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| 1 | Mutation analysis of novel human liver-related putative tumor suppressor gene in hepatocellular carcinoma显示文摘AIM: To find the point mutations meaningful for inactivationof liver-related putative tumor suppressor gene (LPTS) gene,a human novel liver-related putative tumor suppressor geneand telomerase inhibitor in hepatocellular carcinoma.METHODS: The entire coding sequence of LPTS genewas examined for mutations by single strand conformationpolymorphism (SSCP) assay and PCR products directsequencing in 56 liver cancer cell lines, 7 ovarian cancerand 7 head & neck tumor cell lines and 70 pairs of HCCtissues samples. The cDNA fragment coding for the mostfrequent mutant protein was subcloned into GST fusionexpression vector. The product was expressed in E. coliand purified by glutathione-agarose column. Telomericrepeat amplification protocol (TRAP) assays wereperformed to study the effect of point mutation totelomerase inhibitory activity.RESULTS: SSCP gels showed the abnormal shifting bandsand DNA sequencing found that there were 5 differentmutations and/or polymorphisms in 12 tumor cell lineslocated at exon2, exon5 and exon7. The main alterationswere A(778)A/G and A(880)T in exon7. The change in siteof 778 could not be found in HCC tissue samples, while themutation in position 880 was seen in 7 (10 %) cases. Themutation in the site of 880 had no effect on telomeraseinhibitory activity.CONCLUSION: Alterations identified in this study arepolymorphisms of LPTS gene. LPTS mutations occur in HCCbut are infrequent and of little effect on the telomeraseinhibitory function of the protein. Epigenetics, such asmethylation, acetylation, may play the key role in inactivationof LPTS. | ChengLiao Mu-junZhao JingZhao HaiSong PascalPineau AgnésMarchio AnneDejean PierreTiollais Hong-YangWang Tsai-PingLi | 2003 | World Journal of Gastroenterology2003，9，1： | 67 |
| 2 | Inhibition of human telomerase in MKN-45 cell line by antisense hTR expression vector induces cell apoptosis and growth arrest显示文摘AIM: To investigate the effects of antisense humantelomerase RNA (hTR) on the biologic behavior of humangastric cancer cell line: MKN-45 by gene transfection and itspotential role in the gene therapy of gastric cancer.METHODS: The hTR cDNA fragment was cloned from MKN-45 through RT-PCR and subcloned into eukaryoticexpression vector (pEF6/V5-His-TOPO) in cis-direction ortrans-direction by DNA recombinant methods. Theconstructed sense, antisense and empty vectors weretransfected into MKN-45 cell lines separately by lipofectin-mediated DNA transfection technology. After drugselection, the expression of antisense hTR gene in stabletransfectants and normal MKN-45 cells was detected by RT-PCR, the telomerase activity by TRAP, the apoptoticfeatures by PI and Hoechst 33258 staining, the cell cycledistribution by flow cytometry and the population doublingtime by cell counting. Comparison among the stabletransfectants and normal MKN-45 cells was made.RESULTS: The sense, antisense hTR eukaryotic expressionvectors and empty vector were successfully constructed andproved to be the same as original design by restrictionendonuclease analysis and sequencing. Then, they weresuccessfully transfected into MKN-45 cell lines separatelywith lipofectin. The expression of antisense hTR gene wasonly detected in MKN-45 cells stably transfected withantisense