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| 1 | KAI1 gene is differently expressed in papillary and pancreatic cancer:influence on metastasis显示文摘AIM To compare KAI1 in cancer of papilla ofVater and pancreas to evaluate whether there aredifferences in biologic behavior which mightaccount for prognosis.METHODS We compared the expression in 24papillay and 29 pancreatic cancers usingNorthern blot analysis,immunochemical assayand in situ hybridization,and investigatedwhether early diagnosis or molecular differencespredict the outcome in these tumor entities.RESULTS By Northern blot analysis there is nostatistical difference of KAI1 levels in normaland cancerous papilla.No association betweenKAI1 mRNA expression and tumor stage or tumordifferentiation was found in the tumors.Byimmunohistochemical assay,KAI1 staining incytoplasm of papillary cancer cells was similarto that of normal papillary cells.By in situhybridization,the results of KAI1 mRNAexpression in normal and cancerous papilla weresimilar to those with immunohistochemicalassay.The normal and cancerous pancreastissues were also analyzed by the methods usedin papillary samples.CONCLUSION Although the biologic roles of KAI1 have not been clarified, our results suggest that KAI1 may restrict the progression of malignant papillary cancer, but its expression might not have any effect on the characteristics of papillary tumor, whereas by the analysis of KAl1 gene, its reduced expression is closely related to the progression and metastases of pancreatic cancer. | Helmut Friess Markus W.Buchler | 2000 | World Journal of Gastroenterology2000，6，6： | 20 |
| 2 | Effect of arsenic trioxide on rat hepatocarcinoma and its renal cytotoxicity显示文摘AIM: To study the effect of arsenic trioxide (As2O3) on rat experimental hepatocarcinoma and its renal cytotoxicity.METHODS: The hepatocarcinoma model was established by diethaylnitrosamine perfusion in stomach of 120 Wistar rats, and the treatment began at the end of 20 weeks.Before the treatment, the rat models were randomly divided into 5 groups. In the treatment groups, three doses of As2O3 were injected into rat abdominal cavity, the total time of drug administration was 4 weeks. Cisplatin control or the blank group was injected into abdominal cavity with equal amount of cisplatin or saline at the same time,respectively. On the 7th, 14th and 28th day after the treatment, the hepatocarcinoma nodules were obtained and the morphologic changes of hepatocarcinoma cells were observed under light and electron microscopes;Immunohistochemistry (S-P methods) was employed to detect the expression of bcl-2, bax and PCNA in hepatocarcinoma tissues; flow cytometry (TUNEL assay)was used to detect the apoptosis of liver cancer cells and the change of cytokinetics. On the 28th day, the kidneys were obtained and their histologic changes were observed under light microscope, and immunohistochemistry (SP stain) was also employed to detect the expression of bcl-2and PCNA. Cisplatin and saline solution were used as the control.RESULTS: As2O3 could induce the apoptosis of rat liver cancer cells and exhibited typical morphologic changes.The incidence of apoptosis of hapatocarcinoma cells was elevated (P=0.001). The elevation was the most higher in the group of middle-dose of As2O3 (1 mg.kg-1), significantly higher than that of the other arsenic groups and the controls (P=0.001). Large dose of As2O3 (5 mg.kg-1) was able to arise the incidence