cancer Hospital,Linzhou 456500,Henan Province,China Ling Yuan,Department of Oncoradiotherapy,Henan Province Tumor Hospital,Zhengzhou 450003,Henan Province,China Yi Zeng,Institute of Virology,Chinese Academy of Preventive Medicine,Beijing 100052,China | 2010 | World Journal of Gastroenterology2010，16，46： | 11 |
| 16 | Is inconsistency of α-fetoprotein level a good prognosticator for hepatocellular carcinoma recurrence?显示文摘AIM: To identify the clinical outcomes of hepato-cellular carcinoma (HCC) patients with inconsistent α-fetoprotein (AFP) levels which were initially high and then low at recurrence.METHODS: We retrospectively included 178 patients who underwent liver resection with high preoperative AFP levels (≥ 200 ng/dL). Sixty-nine HCC patients had recurrence during follow-up and were grouped by their AFP levels at recurrence: group Ⅰ, AFP ≤ 20 ng/dL (n = 16); group Ⅱ, AFP 20-200 ng/dL (n = 24); and group Ⅲ, AFP ≥ 200 ng/dL (n = 29). Their preoperative clinical characteristics, accumulated recurrence rate, and recurrence-to-death survival rate were compared. Three patients, one in each group, underwentliver resection twice for primary and recurrent HCC. AFP immunohistochemistry of primary and recurrent HCC specimens were examined.RESULTS: In this study, 23% of patients demon-strated normal AFP levels at HCC recurrence. The AFP levels in these patients were initially high. There were no significant differences in clinical characteristics between the three groups except for the mean recur-rence interval (21.8 ± 14.6, 12.3 ± 7.7, 8.3 ± 6.6 mo, respectively, P < 0.001) and survival time (40.2 ± 19.9, 36.1 ± 22.4, 21.9 ± 22.0 mo, respectively, P = 0.013). Tumor size > 5 cm, total bilirubin > 1.2 mg/dL, vessel invasion, Child classification B, group Ⅲ, and recurrence interval < 12 mo, were risk factors for survival rate. Cox regression analysis was performed and vessel invasion, group Ⅲ, and recurrence interval were independent risk factors. The recurrence inter-val was significant longer in group Ⅰ (P < 0.001). The recurrence-to-death survival rate was significantly bet-ter in group Ⅱ (P = 0.016). AFP staining was strong in the primary HCC specimens and was reduced at recur-rence in group Ⅰ specimens.CONCLUSION: Patients in group Ⅰ with inconsistent AFP levels had a longer recurrence interval and worse recurrence-to-death survival rate than those in group Ⅱ. This clinical presentation may be caused by a delay in the detection of HCC recurrence. | Chung-Bao Hsieh, Teng-Wei Chen, Division of General Sur-gery, Tri-Service General Hospital, Taipei 114, Taiwan, China Chung-Bao Hsieh, Kuo-Piao Chung, Graduate Institute of Health Care Organization Administration, National Taiwan University, Taipei 100, Taiwan, China Chi-Ming Chu, Section of Biostatistics and Informatics, De-partment of Epidemiology, School of Public Health, National Defense Medical Center, Taipei 114, Taiwan, ChinaHeng-Cheng Chu, Department of Internal Medicine, Tri-Service General Hospital, Taipei 114, Taiwan, ChinaCheng-Ping Yu, Department of Pathology, Tri-Service General Hospital, Taipei 114, Taiwan, China | 2010 | World Journal of Gastroenterology2010，16，24： | 11 |
| 17 | FOXP3 expression and clinical characteristics of hepatocellular carcinoma显示文摘AIM: To study the biological and clinical characteristics of transcription factor forkhead box protein 3 (FOXP3) in hepatocellular carcinoma (HCC). METHODS: We analyzed the expression and localization of FOXP3 in HCC tissues and cell lines to evaluate its biological features. The relationship between FOXP3 staining and clinical risk factors of HCC was assessedto identify the clinical characteristics of FOXP3 in HCC. RESULTS: The mRNA and protein expression of FOXP3 were found in some hepatoma cell lines. Immunohistochemical (IHC) analysis of HCC sections revealed that 48% of HCC displayed FOXP3 staining, but we did not find any FOXP3 staining in normal liver tissues and