hTR vector (named as MKN-45-ahTR) but not inthe control cells. In MKN-45-ahTR, the telomerase activitywas inhibited by 75 %, the apoptotic rate was increased to25.3 %, the percentage of cells in the G0/G1 phase wasincreased to 65 %, the proliferation index was decreased to35 % and the population doubling time was prolonged to 35.3hours. However, the telomerase activity, the apoptotic rate,the distribution of cell cycle, the proliferation index and thepopulation doubling time were not different among the controlcells.CONCLUSION: Antisense hTR can significantly inhibittelomerase activity and proliferation of MKN-45 cells andinduce cell apoptosis. Antisense gene therapy based onteiomerase inhibition can be a potential therapeuticapproach to the treatment of gastric cancer. | FengRH ZhuZG 等 | 2002 | World Journal of Gastroenterology2002，8，3： | 31 |
| 3 | 二烯丙基二硫对人胃癌MGC803细胞生长的影响显示文摘目的:研究二烯丙基二硫(DADS)对人胃癌MGC803细胞生长的抑制作用。方法:采用MTT法、生长曲线分析、细胞活力检测、双层软琼脂集落形成率、及倒置显微镜等方法,观察DADS对体外培养的人胃癌MGC803细胞的影响。结果:DADS对MGC803细胞具有明显的生长抑制效应,且呈剂量-效应依赖关系(P<0.05)。培养96 h,35mg/LDADS的抑制作用呈时间-效应依赖关系(P<0.05)。细胞群体倍增时间由33.8 h处长至DADS处理后的84.0 h(P<0.05);细胞存活率分别为阴性对照组97.4%和DADS处理组80.4%(P>0.05);软琼脂集落形成率由 1.23%下降到0.33%(P<0.05)。阴性对照组细胞多角形、圆形,体积大,多形性明显,核大小不一,见双核及核仁,细胞生长紧密呈堆叠生长,DADS处理后细胞异型性降低,为形态一致的梭形,体积小,境界清楚而分散,胞质丰富,核明显变小。结论:DADS对体外培养的MGC803细胞具有明显的增生抑制作用,且呈现剂量-效应依赖关系。 | 张良运 凌晖 苏琦 宋颖 梁晓秋 | 2003 | 世界华人消化杂志2003，11，9： | 29 |
| 4 | Expression and function of classical protein kinase C isoenzymes in gastric cancer cell line and its drugresistant sublines显示文摘AIM: To investigate the expression and function of classicalprotein kinase C (PKC) isoenzymes in inducing MDRphenotype in gastric cancer cells.METHODS: Two cell lines were used in the study: gastriccancer cell SGC7901 and its drug-resistant cell SGC7901/VCRstepwise-selected by vincristine 0.3, 0. 7 and 1.0 mg@ L-1 ,respectively. The expression of classical PKC (cPKC)isoenzymes in SGC7901 cells and SGC7901/VCR cells weredetected using immunofluorescent cytochemistry, laserconfocal scanning microscope and Wsstern blot. The effectsof anti-PKC isoenzymes antibody of adriamycinaccumulation in SGC7901/VCR cells were determined usingflow cytometric analysis.RESULTS: (1) SGC7901 cells exhibited positive staining ofPKC-α. SGC7901/VCR cells exhibited stronger staining ofPKC-α than SGC7901 cells. The higher dosage vincristineselected, the much stronger staining of PKC-α was observedon SGC7901/VCR cells. (2) Both SGC7901 and SGC7901/VCRcells exhibited positive staining of PKC-βⅠ and PKC-βⅡ withno significant difference. ( 3 ) Compared with SGC7901,SGC7901/VCR cells had decreased adriamycin accumulationand retention. Accumulation of adriamycin in SGC7901 was5.21 + 2.56 mg@ L-1, in SGC7901/VCR 0.3 was 0.85 + 0.29 mg@L-1 , in SGC7901/VCR 0.7 was 0.81 + 0.32 og@ L-1 , and inSGC7901NCR 1.0 was 0.80 + 0.33 mg @ L-1; Retention ofadriamycin in SGC 7901 was 2.51 + 1.23 mg@L-1, in SGC7901/VCR 0.3 was 0.47 + 0.14 mg@ L-1 , in SGC7901/VCR 0.7 was 0.44 + 0.15 mg@ L-1, and in SGC 7901/VCR 1.0 was 0.41 + 0.1 1mg @ L-1 . (4) Fluorescence intensity presented adriamycinaccumulation in SGC7901/VCR cells was increased from 1.14+0.36 to 2.71 +0.94 when cells were co-incubated with anti-PKC-αbut not with anti-PKC-βⅠ, PKC-βⅡ and PKCγ antibodies.CONCLUSION: PKC-α, but not PKC-βⅠ, PKC-βⅡ or PKCγ,may play a role in multidrug resistance of gastric cancercells SGC7901/VCR. | Ying Han Zhe-Yi Han Xin-Min Zhou Ru Shi Yue Zheng Yong-Quan Shi Ji-Yan Miao Bo-Rong Pan Dai-Ming Fan | 2002 | World Journal of Gastroenterology2002，8，3： | 25 |