of apoptosis, but also produced a large amount of necrosis and inflammatory reaction. Middle dose of As2O3 dramatically increased the cell number in G2/M phase (P=0.0001), and apoptosis happened apparently.The expression of bcl-2 and bax was related to the dose of As2O3. With the up-regulation of apoptotic incidence, the ratio of bcl-2/bak decreased. But the incidence of apoptosis was not the highest status and the ratio of bcl-2/bax was at the lowest when the highest-dose of As2O3 was used.There was significant difference among the PCNA indexes (PCNA L1) of the five groups. Of them, three arsenic groups all showed decrease of different degrees, and this downregulation was most obvious in group A. There was significant difference among the three groups (P=0.016).Under the light microscope, the rat kidney in the cisplatin group exhibited tubular epithelium swelling and degeneration, protein casts in collecting tubules; While all arsenic groups didn't show the significant changes (P=0.013).In the arsenic groups, the expression of bcl-2 in the renal tubular epithelium was increased (P=0.005), no obvious changes happened to PCNA L1. But in the group of cisplatin,the PCNA L1 increased significantly (P=0.001).CONCLUSION: AS2O3 can induce apoptosis of rat hepatocellular carcinoma cells. And there is optimum dose;too high dose will induce the cytotoxic effect, while certain dose of As2O3 is able to block the cell cycle at G2/M phase.As2O3 had the most remarkable influence on G2/M cells,and it can also induce apoptosis to cells at other phases.As2O3 can restrain the proliferation of rat hepatocellular carcinoma cells, in a dose-time dependent manner.Compared with cisplatin, As2O3 didn't show obvious renal toxicity, which was related to the increasing expression of bcl-2 in renal tubular epithelium, the inhibition of apoptosis and the anti-oxidation effects. | Shao-Shan Wang Ti Zhang Xi-Lu Wang Li Hong Department of Surgery of Dagang Hospital 300270,Tianjin,China Qing-Hui Qi Department of Chinese and Western Integral Surgery of Master Hospital of Tianjin Medical University 300052,Tianjin,China | 2003 | World Journal of Gastroenterology2003，9，5： | 17 |
| 3 | Methylation status of c-fms oncogene in HCC and its relationship with clinical pathology显示文摘INTRODUCTIONThe mechanism that DNA hypomethylation leads toactivation of oncogene and occurrence of malignantneoplasm is being increasingly recognized byresearchers. Normal DNA methylation playsimportant role in stabilizing the phenotype of cell.DNA methylation status reduction and/or patternalteration are related to activation and abnormallyhigh expression of some oncogenes and cellularmalignancy[1-6]. c-fms oncogene encodes for colonystimulating factor 1 receptor (CSF-1R)[7], c-fms/CSF-1R was highly expressed in hepatocellularcarcinoma (HCC) tissue, but the mechanismremained obscure[8,9]. | Jun Cui Dong Hua Yang Xiang Jun Bi Zi Rong Fan Department of Gastroenterology, Zhujiang Hospital, The First Military Medical University, Guangzhou 510282, Guangdong Province, China | 2001 | World Journal of Gastroenterology2001，7，1： | 16 |