para-tumor tissues. IHC and Confocal analysis showed that the expressions of FOXP3 were mainly present in the nucleus and cytoplasm of tumor cells in tissues or cell lines. In HCC, the distribution of FOXP3 was similar to that of the cirrhosis, but not to the hepatitis B virus. Those findings implicate that FOXP3 staining seems to be associated with the high risk of HCC. CONCLUSION: The clinical characteristics of FOXP3 in HCC warrants further studies to explore its functions and roles in the cirrhosis and development of HCC. | Wei-Hua Wang, Jun-Zhi Wang, National Center for Safety Evaluation of Drugs, National Institute for the Control of Pharmaceutical and Biological Products, Beijing 100050, China Wei-Hua Wang, Chang-Li Jiang, Cun Zhang, Bo Yan, Wei Zhang, Wei Han, Ying-Qi Zhang, Biotechnology Center, School of Pharmacy, the Fourth Military Medical University, Xi’an 710032, Shaanxi Province, China Wei-Hua Wang, Chang-Li Jiang, Cun Zhang, Bo Yan, Wei Zhang, Wei Han, Ying-Qi Zhang, State Key Laboratory of Cancer Biology, Xi’an 710032, Shaanxi Province, China Wei Yan, Department of Pathology, Xijing Hospital, The Fourth Military Medical University, Xi’an 710032, Shaanxi Province, China Yu-Hai Zhang, Department of Health Statistics, The Fourth Military Medical University, Xi’an 710032, Shaanxi Province, China Jiang-Tao Yang, Department of Pathology, Xi’an Gaoxin Hospital, Xi’an 710032, Shaanxi Province, China | 2010 | World Journal of Gastroenterology2010，16，43： | 10 |
| 18 | A new role for T cells in dampening innate inflammatory responses显示文摘The inflammatory response is an attempt by a host to protect itself against injurious stimuli and initiate the tissue healing process [1,2]. Although the production of both pro-and anti-inflammatory mediators which occurs mainly within tissues is a systemic process, | TANG Hong1 & FU YangXin1,2 1 Key Laboratory of Infection and Immunity,Institute of Biophysics,Chinese Academy of Sciences,Beijing 100101,China 2 Department of Pathology,Committee of Immunology,University of Chicago,Chicago,IL 60637,USA | 2010 | Science China(Life Sciences)2010，53，2： | 9 |
| 19 | Impact of KRAS mutation and PTEN expression on cetuximab-treated colorectal cancer显示文摘AIM:To investigate the prognostic value of KRAS mutation,and phosphatase and tensin (PTEN) expression in Chinese metastatic colorectal cancer metastatic colorectal cancer (mCRC) patients treated with cetuximab.METHODS:Ninety Chinese mCRC patients treated with cetuximab were evaluated for KRAS mutation and PTEN protein expression by DNA sequencing of codons 12 and 13 and immunohistochemistry,respectively.We then selected 61 patients treated with cetuximab,either in combination with chemotherapy,or alone as a second-line or third-line regimen to assess whether KRAS mutation or PTEN protein expression is associated with the response and the survival time of mCRC patients treated with cetuximab.RESULTS:KRAS mutation was found in 30 (33.3%) tumor samples from the 90 patients,and positive PTEN expression was detected in 58 (64.4%) of the 90 patients.Among the 61 patients who were treated with cetuximab as a second-line or third-line regimen,the resistance to cetuximab was found in 22 patients with KRAS mutation and in 39 patients without KRAS mutation,with a response rate of 4.5% and 46.1% respectively (P=0.001),a shorter median progression-free survival (PFS) time of 14 ± 1.3 wk and 32 ± 2.5 wk respectively (P < 0.001),a median overall survival (OS) time of 11 ± 1.2 mo and 19 ± 1.8 mo respectively (P < 0.001),as well as in 24 patients with negative PTEN expression and in 37 patients with positive PTEN expression respectively (P < 0.001),with a responsive rate of 4.2% and 48.6% respectively,a shorter median PFS survival time of 17 ± 2.0 wk and 28 ± 1.9 wk respectively (P=0.07),and a median OS time of 11 ± 1.3 mo and 18 ± 1.9 mo respectively (P=0.004).Combined KRAS mutation and PTEN expression analysis showed