| 5 | The role of KDR in the interactions between human gastric carcinoma cell and vascular endothelial cell显示文摘AIM:To study the interactions between human gastriccarcinoma cell (HGCC) and human vascular endothelialcell (HVEC), and the role of KDR in these interactions.METHODS:Antisense oligodexynucleotide(ASODN)specific to KDR gene was devised and added to theculture medium of HGCC and HVEC. After the action ofASODN, the proliferation of two cells was measured byMTT method.The role of KDR in regulating theproliferation of two kinds of cells was known throughobserving the effect of ASODN on them. The conditionedmediums (CMs) of HGCC and HVEC were prepared. TheCM of one kind of cell was added acting on the otherkind of cell, then the cell proliferation was measuredby MTT. After the action of ASODN or CM, the cellularexpression of KDR gene was detected with in situhybridization(ISH) for mRNA level and withimmunohistochemical staining for protein level. ABC-ELISA was used to detect/NEGF in the CMs of two cells.RESULTS: KDR ASODN could specifically inhibit theproliferation of HGCC and HVEC significantiy. The growthinhibitory rate amounted to 55.35 % and 54.83 %,respectively (P<0.01). HGCC and HVEC could secret acertain level of hVEGF(92.06±1.69 ng/L, 77.70±8.04ng/L). The CM of HGCC could significantiy stimulate thegrowth(2.70±0.01 times) and KDR gene expression ofHVEC(P<0.01) while the CM of HVEC could significantiyinhibit the growth(52.97±0.01%) and KDR geneexpression of HGCC (P <0.01).CONCLUSION: KDR plays a key role in regulating theproliferation of HGCC and HVEC. There existcomplicated interactions between HGCC and HVEC.HGCC can significantly stimulate the growth of HVECwhile HVEC can significantly inhibit the growth of HGCC.KDR is involved in the interactions between them. | Juan Ren Lei Dong Cang-Bao Xu Bo-Rong Pan | 2002 | World Journal of Gastroenterology2002，8，4： | 23 |
| 6 | Methylation and mutation analysis of p16 gene in gastric cancer显示文摘AIM: To study methylation, frequencies of homozygous deletion and mutation of p16 gene in gastric carcinoma.METHODS: The methylation pattern in exon 1 and exon 2of p16 gene was studied with polymerase chain reaction (PCR), using methylation sensitive restriction endonuclease HpaⅡ and methylation insensitive restriction endonudease MspⅠ. PCR technique was used to detect homozygous deletions of exon 1 and exon 2 of p16 gene and single strand conformation polymorphism (SSCP) technique was used to detect the mutation of the gene.RESULTS: Hypermethylation changes in exon 1 and exon 2 of p16 gene were observed in 25 % and 45 % of 20gastric cancer tissues, respectively, while no methylation abnormality was found in normal tissues. The homozygous deletion frequency of exon 1 and exon 2 of p16 gene in 20gastric cancer tissues was 20 % and 10 %, respectively. No mutation was found in exon 1 of p16 gene, while abnormal single strands were found in 2 (10 %) cases in exon 2 as detected by SSCP.CONCLUSION: The results suggest that hypermethylation and abnormality of p16 gene may play a key role in the progress of gastric cancer. Hypermethylation of exon 2 of p16 gene may have effects on the carcinogenesis of gastric mucosa and may be a later event. | YiDing Xiao-PingLe Qin-XianZhang PengDu | 2003 | World Journal of Gastroenterology2003，9，3： | 21 |