| 4 | p73β inhibits transcriptional activities of enhancer I and X promoter in hepatitis B virus more efficiently than p73α显示文摘AIM: p73, as a novel member of a family of p53-related transcription factors, shares redundant functions with p53, such as the abilities of inducing apoptosis and suppressing growth. It is well known that p53 can repress HBV expression and transcription efficiently. The aim of this paper is to investigate the transcriptional effect of p73α and p73β on hepatitis B virus (HBV) and to understand the correlation between HBV and p73.METHODS: To construct an x-gene inactivated HBV plasmid which was cotransfected with p73α or p73β expression vectors into HepG2 cells. After transiently transfecticn, HBV surface antigen (HBsAg) and HBV e antigen (HBeAg) were detected by ELISA. Viral transcripts synthesized by HBV were evaluated by Northern blotting analysis. The activities of HBV regulatory elements, including enhancer Ⅰ/X promoter (ENI/Xp) and enhancer Ⅱ/core promoter (ENⅡ/Cp) were monitored by luciferase assays.RESULTS: Both p73α and p73β could repress HBsAg and HBeAg expression by downregulating the ENⅠ/Xp and ENⅡ/Cp activities. But p73β exerted stronger inhibition on the activity of ENI/Xp than p73α, resulting in much lower level of viral transcripts and the antigens expression.CONCLUSION: p73β as a novel member of p53 family can efficiently inhibit HBV transcription mainly through downregulating the activities of the HBV ENI/Xp regulatory elements. | Tsai-Ping Li | 2002 | World Journal of Gastroenterology2002，8，6： | 14 |
| 5 | 腺病毒介导的p16和顺铂的联合应用对胆管癌细胞系QBC939的生长抑制作用显示文摘目的研究 p16基因和顺铂联合应用对胆管癌细胞的作用.方法将重组体腺病毒 p16(Ad-p16)和顺铂联合作用于人胆管癌细胞 QBC939,对 p16基因的表达、细胞的生长抑制及机制进行分析.结果用 Ad-LacZ 进行重组体腺病毒转导效率的检测,发现当MOI 为100以上时,重组体腺病毒可使90%以上的培养的人胆管癌 QBC939细胞被转导.用 RT-PCR 方法检测,在胆管癌QBC939细胞系中 p16呈低表达.重组体腺病毒能介导外源基因 p16在胆管癌 QBC939细胞系中高效表达,重组体腺病毒介导的 p16在 QBC939细胞中表达,能抑制 QBC939细胞的生长和集落形成.其与顺铂联合应用对 QBC939细胞的生长抑制具有明显作用.并显著地抑制该肿瘤细胞的克隆形成能力.流式细胞计数证实 p16能诱导 PBC939细胞发生凋亡并导致其发生 G_1期阻滞,顺铂能诱导 QBC939细胞发生凋亡并导致细胞发生明显的 G_2期阻滞.结论 p16基因能够增加 QBC939细胞对顺铂的敏感性. | 鲁建国 林晨 黄志强 吴金生 付明 张雪艳 梁萧 要秀 吴旻 | 2000 | 世界华人消化杂志2000，8，6： | 12 |
| 6 | 腺病毒载体介导四环素调控的DT/VEGF体系的基因治疗显示文摘目的研究重组腺病毒在四环素调控下传递 DT_(390)-VEGF_(165)及DT_(390)-VEGF_(exon7)融合基因治疗肝癌的可行性.方法构建4种四环素 tet-off 调控的 DT_(39)-VEGF_(165)或 DT_(390)-VEGF_(exon7)融合基因重组腺病毒载体,用脂质体介导包装出4种重组腺病毒,分别感染肝细胞癌 HepG2细胞,在没有四环素的情况下观察肝癌细胞的形态变化,用2种粗制重组腺病毒治疗荷肝癌裸鼠,用免疫组化鉴定融合基因的表达.结果在培养液中加入 3mg·L^(-1)的四环素可包装出携带毒素融合基因的重组腺病毒,用噬斑分析法测定重组腺病毒滴度均为1×10^(10)pfu·L^(-1);粗制重组腺病毒感染 HepG2细胞8h 后换以无四环素的正常培养液,发现72h 后 HepG2细胞发生病变,细胞死亡率达95%;感染细胞经白喉抗毒素-FITC 免疫荧光抗体染色均呈现黄绿色荧光;用粗制重组腺病毒AdCA13-tTA-TRE-DT_(390)-VEGF_(165)和 AdCA13-tTA-VEGF_(165)-DT_(390)-TRE 注射肝癌瘤体可观察到瘤体生长明显得到抑制,AFP 值显著下调,免疫组化结果显示融合基因在瘤体内得到了表达.结论重组腺病毒可以提高转基因效率. | 潘欣 潘卫 柯重伟 张斌 曹广文 戚中田 | 2000 | 世界华人消化杂志2000，8，10： | 11 |
| 7 | Biological characteristics of HCC by ultrasound-guided aspiration biopsy and its clinical application显示文摘AIM: To probe the pathological biological characteristics of hepatocellular carcinoma (HCC) by the ultrasound-guided aspiration biopsy and assess the clinical application value of this method.METHODS: The biopsy and DNA analysis by flow cytometry (FCM) were taken in 46 cases with HCC nodules, including 26 cases and 20 cases with nodules ≤3 cm and >3 cm in diameters respectively, and 12 cases with intrahepatic benign hyperplastic nodules. They were taken in 22 cases of 46cases with HCC before and after the therapy. Fine-needles and automatic histological incised biopsy needles were used.The fresh biopsy tissue was produced into the single cell suspension, which was sent for DNA detection and ratio analysis of cell period. The ratio of each DNA period of cell proliferation of each group was calculated and compared with each other. The DNA aneuploid (AN) and apoptosis cell peak were observed and their