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| 1 | The prognostic molecular markers in hepatocellular carcinoma显示文摘The prognosis of hepatocellular carcinoma (HCC) stillremains dismal, although many advances in its clinicalstudy have been made. It is important for tumor control toidentity the factors that predispose patients to death. Withnew discoveries in cancer biology, the pathological andbiological prognostic factors of HCC have been studied quiteextensively. Analyzing molecular markers (biomarkers) withprognostic significance is a complementary method. A largenumber of molecular factors have been shown to associatewith the invasiveness of HCC, and have potential prognosticsignificance. One important aspect is the analysis ofmolecular markers for the cellular malignancy phenotypeThese include alterations in DNA ploidy, cellularproliferation markers (PCNA, Ki-67, Mcm2, MIB1, MIA, andCSE1L/CAS protein), nuclear morphology, the p53 geneand its related molecule MDM2, other cell cycle regulators(cyclin A, cyclin D, cyclin E, cdc2, p27, p73), oncogenesand their receptors (such as ras, c-myc, c-fms, HGF, c-met, and erb-B receptor family members ), apoptosisrelated factors (Fas and FasL), as well as telomeraseactivity. Another important aspect is the analysis ofmolecular markers involved in the process of cancerinvasion and metastasis. Adhesion molecules (E-cadherin,catenins, serum intercellular adhesion molecule-1, CD44variants), proteinases involved in the clegradation ofextracellular matrix (MMP-2, MMP-9, uPA, uPAR, PAl), aswell as other molecules have been regarded as biomarkersfor the malignant phenotype of HCC, and are related toprognosis and therapeutic outcomes. Tumor angiogenesisis critical to both the growth and metastasis of cancersincluding HCC, and has drawn much attention in recentyears. Many angiogenesis-related markers, such as vascularendothelial growth factor (VEGF), basic fibroblast growthfactor (bFGF), platelet-derived endothelial cell growth factor( PD-ECGF ), thrombospondin ( TSP ), angiogenin,pleiotrophin, and endostatin (ES) levels, as well asinratumor microvessel density (MVD) have been evaluatedand found to be of prognostic significance. Body fluid(particularly blood and urinary) testing for biomarkers iseasily accessible and useful in clinical patients. Theprognostic significance of circulating DNA in plasma orserum, and its genetic alterations in HCC are otherimportant trends. More attention should be paid to thesetwo areas in future. As the progress of the human genomeproject advances, so does a clearer understanding of tumorbiology, and more and more new prognostic markers withhigh sensitivity and specificity will be found and used inclinical assays. However, the combination of some items, i.e., the pathological features and some biomarkersmentioned above, seems to be more practical for now. | Lun-Xiu Qin Zhao-You Tang,Liver Cancer Institute and Zhongshan Hospital,Fudan University,Shanghai,China | 2002 | World Journal of Gastroenterology2002，8，3： | 162 |