| 7 | 大肠癌hTERT和p16表达与端粒酶活性的关系显示文摘目的:探讨端粒酶催化亚单位(hTERT)和p16基因表达与端粒酶活性的关系及其在大肠癌发生过程中的作用。 方法:采用原位逆转录聚合酶链反应(RT-PCR)和免疫组化SP法分别检测46例大肠癌及其相应正常组织中hTERTmRNA与P16蛋白表达。用端粒重复序列扩增法(TRAP)测定上述组织标本中的端粒酶活性。 结果:hTERTmRNA与端粒酶活性在大肠癌组织中阳性率分别为87.0%和80.4%,而在相应正常组织中均为阴性。大肠癌中hTERTmRNA表达与端粒酶活性呈显著正相关(r=0.70,P<0.01)。P16蛋白在大肠癌与正常组织中阳性表达率为41.3%和93.5%,二者比较差异有非常显著性(p<0.01)。大肠癌组织P16蛋白表达与端粒酶活性呈显著负相关(r=0.59,P<0.01)。 结论:hTERTmRNA表达和p16基因失活在大肠癌发生过程中起重要作用,大肠癌中端粒酶激活可能与hTERTmRNA表达及p16基因失活有关。 | 方向明 于皆平 罗和生 | 2002 | 世界华人消化杂志2002，10，1： | 13 |
| 8 | 奥沙利铂综合治疗胃癌的疗效及机制显示文摘目的:评价奥沙利铂(Oxaliplatin,L-OHP)对人胃癌的疗效,探讨其治疗胃癌的作用机制。方法:Ⅳ期胃癌患者22例接受包含L-OHP的联合化疗方案(L-OHP 85 mg/m^2,静脉点滴,1h,第1d;四氢叶酸钙200 mg/m^2,静脉点滴,1h,第1-5 d;5-FU 300mg/m^2,静脉注射,第1-2d,5-FU,持续静脉点滴,48h;2wk1疗程)4-6(平均4.6)个疗程.观察有效率,无进展生存时间(progression-free survival,PFS),总体生存时间及毒副作用。体外培养人中分化胃癌细胞株SGC-7901,应用MTT法检测L-OHP对细胞生长的抑制作用,并计算50%抑制浓度(IC_(50));将不同浓度梯度的L-OHP与细胞株作用后,应用流式细胞仪(ANEXIN-V标记)及TUNEL检测细胞凋亡情况。应用RT-PCR检测caspase-3m-RNA的表达。结果:有效(完全有效及部分有效)9例(40.9%)。平均PFS4.2mo,总体生存时间7.2mo。蓄积性神经毒性(全部为Ⅰ-Ⅱ级),呕吐及腹泻(1例Ⅲ级腹泻),骨髓抑制发生率分别为93.5%,20%,32.9%.浓度为1mmol/L的L—OHP与细胞株作用30min,流式细胞仪即可检测出细胞凋亡水平升高,但无统计学差异(P>0.05),1mmol/L作用2d,流式细胞仪及TUNEL均可检测到细胞凋亡水平显著性升高(P<0.05)。L-OHP作用后的细胞caspase-3 m-RNA表达升高,并与药物诱导的凋亡相关。结论:L-OHP治疗进展期胃癌安全有效.L-OHP在体外可明显抑制胃癌细胞株SGC-7901的生长,诱导细胞caspase-3m-RNA表达及凋亡。 | 林万隆 李定国 陈强 陆汉民 马小明 孙培龙 | 2003 | 世界华人消化杂志2003，11，10： | 12 |
| 9 | Expression of p21^(WAF1) and p53 and polymorphism of p21^(WAF1) gene in gastric carcinoma显示文摘To investigate the relationship between expression of p21WAF1 and p53 gene, and to evaluate the deletion and polymorphism of p21WAF1 gene in gastric carcinoma (GC). | Hai-LongXie Qisu Xiu-ShengHe xiao-QiuLiang Jian-GuoZhou YinSong Yi-QinLi | 2004 | World Journal of Gastroenterology2004，10，8： | 12 |
| 10 | 人胃癌细胞端粒酶RNA组分hTR基因片段的克隆及其正反义真核表达载体的构建显示文摘目的克隆人胃癌细胞端粒酶RNA组分(hTR)基因片段并构建其正义和反义真核表达载体,为以端粒酶为靶目标的肿瘤基因治疗奠定基础。方法采用RT-PCR方法从人胃癌细胞株MKN-45中扩增出人hTR部分cDNA序列。将该片段插入pEF6/V5-His-TOPO载体后构建人端粒酶RNA组分(hTR)基因正义真核表达载体(pEF-hTR)。随后采用EcoRV和SpeⅠ从pEF-hTR上切下该目的基因片段并反向插入pBluescriptⅡKS载体上的EcoRV/SpeⅠ酶切位点上。最后采用KpnⅠ和NotⅠ从pBluescriptⅡKS载体上切下该目的基因片段并正向插入pEF-hTR的KpnⅠ/NotⅠ酶切位点上从而构建出人端粒酶RNA组分(hTR)基因反义真核表达载体(pEF-ahTR)。对所构建的载体均进行酶切鉴定和测序确认。结果所克隆的基因片段其碱基序列与文献报道完全一致,且插入载体的方向完全正确。结论本实验已成功克隆了人端粒酶RNA组分(hTR)基因的部分序列并成功构建其正义、反义真核表达载体,从而为研究反义抑制人胃癌细胞端粒酶活性对胃癌细胞生物学行为的影响奠定了基础。 | 冯润华 李建芳 刘炳亚 朱正纲 尹浩然 | 2001 | 世界华人消化杂志2001，9，12： | 11 |
| 11 | A novel gene,GCRG224,is differentially expressed in human gastric mucosa显示文摘AIM: To clone genes that may predispose us to humangastric cancer and to analyze it's expression in gastric tissues.METHODS: Specimens of paired tumor, paratumor andnormal gastric mucosa tissues collected from fifteen patientswho suffered from stomach antrum adenocarcinoma wereused for analysis. Seven out of the fifteen cases were firststudied by fluorescent differential display reversetranscription polymerase chain reaction (DDTR-PCR) analysis.The differentially expressed bands of interest were cloned,analyzed by Northern blot, sequencing and RT-PCR. ThroughBLAST, the sequencing results were compared with GenBankdatabase for homology analysis. In situ hybridization withDIG-labeled cRNA probes was used to analyze the expressionof interesting cDNA bands in paraffin embedded pairednormal gastric mucosa and cancer tissues isolated from 30gastric adenocarcinoma patients.RESULTS: DDRT-PCR showed that one of the interestingcDNA bands, which was