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| 1 | β-catenin up-regulates the expression of cyclinD1, c-myc and MMP-7 in human pancreatic cancer: Relationships with carcinogenesis and metastasis显示文摘AIM: To investigate whether abnormal expression of β catenin in conjunction with overexpression of cyclinD1, cmyc and matrix metalloproteinase-7 (MMP-7) correlated with the carcinogenesis, metastasis and prognosis of pancreatic cancer, and to analyze the relationship of βcatenin expression with cyclinD1, c-myc and MMP-7 expression.METHODS: Using immunohistochemistry, we examined the expression of β-catenin, cyclinD1, c-myc and MMP-7 in 47 pancreatic adenocarcinoma tissues, 12 pancreaticintraepithelial neoplasia (PanIN) and 10 normal pancreases, respectively. Proliferation cell nuclear antigen was also tested as the index of proliferative activity of pancreatic cancer cells.RESULTS: In 10 cases of normal pancreatic tissues, epithelial cells showed equally strong membranous expression of β-catenin protein at the cell-cell boundaries, but the expression of cyclinD1, c-myc and MMP-7 was negative. The expression of β-catenin, cyclinD1, c-myc and MMP-7 in PanIN and pancreatic adenocarcinoma tissues had no significant difference [6/12 and 32/47 (68.1%), 6/12 and 35/47 (74.5%), 5/12 and 33/47 (70.2%), 7/12and 30/47 (63.8%), respectively]. The abnormal expression of β-catenin was significantly correlated to metastasis and one-year survival rate of pancreatic cancer, but had no relation with size, differentiation and cell proliferation. The expression of cyclinD1 was correlated with cell proliferation and extent of differentiation, but not with size, metastasis and one-year survival rate of the pancreatic cancer. The expression of c-myc was not correlated withsize, extent of differentiation, metastasis and 1-year survival rate, but closely with cell proliferation of pancreatic cancer. The overexpression of MMP-7 was significantly associated with metastasis and 1-year survival rate ofpancreatic cancer, but not with size, extent of differentiation and cell proliferation. There was a highly significant positive association between abnormal expression of β-cateninand overexpression of cyclinD1, c-myc and MMP-7 not only in PanIN (r = 1.000, 0.845, 0.845), but also in pancreatic cancer (r = 0.437, 0.452, 0.435).CONCLUSION: The abnormal expression of β-catenin plays a key role in the carcinogenesis and progression of human pancreatic carcinoma by up-regulaling the expression of cyclinD1, c-myc and MMP-7, resulting in the degradation of extracellular matrix and uncontrolled cell proliferation and differentiation. β-catenin abnormal expression and MMP-7 overexpression may be considered as two useful markers for determining metastasis and prognosis of human pancreatic cancer. | Yu-JunLi Zhi-MinWei Yun-XiaoMeng Xiang-RuiJi | 2005 | World Journal of Gastroenterology2005，11，14： | 68 |