| 2 | 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 |
| 3 | MDM2、P53与P14ARF在结肠肿瘤中的表达及意义显示文摘目的:探讨MDM2、P53和P14ARF在人结肠癌组织中的表达及其意义。 方法:用免疫组织化学方法检测36例癌旁正常结肠组织,28例结肠腺瘤及42例结肠癌中三者的表达及其相互关系。 结果:MDM2、P53、P14ARF在癌旁正常结肠组织,结肠腺瘤,结肠癌中的阳性表达率分别为0,0,21.4%;0.25%,67%和100%,82.1%,80.9%。P53和MDM2在结肠癌中的表达率均明显高于癌旁正常结肠组织(P<0.05),P14ARF在结肠腺瘤和结肠癌中的表达率均明显低于癌旁正常结肠组织(P<0.05)。P53、MDM2和P14ARF在不同分化程度结肠癌中的表达率分别为44.4%,68.0%,87.5%;11.1%,24.0%,25.0%和88.9%、92%、37.5%。P53和MDM2在不同分化程度结肠癌中的表达无明显差异(P>0.05),而P14ARF在低分化结肠癌中的表达明显低于高分化和中等分化的结肠癌(P<0.05)。三者的相关分析提示P53和MDM2之间存在正相关(r=0.8805),P53和P14ARF之间为负相关(r=-0.8169),MDM2和P14ARF之间亦存在负相关,但相关不显著(r=-0.5475)。 结论:P53、MDM2和P14ARF在人结肠癌中的表达异常可能与结肠癌的发生发展有关,联合检测三者的表达可作为早期诊断结肠癌的重要指标。 | 郭洁 沈志祥 谭诗云 罗和生 李海霞 冯志强 杨军 | 2002 | 世界华人消化杂志2002，10，5： | 13 |
| 4 | Distribution of nitric oxide synthase in stomach myenteric plexus of rats显示文摘AIM: To study the distribution of nitric oxide synthase (NOS) in rat stomach myenteric plexus.METHODS: The distribution of NOS in gastric wall was studied in quantity and location by the NADPH-diaphorase (NDP) histochemical staining method and whole mount preparation technique.RESULTS: NOS was distributed in whole stomach wall, most of them were located in myenteric plexus, and distributed in submucosal plexus. The shape of NOS positive neurons was basically similar, most of them being round and oval in shape. But their density, size and staining intensity varied greatly in the different parts of stomach. The density was 62 -± 38 cells/mm2(antrum), 43 ± 32 cells/mm2(body), and 32 ± 28 cells/mm2 (fundus), respectively. The size and staining intensity of NOS positive neurons in the fundus were basically the same, the neurons being large and dark stained, while they were obviously different in antrum. In the body of the stomach, the NOS positive neurons were in an intermediate state from fundus to antrum. There were some beadlike structures which were strung together by NOS positive varicosities in nerve fibers, some were closely adherent to the outer walls of blood vessels.CONCLUSION: Nitric oxide might he involved in the modulation of motility, secretion and blood ciroulation of the stomach, and the significant difference of NOS positive neurons in different parts of stomach myenteric plexus may be related to the physiologic function of stomach. | Xi Peng Jin-Bin Feng Hong Yan Yun Zhao Shi-Liang Wang Institute of Burn Research,Southwest Hospital,Third Military Medical University,Chongqing 400038,China | 2001 | World Journal of Gastroenterology2001，7，6： | 11 |
| 5 | CpG岛甲基化与胃肠道肿瘤显示文摘基因和表遗传性改变是恶性肿瘤发生的主要机制.表遗传性修饰-DNA甲基化在胃肠道恶性肿瘤的发生、发展中起重要作用.细胞周期、DNA修复、血管生成和凋亡等都涉及到相关基因的CpG岛甲基化.CpG岛甲基化导致基因失活的分子机制包括DNA甲基转移酶(DNMTs)、CpG甲基化结合蛋白(MBDs)以及组蛋白去乙酰化酶(HDACs)等相关蛋白.MBD可直接抑制转录,并与HDAC形成复合体.DNMT催化甲基化生成,并与HDAC协同作用导致基因转录失活.与衰老相关的甲基化可影响众多基因CpG岛,是老年人恶性肿瘤发生的主要危险因素;甲基化的另一种方式CpG岛甲基化表型(CIMP)具有肿瘤独特性,P16、hMLH1、E-cadherin等重要肿瘤抑制基因失活与此有关.DNA甲基化的相关深入研究将对揭示包括消化道等恶性肿瘤的发生机制以及未来临床诊断和治疗展示了广阔前景. | 周永宁 徐采朴 房殿春 | 2003 | 世界华人消化杂志2003，11，1： | 10 |