named W2, expressed much higherin all seven tested tumor and paratumor samples than intheir normal counterparts, it was sub-cloned into a pGEM-TEasy vector. Two subclones were subsequently obtained.One of the subclone, GCRG224, was studied further. Thesequencing result showed that GCRG224 consisted of 1 159base pairs and had one open reading frame (ORF). It locatedat human chromosome 11q14. No homologue was found inGenBank database with GCRG224-ORF. This nucleotidesequence data were submitted to GenBank with accessionNo. AF438406. RT-PCR showed that GCRG224 expressedhigher in 11/15 gastric cancer tissues than in non-tumortissues. However, the result of Northern blot analysis showeda higher GCRG224 expression in the non-tumor tissue thanin the tumor one. Human multiple tissue Northern blot analysisrevealed that GCRG224 also expressed in human normal colontissue, and peripheral blood leukocyte. In situ hybridizationanalysis showed that only 5/30 adenocarcinoma, 3/18dysplasia and 6/18 intestinal metaplasia showed higherGCRG224 expression level than the normal gastric glands.However, GCRG224 was over-expressed predominantly in 26/30 cases of normal mucosal epithelium.CONCLUSION: A novel gene named GCRG224 wasidentified from human gastric mucosal tissue. Itoverexpressed in almost all gastric mucos al epithelium butonly a small portion of cancer and precancerous leisions.The role of GCRG224 expression in gastric epithelium needsfurther study. | Gang-Shi Wang Meng-Wei Wang Ben-Yan Wu Wei-Di You Xin-Yan Yang Department of Gastroenterology,General Hospital of Chinese PLA,Beijing 100853,China | 2003 | World Journal of Gastroenterology2003，9，1： | 11 |
| 12 | Relationship between inactivation of p16 gene and gastric carcinoma显示文摘AIM: To investigate the relationship between inactivation of p16 gene and gastric carcinoma, and the mechanism of inactivation of p16 gene in gastric carcinogenesis.METHODS: 40 fresh tumor tissue specimens were taken from primary gastric cancer patients. Expression of P16protein was detected by immunohistochemical method.Deletion and point mutation of p16 gene were analyzed by polymerase chain reaction (PCR) and DNA sequencing,respectively.RESULTS: The frequency of loss of P16 protein expression in the gastric cancer tissue, adjacent nontumor tissue, and distal normal tissue was 77.5 %(31/40), 55.0 %(22/40),and 17.5 % (7/40), respectively (P<0.005). Homozygous deletion of exon 1 and exon 3 was observed in two and three cases, respectively, giving an overall frequency of homozygous deletion of 12.5 %. All five cases had diffuse type gastric carcinoma. No p16 gene point mutation was detected.CONCLUSION: These findings suggest a close correlation between inactivation of p16 gene and gastric carcinoma.Further investigations are needed to testify the mechanism of inactivation of p16 gene in gastric carcinogenesis. | Guo-HaiZhao Tie-ChenLi Liang-HuiShi Ya-BinXia Lin-MingLu Wen-BinHuang Hui-LanSun Yi-ShengZhang | 2003 | World Journal of Gastroenterology2003，9，5： | 10 |