| 2 | 肝癌发生的分子遗传学和表遗传学研究显示文摘肝细胞癌(简称肝癌)是原发性肝癌的主要类型,也是全世界最高发的恶性肿瘤之一。肝癌最主要的危险性因素是慢性肝炎病毒感染(HBV和HCV)、食物中黄曲霉毒素B1摄入、长期过量饮酒和遗传性肝病肝硬化等。肝癌的发生是遗传和环境因素相互作用的结果,遗传决定了个体遗传易感性,而环境因素决定了什么样的易感个体患癌。肝癌发生的遗传学和表遗传学机制研究结果提示,肝癌发生是一个多基因、多途径的复杂多阶段过程;由遗传学和表遗传学改变引起的原癌基因的活化和抑癌基因的灭活,是肝癌发生的核心生物学过程;在不同病因的肝癌中通常受影响的是RB1途径、p53途径和Wnt途径等,这可能反映了共同的肝癌发生的病理顺序:慢性肝损伤、肝硬化、不典型增生结节和早期癌。在肝炎病毒感染为主的相关肝癌主要是RB1途径的改变,包括p16INK4a和RB1基因的甲基化、细胞周期蛋白D1扩增等;在AFB1暴露相关的肝癌,受影响最明显的是p53途径,p53基因密码子249的G→T颠换突变已成为这类肝癌的遗传学标志;而酒精中毒相关的肝癌更多的改变发生在RB1和p53两种途径。一些与细胞凋亡、DNA修复、药物代谢和转移等相关的重要基因,在肝癌发生中的意义也被评述。 | 薛开先 | 2005 | 癌症2005，24，6： | 17 |
| 3 | Wnt/β-catenin信号通路重要分子及其靶基因在原发性肝癌中的作用机制显示文摘肝癌是我国及某些亚非地区常见的恶性肿瘤之一,死亡率较高。近年来我国肝癌的发生率有上升趋势,因此了解肝癌的发生发展机制及其治疗刻不容缓。但目前对其发生机制仍不清楚。其中细胞信号转导对其发生、发展、转移起着至关重要的作用。 | 周威 熊奇如 | 2013 | 肝胆外科杂志2013，21，2： | 11 |
| 4 | 肝细胞癌组织中β-Catenin的表达与第三外显子突变的关系显示文摘背景与目的:广西南部是肝细胞癌(hepatocellular carcinoma,HCC)高发地区,也是粮食受黄曲霉毒素B1(aflatoxin B1,AFB1)污染较重的地区。β-Catenin的异常表达与多种肿瘤有关,而AFB1是诱发HCC的重要因素。本研究旨在探讨AFB1高暴露地区HCC患者癌组织中β-Catenin基因突变及表达情况。方法:用基因直接测序、RT-PCR、免疫组化和Western blot等方法,检测52例来自广西南部AFB1高暴露地区HCC患者癌、癌旁组织和18例非肝癌肝组织中β-Catenin基因的表达。结果:癌组织中未见β-Catenin基因第三外显子的突变。β-Catenin mRNA在癌、癌旁和正常肝组织中的表达分别为0.42±0.24、0.20±0.16和0.23±0.12,癌组织中的表达显著高于癌旁组织或正常肝组织(P<0.01);免疫组化染色癌组织中阳性率为55.8%(29/52),显著高于癌旁组织[36.5%(19/52)](P<0.05)。β-Catenin蛋白表达与肝外转移、术后复发、门静脉癌栓和临床分期有关(P<0.05),而mRNA的表达与上述临床参数均无明显关系(P>0.05)。结论:β-Catenin在HCC组织中高表达,但其异常表达不是由基因第三外显子上GSK-3β磷酸化位点的突变引起。 | 焦杨 班克臣 曹骥 岳海英 罗元 苏建家 | 2007 | 癌症2007，26，10： | 6 |
| 5 | 成纤维细胞生长因子20研究进展显示文摘成纤维细胞生长因子20(FGF20)是成纤维细胞生长因子家族(FGFs)的成员之一。研究发现,FGF20具有广泛生物学活性,不仅在退行性神经系统疾病,如帕金森病中起着重要作用,还在组织修复,肿瘤发生、器官发育等方面具有重要的生物学功能。尽管作为重组蛋白药物的开发其功能和机制仍有待进一步研究,但FGF20所具备的生物学特性将会有非常广阔的研究领域和应用价值。 | 赵央 田海山 李校堃 姜潮 | 2015 | 中国生物工程杂志2015，35，8： | 4 |
| 6 | hTERT和β-Catenin在胆囊癌细胞系中的表达及其与癌细胞增殖、侵袭关系研究显示文摘目的:检测hTERT和β-Catenin在人胆囊癌细胞系中的表达;初步探讨其与癌细胞增殖、侵袭关系。方法:采用端粒酶TRAP、半定量RT-PCR和Western印迹方法检测3种体外培养人胆囊癌细胞系端粒酶活性、hTERT基因和β-Catenin基因mRNA、蛋白质表达水平。四甲基偶氮唑盐(MTT)光吸收法检测琥珀酸脱氢酶(SDH)活性并做细胞增殖计数、运用Transwell小室和划线了解癌细胞侵袭与运动情况。结果:(1)TGBC1TKB、TGDC2TKB和GB-SD端粒酶活性OD值分别为0.183±0.001、0.257±0.002和0.260±0.002;β-Catenm基因mRNA值分别为44718±567、50279±545和50802±371;hTERT基因值分别为51287±1818、62346±733和63345±1154;后两组均高于第1组(P<0.05)。β-Catenm蛋白质值分别为35289±154、32636±345和32510±346;hTERT蛋白质值分别为34515±454、32562±571和32083±163。后两组均低于第1组(P<0.05),有显著差异。(2)TGBC1TKB、TGBC2TKB和GB-SD琥珀酸脱氢酶活性第5天OD值分别为1.324±0.792、1.573±0.(143和1.647±0.033;24h穿膜细胞数分别为60.667±3.512、113.333±5.508和124.667±6.506;24h过线细胞数分别为23.667±1.155、40.000±1.000和42.667±2.082。后两组均高于第1组(P<0.05),有显著差异。结论:端粒酶、hTERT和β-Catenin基因蛋白在人胆囊癌细胞系呈阳性表达;它们可提示胆囊癌细胞的生物学特性,可能影响胆囊癌细胞的增殖、运动和侵袭力。 | 丁昂 童赛雄 锁涛 | 2005 | 中国临床医学2005，12，3： | 4 |