that the PFS and OS time of patients with two favorable prognostic factors were longer than those of patients with one favorable prognostic factor or no favorable prognostic factor (P < 0.001).CONCLUSION:KRAS mutation and PTEN protein expression are significantly correlated with the response rate and survival time of Chinese mCRC patients treated with cetuximab. | Fang-Hua Li,Zhuang-Hua Li,Hui-Yan Luo,Miao-Zhen Qiu,Yu-Hong Li,Rui-Hua Xu,State Key Laboratory of Oncology in Southern China,Department of Medical Oncology,Sun YatSen University Cancer Center,Guangzhou 510060,Guangdong Province,China Fang-Hua Li,Department of Medical Oncology,Shengli Oil Field Central Hospital,Dongying 257034,Shandong Province,China Lin Shen,Department of GI Oncology,Peking University School of Oncology,Beijing Cancer Hospital and Institute,Beijing 100142,China Hui-Zhong Zhang,State Key Laboratory of Oncology in Southern China,Department of Pathology,Sun Yat-Sen University Cancer Center,Guangzhou 510060,Guangdong Province,China | 2010 | World Journal of Gastroenterology2010，16，46： | 9 |
| 20 | Progressive transformation of immortalized esophageal epithelial cells显示文摘AIM: To investigate the progressive transformation of immortal cells of human fetal esophageal epithelium induced by human papillomavirus, and to examine biological criteria of sequential passage of cells, including cellular phenotype, proliferative rate, telomerase, chromosome and tumorigenicity.METHODS: The SHEE cell series consisted of immortalized embryonic esophageal epithelium which was in malignant transformation when cultivated over sixty passages without co-carcinogens. Cells of the 10th, 31st, 60th and 85th passages were present in progressive development after being transfected with HPV. Cells were cultivated in a culture flask and 24-hole cultural plates. Progressive changes of morphology, cell growth, contact-inhibition, and anchoragedependent growth characteristics were examined by phase contrast microscopy. The cell proliferation rate was assayed by flow cytometry. The modal number of chromosomes was analyzed. HPV18E6E7 was detected by Western blot methods and activities of telomerase were analyzed by TRAP.Tumorigenicity of cells was detected with soft agar plates cultivated and with tumor formation in SCID mice.RESULTS: In morphological examination the 10th passage cells were in good differentiation, the 60th and 85th passages cells were in relatively poor differentiation, and the 31st passage cells had two distinct differentiations. The characteristics of the 85th and 60th passage cells were weakened at contact-inhibition and anchorage-dependent growth. Karyotypes of four stages of cells belonged to hyperdiploid or hypotriploid, and bimodal distribution of chromosomes appeared in the 31st and 60th passage cells. All of these characteristics combined with a increasing trend. The activities of telomerase were expressed in the latter three passages. Four fourths of SCID mice in the 85th passage cells and one fourth of SCID mice in the 60th passage cells developed tumors, but the cells in the 10th and 31st passage displayed no tumor formation.CONCLUSION: In continual cultivation of fetal esophageal epithelial cells with transduction of HPV18E6E7, cells from the 10th to the 85th passage were changed gradually from preimmortal, immortal, precancerous to malignantly transformed stages. All of these changes were in a dynamic progressive process. The establishment of a continuous line of esophageal epithelium may provide a in vitro model of carcinogenesis induced by HPV. | Zhong-Ying Shen Li-Yan Xu Min-Hua Chen Jian Shen WeiJia Cai,Department of Tumor Pathology Medical College of Shantou University,Shantou 515031,Guangdong Province,China Yi Zeng,Institute of Virology,Chinese Academy of Preventive Medicine.Beijing 100052,China | 2002 | World Journal of Gastroenterology2002，8，6： | 8 |
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