| 13 | Expression of tumor related genes NGX6,NAG-7,BRD7 in gastric and colorectal cancer显示文摘AIM: NGX6, NAG-7 and BRD7 genes are tumor related genes, which have been newly cloned by positional candidate cloning strategy. This study was designed to investigate the expression levels of NGX6, NAG-7 and BRD7 genes in human gastric and colorectal cancer tissues, and their corresponding normal tissues, and to investigate whether these genes play a role in the pathogenesis of gastric and colorectal cancers.METHODS: Reverse transcription-polymerase chain reaction (RT-PCR), dot hybridization and Northern blot analysis were used to compare the expression levels of NGX6, NAG-7 and BRD7 genes in 34 gastric cancer tissues and 34 colorectal cancer tissues with their corresponding normal tissues of the same patients, respectively.RESULTS: Among the 34 colorectal cancer specimens and the 34 gastric cancer specimens, the expression of NGX6 in 25 colorectal cancer tissues was absent or very weak (73.5 %) by RT-PCR analysis. The down-regulation rate of NGX6 in colorectal cancer tissues was significantly higher than that in corresponding normal tissues (26.5 %,9/34)(P<0.005). Moreover, the down-regulation of NGX6 was significantly correlated with lymph node and/or distance metastases. Patients with lymph node and/or distance metastasis had much higher down-regulation rate of NGX6 than patients without metastases (93.8 % vs 55.6 %, P<0.05).However no correlation was found between the expression of NGX6 and pathologic type of colorectal cancer in this study, and also the expression of NGX6 did not display any difference between gastric cancer and corresponding normal tissues (58.8 % vs 70.6 %, P>0.25). Dot hybridization and Northern blot analysis confirmed the results of RT-PCR.Furthermore, NAG-7 and BRD7 mRNA was not up- or downregulated in gastric and colorectal cancers compared with their corresponding normal tissues in our study.CONCLUSION: The down-regulation of NGX6 may be closely associated with tumorigenesis and metastasis of colorectal carcinoma. However, it may not contribute to the development and progression of gastric carcinoma. In addition, the expression levels of NAG-7, and BRD7 did not alter in gastric and colorectal cancers. This seems to suggest that NAG-7and BRD7 genes may not play a role in gastric and colorectal carcinogenesis. | Xiao-MeiZhang Shou-RongSheng Xiao-YanWang Jie-RuWang JiangLi | 2003 | World Journal of Gastroenterology2003，9，8： | 10 |
| 14 | Expression of TFF2 and Helicobacter pylori infection in carcinogenesis of gastric mucosa显示文摘AIM: To investigate the expression of TFF2 and Helicobacter pyloriinfection in carcinogenesis of gastric mucosa.METHODS: The expression of TFF2 was immunohistochemically analyzed in paraffin-embedded samples from 119 patients with endoscopic biopsy and subtotal gastrectomy specimens of gastric mucosal lesions, including 16 cases of chronic superficial gastritis (CSG), 20 chronic atrophic gastritis (CAG),35 intestinal metaplasia (IN), 23 gastric epithelial dysplasia (GED) and 25 gastric carcinoma (CA), and Helicobacter pylori infection was detected by Warthin-Starry staining.RESULTS: 1:TFF2 was located in the cytoplasm of gastrk mucous neck cell. The expression of TFF2 was 100 %,100 %, 0, 56.5 % and 0 in CSGs, CAGs, INs, GEDs and CAs, respectively. 