percentages were calculated.RESULTS: The ratios of S and G2/M periods of DNA, which reflect cell hyperproliferation, in the group with HCC tumors >3 cm in diameter were markedly higher than those of the group with HCC nodules ≤3 cm in diameter and the group with the benign hyperplastic nodules (P<0.01 except A:B of S period, P<0.05). The ratios of the middle group were also apparently higher than those of the latter group (P<0.01).The ratio of DNA AN of 46 cases with HCC nodules was 34.8 % (16/46). None of the cases with the intrahepatic hyperplastic nodules appeared AN. The DNA AN appeared more apparently with the growth of the tumors. The AN ratio of the group with tumors >3 cm in diameter was 55 %(11/20), markedly higher than that of the group with tumors ≤3 cm in diameter which was 19.2 % (5/26) (P<0.01). The FCM DNA analysis of 22 specimens of hepatic carcinoma tissue before therapy showed that the aneuploid peaks appeared in 5 cases (22.7 %). The ratio of G1 period rose after therapy while the S period and G2/M ratios fell (P<0.01).The aneuploid peak disappeared in the 5 cases after the therapy, while the apoptosis peaks in 12 cases (54.5 %)appeared.CONCLUSION: Addition to supply the information of the pathological morphology of the tumor, the ultrasound-guided fine-needle aspiration tissue could be sent for FCM DNA analysis to comprehend its pathological biological characteristics. This can not only provide the clinic the reliable information about the occurrence, development,diagnosis, curative effect and prognosis of tumors but also supply biological information for clinic to choose therapeutic schemes. | Li-Wu Lin Xue-Ying Lin Yi-Mi He Shang-Da Gao Xiao-Dong Lin Fujian Provincial Ultrasonic Medicine Institute,Ultrasound Department,Union Hospital of Fujian Medical University,Fuzhou 350001,Fujian Province,China | 2003 | World Journal of Gastroenterology2003，9，5： | 7 |
| 8 | 肝移植体保存—再灌注损伤的研究现状显示文摘植体的保存是肝脏移植的三大支柱之一,获取高质量的供肝是保证肝移植成功的先决条件.近10 a来,国内外学者对于肝脏的保存损伤机制及方法进行了大量的研究,使肝保存的安全时限有了很大的提高.本文就肝移植体保存一再灌注损伤机制及研究现状作一综述. | 赵子粼 张云生 俞金龙 高毅 | 2001 | 世界华人消化杂志2001，9，1： | 5 |
| 9 | 肝细胞癌热休克蛋白27,70,90_α的表达意义显示文摘目的探讨HSP27,HSP70和HSP90α在肝细胞癌(HCC)中的表达及其意义.方法采用免疫组化技术对44例HCC和癌旁组织中HSP27,HSP70和HSP90α的表达进行检测结果 HCC和癌旁组织中HSP27阳性率分别为18%和30%,HSP70阳性率分别为68%和27%,HSP90α阳性率分别为63%,和23%.HCC中HSP70和HSP90α阳性率明显高于癌旁组织(x_1~2=7.3,x_2~2=7.8,P<0.01.而HSP27阳性率变化不大(X^2=1.6,P>0.05).HSP70和HSP90α在分化较好和分化不良的HCC中的阳性率分别为54%,85%和50%,80%,两者相比差异显著(X_1~2=4.5,X_2~2=4.2,P<0.05),但与癌周淋巴细胞浸润(X_1~2=3.2,X_2~2=1.4,P>0.05)和转移(X_1~2=2.3,X_2~2=2. 7,P>0.05)无关结论 HCC是HSP70和HSP90α高表达肿瘤.HSP70和HSP90α与HCC分化有关,在HCC发生和发展中起重要作用. | 蒋业贵 王宇明 李奇芬 | 2001 | 世界华人消化杂志2001，9，7： | 5 |
| 10 | 不同载体表达核酶对HBV mRNA细胞内表达的阻断作用显示文摘目的:探讨多位点自剪切核酶及突变核酶对细胞内HBVmRNA的切割作用.方法:构建5个不同的多位点核酶及突变核酶的真核表达载体,将他们分别与乙型肝炎病毒全基因序列共转染HepG2细胞,用ELISA,共聚焦定量及图像分析的方法观察多位点核酶在细胞内对HBVmRNA切割作用.结果:构建的真核表达载体在细胞内确可表达出多位点核酶,核酶及突变核酶在细胞内对HBV基因的表达均有抑制作用,不同表达载体的抑制率不同,以tRNA启动子的表达载体抑制效率最高,达81%,突变核酶亦有部分反义RNA的抑制效果.结论:抗乙型肝炎病毒核酶在细胞内可抑制HBV基因的表达,不同表达载体其核酶的表达效率不同. | 李谨革 连建奇 贾战生 冯志华 聂青和 王九平 黄长形 白雪帆 | 2003 | 世界华人消化杂志2003，11，2： | 3 |
| 11 | 抗乙型肝炎病毒核酶的研究进展显示文摘全世界大约有3.5亿乙型肝炎病毒(HBV)携带者,这种感染者集中分布于包括我国在内的东南亚、东亚及非洲的撒哈拉地区.HBV的持续存在常可导致肝硬化以及肝癌,对于已感染HBV者,目前常用的化学及免疫疗法通常无效.因此,寻找新的抗HBV感染的手段成为热点.核酶做为一种成熟的、可剪切特异性RNA的分子生物学方法受到广泛重视.由于核酶有严格的序列特异性,长期使用对细胞无副作用,并且结构简单,可人工设计,因此,很有希望成为治疗HBV感染的新方法.目前,核酶已广泛用于抗病毒及抗肿瘤的研究,尤其对HIV的研究,已进入临床工作阶段.本文将从核酶的构成、核酶研究的热点以及抗HBV感染等方面进行阐述. | 李谨革 聂青和 黄长形 | 2003 | 世界华人消化杂志2003，11，2： | 1 |
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