| 7 | T细胞转录因子-4在大鼠脑缺血再灌注海马齿状回神经干细胞中的表达显示文摘目的:检测T细胞转录因子-4(Tcf-4)在大鼠脑缺血再灌注海马组织神经干细胞中的表达及其变化。探讨影响神经干细胞早期增殖分化的分子调控机制。方法:采用大脑中动脉栓塞(MCAO)制作大鼠脑缺血再灌注模型。用免疫组织化学SP法及RT-PCR法检测海马神经干细胞BrdU、Tcf-4中的表达。结果:随着脑缺血再灌注第3日齿状回神经元BrdU阳性细胞明显增多,第7日达高峰,然后逐渐减少。Tcf-4 mRNA反应产物随脑缺血再灌注时间延长逐渐增多,第21日表达最强,以后表达逐渐减少。结论:Tcf-4时间依赖性表达与神经干细胞增殖分化进程相吻合,说明其在神经干细胞晚期分化中起重要调控作用。 | 邢雪松 张莹 王玉 叶丽萍 孙黎光 | 2008 | 解剖学杂志2008，31，2： | 2 |
| 8 | 黄曲霉毒素B1诱发大鼠肝癌过程中β连环蛋白的变化显示文摘许多研究表明,黄曲霉毒素B1(aflatoxin B1,AFB1)与HCC密切相关,而β连环蛋白是近年肿瘤研究的一个热点,其基因突变和表达异常与HCC等肿瘤密切相关。研究人HCC往往只能对癌及癌旁组织(或加上正常组织)进行比较,无法知道基因在哪个阶段开始出现异常,而且患者往往在发病前接触过很多致癌因素,很难明确是哪些引起β连环蛋白表达量增高。本研究仅用AFB1处理大鼠诱发HCC,于不同时段进行肝活组织检查, | 焦杨 班克臣 曹骥 岳海英 陈茂伟 苏建家 | 2007 | 中华肝脏病杂志2007，15，10： | 2 |
| 9 | Implantation of a drug delivery system during surgery for patients with primary hepatocarcinoma显示文摘BACKGROUND: Postoperative regional chemotherapy is one of the most effective methods to decrease the recurrent rate and improve the prognosis of primary hepatocarcinoma (PHC). This study was undertaken to assess the optimal pathway to implant the drug delivery system (DDS) in the different ways of resecting PHC so as to offer a valuable reference to clinical implantation of the DDS. METHODS: One hundred and ninety cases were divided into two groups according to whether the tumors were resected completely (A) or not (B). Groups A and B were subdivided into three groups a, b and c according to the pathway selected for DDS implantation. The patients in subgroup a received DDS implantation through both the hepatic artery and portal vein (A+P-implanted group), the patients in subgroup b received DDS implantation through the portal vein (P-implanted group), and the patients in subgroup c received DDS implantation through the hepatic artery (A-implanted group). RESULTS: The 1- and 3-year recurrent rates of subgroup c in group A were higher than those of subgroup b, and there was no significant difference between subgroups a and b. Compared with subgroups a and c, the 1- and 3-year survival rates of subgroup b were similar to those of group a but higher than those of group c. The 1- and 3-year survival rates between subgroups a and b in group B were significantly different. The prognosis of subgroup c was lower than that of subgroup a and no significant difference was observed between subgroups b and c. CONCLUSIONS: The DDS should be implanted into the portal vein when PHC is resected completely. It may be better to implant it into both portal vein and hepatic artery if the tumor cannot be completely resected. | Wan-Ping Chen, Xin He, Qi-Fa Ye and Ke Li Institute of Organ Transplantation, Third Xiangya Hospital, Xiangya Medical College, Central South University, Changsha 410013, China, and Institute of Clinical Pharmacology, Xiangya Medical College, Central South University, Changsha 410078, China | 2006 | Hepatobiliary & Pancreatic Diseases International2006，5，3： | 2 |
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