2: The value of TFF2 positive cell density in CSG with Helicobacter pyloriinfection was higher than that without Helicobacter pyloriinfection. (52.89±7.27vs46.49±13.04, P>0.05); But the value of TFF2 positive cell density in CAG and GED with Helicobacter pyloriinfection was significantly lower than that without Helicobacter pylori infection (18.17±4.09 vs 37.93±13.80, P<0.01 and 14.44±9.32 vs 24.84±10.22, P<0.05).CONCLUSION: Increase of TFF2 expression in CSG is perhaps associated with the protective mechanism after gastric mucosal injury. Decrease of TFF2 expression in CAG possibly attributes to the decrease in the number of gastric gland cell expressing TFF2. Re-expression of TFF2 in gastric epithelial dysplasia implies that TFF2 possibly contributes to the initiation of gastric carcinoma. The effect of Helicobacter pylori on the expression of TFF2 depends on the status of gastric mucosa. | Guo-Yong Hu Bao-Ping Yu Wei-Guo Dong Mu-Qi Li Jie-Ping Yu He-Sheng Luo Zong-Xue Rang Gastroenterology Department,Renmin Hospital of Wuhan University,Wuhan 430060,Hubei Province,China | 2003 | World Journal of Gastroenterology2003，9，5： | 10 |
| 15 | p16蛋白和VEGF在乳腺癌组织中的表达及相关性研究显示文摘目的 探讨 p16蛋白、VEGF在乳腺癌组织中的表达及其相关性。 方法 采用SABC免疫组化技术 ,检测 5 3例乳腺癌标本中p16蛋白及VEGF的表达。结果 p16蛋白、VEGF的阳性表达率分别为5 4 .7%和 79.2 5 % ,其表达均与患者的年龄、肿瘤大小、绝经状况、ER、PR的表达无关 (P >0 .0 5 ) ,p16蛋白的表达与乳腺癌的组织学分级、TNM分期及淋巴结转移呈负相关 (P <0 .0 5 ) ;VEGF的表达则与组织学分级及淋巴结转移密切相关 (P <0 .0 5 )。结论 p16蛋白与VEGF在乳腺癌中的表达具有相关性 ,两者在乳腺癌的发生、发展中可能起协同作用 ,并可作为判断乳腺癌生物学行为的有用指标。 | 曾谷清 周秀田 程爱兰 邹飞燕 谷依学 高天舒 | 2004 | 肿瘤防治研究2004，31，5： | 10 |
| 16 | 乳腺癌组织p16蛋白和VEGF的表达及其临床意义显示文摘目的 探讨乳腺癌组织中p16蛋白、VEGF的表达与乳腺癌临床病理指标及预后的关系。方法 采用SABC免疫组织化学技术 ,检测 5 3例乳腺癌标本中p16蛋白及VEGF的表达 ,结合临床病理和随访资料作统计分析。结果 5 3例乳腺癌组织中p16蛋白的阳性表达率为 5 4 7%,其表达与患者的年龄、肿瘤大小、绝经状况、ER、PR的表达无关 (P >0 0 5 ) ,而与乳腺癌的组织学分级、TNM分期、淋巴结转移及 5年生存率相关 (P <0 0 5 ) ;VEGF的阳性表达率为 79 2 5 %,其表达与患者的年龄、肿瘤大小、绝经状况、ER、PR的表达、TNM分期及 5年生存率无显著相关性 (P >0 0 5 ) ,而与组织学分级及淋巴结转移密切相关 (P <0 0 5 )。结论 p16蛋白和VEGF的表达与乳腺癌的浸润、转移密切相关 ,可作为乳腺癌的生物学标记。p16可作为临床上判定乳腺癌预后的一个新指标。 | 曾谷清 王汉群 方松清 谷依学 邹飞燕 高勇强 | 2004 | 中国医师杂志2004，6，2： | 9 |
| 17 | Expression of sphingosine kinase gene in the interactions between human gastric carcinoma cell and vascular endothelial cell显示文摘AIM: To study the interactions between human gastriccarcinoma cell (HGCC) and human vascular endothelialcell (HVEC), and if the expression of sphingosine kinase(SPK) gene was involved in these interactions.METHODS: The specific inhibitor to SPK, dimethylsphingosine (DMS), was added acting on HGCC andHVEC, then the cell proliferation was measured by MTT.The conditioned mediums (CMs) of HGCC and HVECwere prepared. The CM of one kind of cell was added tothe other kind of cell, and the cell proliferation wasmeasured by MTr. After the action of CM, the cellularexpression of SPK gene in mRNA level was detectedwith in situ hybridization(ISH).RESULTS: DMS could almost completely inhibit theproliferation of HGCC and HVEC. The growth inhibitoryrates could amount to 97.21%, 83.42 %, respectively(P<0.01). The CM of HGCC could stimulate the growthof HVEC (2.70±0.0:1, P<0.01) while the CM of HVEC couldinhibit the growth of HGCC (52.97±0.01 %, P<0.01).There was no significant change in the mRNA level ofSPK gene in one kind of cell after the action of the CM ofthe other kind of cell.CONCLUSION: SPK plays a key role in regulating theproliferation of HGCC and HVEC. There exist complicatedinteractions between HGCC and HVEC. HGCC cansignificantly stimulate the growth of HVEC while HVECcan significantly inhibit the growth of HGCC. Theexpression of SPK gene is not involved in the interactions. | Juan Ren Lei Dong Cang-Bao Xu Bo-Rong Pan | 2002 | World Journal of Gastroenterology2002，8，4： | 8 |