| 6 | Influence of methionine/valine-depleted enteral nutrition on nucleic acid and protein metabolism in tumor-bearing rats显示文摘AIM: To investigate the effects of methionine/valine-depleted enteral nutrition (EN) on RNA, DNA and protein metabolism in tumor-bearing (TB) rats.METHODS: Sprague-Dawlley (SD) rats underwent jejunostomy for nutritional support. A suspension of Walker256 carcinosarcoma cells was subcutaneously inoculated.48 TB rats were randomly divided in 4 groups: A, B, C and D. The TB rats had respectively received jejunal feedings supplemented with balanced amino acids, methioninedepleted, balanced amino acids and valine-depleted for 6days before injection of 740 KBq 3H- methionine/valine via jejunum. The 3H incorporation rate of the radioactivity into RNA, DNA and proteins in tumor tissues at 0.5, 1, 2, 4 h postinjection of tracers was assessed with liquid scintillation counter.RESULTS: Incorporation of 3H into proteins in groups B and D was (0.500±0.020) % to (3.670±0.110) % and (0.708±0.019) % to (3.813±0.076) % respectively, lower than in groups A [(0.659±0.055) % to (4.492±0.108) %]and C r(0.805±0.098) % to (4.180±0.018) %]. Incorporation of 3H into RNA, DNA in group B was (0.237±0.075) %and (0.231±0.052) % respectively, lower than in group A (P<0.01). There was no significant difference in uptake of 3H by RNA and DNA between group C and D (P>0.05).CONCLUSION: Protein synthesis was inhibited by methionine/valine starvation in TB rats and nucleic acid synthesis was reduced after methionine depletion, thus resulting in suppression of tumor growth. | Yin-Cheng He Jun Cao Ji-Wei Chen Ding-Yu Pan Ya-Kui Zhou Department of general surgery,Zhongnan Hospital,Wuhan University,Wuhan 430071,China | 2003 | World Journal of Gastroenterology2003，9，4： | 10 |
| 7 | Expression of liver cancer associated gene HCCA3显示文摘AIM: To study and clone a novel liver cancer reisted gene,and to explore the molecular basis of liver cancer genesis.METHODS: Using mRNA differential display polymerasechain reaction (DDPCR), we investigated the difference of mRNA in human hepatocellular carcinoma (HCC) and paired surrounding liver tissues, and got a gene probe. By screening a human placenta cDNA library and genomic homologous extend, we obtained a full-length cDNA named HCCA3. We analyzed the expression of this novel gene in 42pairs of HCC and the surrounding liver tissues, and distribution in human normal tissues by means of Northern blot assay.RESULTS: A full-length cDNA of liver cancer associated gene HCCA3 has been submitted to the GeneBank nucleotide sequence databases ( Accession No. AF276707 ). The positive expression rate of this gene was 78.6% (33/42) in HCC tissues, and the clinical pathological data showed that the HCCA3 was closely associated with the invasion of tumor capsule ( P = 0.023) and adjacant small metastasis satellite nodules lesions ( P= 0.041). The HCCA3 was widely distributed in the human normal tissues, which was intensively expressed in lungs, brain and colon tissues,while lowly expressed in the liver tissues.CONCLUSION: A novel