| 18 | 复发脑胶质瘤的诊断与治疗进展显示文摘复发脑胶质瘤,是指原发性脑胶质瘤术后以及其他治疗后再次复发,既可单发,也可多发.复发脑胶质瘤的部位大多较局限,约80%左右的复发病灶在其原发灶周围2 cm处[1].脑胶质瘤的复发与手术切除程度、肿瘤的病理分级、术后放化疗等因素有关.脑胶质瘤术后复发率可达50%以上,复发后的胶质瘤恶性程度增加,侵袭力更强[2],其组织学分化的恶性特征也更加明显[3],成为加速患者死亡的主要危险因素[4].随着影像学诊断技术的提高,显微技术、神经导航等神经外科技术的普及,间质内放化疗等新技术、新疗法手段的应用,使复发脑胶质瘤的诊断与治疗取得显著进步.关键词:脑肿瘤;外科手术;放射疗法分类号:R739.41 | 吕冬芳 武江 岳向勇 | 2013 | 临床误诊误治2013，26，11： | 8 |
| 19 | CD44v6和P16表达与非小细胞肺癌生物学行为关系显示文摘目的探讨非小细胞肺癌组织细胞黏附分子CD44v6和新型抑癌基因p16的表达及其与肿瘤生物学行为的关系。方法应用免疫组织化学方法对72例非小细胞肺癌组织进行CD44v6和P16蛋白检测。结果CD44v6阳性染色定位于肺癌细胞的细胞质,阳性表达率为68.05%,其表达强度与非小细胞肺癌的组织学分级、淋巴结转移及临床分期显著相关(χ2=9.90~16.86,P均<0.01),鳞癌的CD44v6的表达率与腺癌比较差异有显著性(χ2=7.27,P<0.05)。P16阳性染色定位于肺癌细胞的细胞核,阳性表达率为41.67%,其表达强度与非小细胞肺癌的组织学分级、临床分期、淋巴结转移及原发癌大小相关(χ2=11.53~17.82,P均<0.05),与病理类型无关(χ2=3.40,P>0.05)。CD44v6和P16的表达强度与病人的年龄、性别均无关(P均>0.05)。非小细胞肺癌组织中CD44v6和P16的表达强度呈显著负相关(r=-0.42,P<0.01)。结论CD44v6和P16在非小细胞肺癌的发生发展过程中有一定的作用,联合检测CD44v6和P16可作为判定非小细胞肺癌恶性程度及评估其侵袭性、转移性的重要方法。 | 张菡菡 祝博 孔丽君 | 2009 | 齐鲁医学杂志2009，24，5： | 8 |
| 20 | Effect of ZNRD1 gene antisense RNA on drug resistant gastric cancer cells显示文摘AIM: To investigate the expression level of ZNRD1 gene in gastric cancer cells SGC7901 and gastric cancer MDR (multidrug resistant) cells SGC7901/VCR, and to observe the drug sensitizing and proliferation effect of ZNRD1 antisense nucleic acid transduction on SGC7901/VCR cells.METHODS: Amplification of sequences encoding ZNRD1 from SGC7901/VCR cDNA by PCR. The levels of ZNRD1 mRNA expression were demonstrated using semiquantitative reverse transcription polymerase chain reaction (RT-PCR).Eukaryotic expression vector pcDNA3.1-anti ZNRD1 was constructed and transfected into SGC7901/VCR cells by lipofectamine. Immunochemical method was used to detect the expression of protein in SGC7901/VCR cells and transfectants. The cell cycle alteration and the intracellular adriamycin (ADM) accumulation were observed by FACS.Growth curve and drug sensitization of cells for vincristine (VCR) were analyzed with MTT assay.RESULTS: We cloned the open reading frame of full-length ZNRD1. The expression of ZNRD1 showed higher in SGC7901/VCR than in SGC7901 cells. The antisense ZNRD1 drug-resistant clones were selected after gene transfection.Immunochemical results showed that the expression level of ZNRD1 protein was lower in anti ZNRD1-SGC7901/VCR cells than that in non-transfectants. Comparing to SGC7901/VCR and pcDNA3.1-SGC7901/VCR, anti ZNRD1-SGC7901/VCR showed gradually accumulated in G1 phase, with aconcomitant decrease of cell population in S phase. FACSalso suggested intracellular ADM accumulation increased2fold in SGC7901/VCR cells after transfected with antisenseZNRD1.MTT assay showed that transfectant cells proliferationwas lagged and more sensitive to vcr than non-transfectants.CONCLUSION: ZNRD1 gene displayed highly expression in VCR resistant gastric cancer cells.Expression of ZNRD1 protein was effectively blockde in anti ZzNRD1-SGC7901/VCR cells by gene transfection.ZNRD1 antisense nucleic acid transfection sensitized drug resistant gastric cancer cells to VCR,increased ADM accumulation and inhibited the cells to VCR,incereased ADM accumulation qand inhibited the cells proliferation.ZNRS1 antisense RNA transduction could reverse the MDR of human drug-resistant gastric cancer cell SGC7901/VCR to a degree. | Yu-Mei Zhang Yan-Qiu Zhao Yang-Lin Pan Yong-Quan Shi Xiao-Hang Jin Hui Yi Dai-Ming Fan Department of Gastroenterology,Xijing Hospital,the Fourth Military Medical University,Xi’an 710033,Shaanxi Province,China | 2003 | World Journal of Gastroenterology2003，9，5： | 7 |
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