full-length cDNA was cloned and differentiated, which was highly expressed in liver cancer tissues. The high expression was closely related to the tumor invasiveness and metastasis, that may be the late heredited change in HCC genesis. | Zheng-Xu Wang~1 Gui-Fang Hu~1 Hong-Yang Wang~2 Meng-Chao Wu~2 1 Department of General Surgery,Chinese PEA General Hospital of Lanzhou Military Command,Lanzhou 730050,Gansu Province,China2 Eastern Hepatobilliary Surgical Hospital,Second Military Medical University,Shanghai 200438,China | 2001 | World Journal of Gastroenterology2001，7，6： | 9 |
| 8 | Clinical application of serial operations with preserving spleen显示文摘AIM: To evaluate the clinical application of serial operations with preservation of spleen.METHODS: Serial operations with preserving spleen were performed on 211 cases in our hospital from 1980 to 2000.The patient's age ranged from 13 to 56 years, averaging 3years. Diseases included splenic injury in 171 cases, portal hypertension in 9 cases, splenic cyst in 10 cases, and the lesion of pancreatic body and tail in 21 cases.RESULTS: All the cases were cured, and 129 patients were followedup from 3 months to 3 years with the leukocyte phagocytosis test, detection of immunoglubin, CT, 99mTc scanning and ultrasonogrsphy. The results were satisfactory.CONCLUSION: The operations with preserving spleen were safe, feasible, and worth of clinical application. | Hong-Chi Jiang~1 Bei Sun~1 Hai-Quan Qiao~1 Jun Xu~1 Da-Xun Piao~1 Hang Yin~2 1 Department of General Surgery,First Clinical Hospital,Harbin Medical University,Harbin 150001,China2 Department of General Surgery,Heilongjiang Provincial Hospital,Harbin 150001,China | 2001 | World Journal of Gastroenterology2001，7，6： | 8 |
| 9 | RNAi及DNA芯片分析肝癌细胞系中受DNMT3B调控的下游基因(英文)显示文摘为揭示DNA甲基转移酶3B(DNMT3B)在肝癌中是否参与了肿瘤的发生,应用Westernblotting及细胞免疫化学方法分析DNMT3B蛋白在人的正常肝细胞株、肝癌癌旁细胞株及肝癌癌细胞株中的表达。构建了DN-MT3B的RNAi稳定表达的重组载体,并转染入肝癌细胞株SMMC-7721中。以半定量RT-PCR及Westernblot-ting分别鉴定DNMT3BRNAi表达载体对内源性DNMT3B的抑制效率。用高通量的cDNA基因芯片分析了SMMC-7721中DNMT3B抑制后有影响的下游基因谱。结果显示,DNMT3B在肝癌细胞株中的表达水平明显高于肝癌癌旁和正常肝细胞株。DNMT3B的RNAi稳定表达重组载体转染SMMC-7721细胞株2个月后,观察到DNMT3B明显受到抑制。cDNA基因芯片分析发现,DNMT3B抑制后诱导26条基因表达下调,115条基因表达上调,包括一些发育相关基因以及肿瘤相关基因,如SNCG、NOTCH1、MBD3、WNT11、MAOA、FACL4等。提示DNMT3B的高表达可能与肝癌的发生有关,并以调控其他相关基因的表达而起作用,包括与发育相关的重要基因。 | 许军 樊红 赵主江 张建琼 谢维 | 2005 | Acta Genetica Sinica2005，32，11： | 8 |
| 10 | 癌基因对大鼠肝卵圆细胞分化和转化的影响显示文摘目的:通过对体外培养的大鼠卵圆细胞进行AFP和c-ras、c-myc基因的动态测定,观察二者在卵圆细胞转化过程中的变化特点,探讨癌基因对细胞分化和转化的影响.方法:用化学致癌剂3’-Me-DAB诱发出SD大鼠肝卵圆细胞增生,采用Percoll密度梯度离心法分离之,并进行长期体外培养.在培养过程中,通过免疫荧光流式细胞仪租RNA-DNAslotblot杂交分别测定细胞AFP及癌基因的表达隋况.结果:AFP及c-ras、c-myc在卵圆细胞体外培养的不同时期呈现同步升高或降低:培养初期,卵圆细胞AFP及癌基因均呈高表达,而后下降;第20代时再次升高,之后维持在较低的表达水平.至第65代时,卵圆细胞不仅呈现出生长速度加快、群体倍增时间缩短、多倍体核型及软琼脂生长,而且癌基因及AFP的表达亦第3次升高.结论:癌基因及其产物不仅参与细胞的转化过程,亦可调节细胞的分化. | 廖冰 薛玲 何萍 赵国强 车丽洪 | 2004 | 世界华人消化杂志2004，12，2： | 3 |
| 11 | 大鼠肝癌形成过程中癌基因表达变化的意义显示文摘目的:探讨癌基因在实验性大鼠肝癌形成过程中的表达变化特点及其生物学意义.方法:应用化学致癌剂3'-Me-DAB建立大鼠肝癌模型,取其肝脏用核酸原位杂交和RNA Slot blot杂交方法,动态检测c-myc、Ha-ras和Ki-ras在实验性大鼠肝癌形成过程中的表达变化.结果:在诱癌全过程中,c-myc和Ha-ras均为同步表达;在诱癌的早期可检测到较多c-myc和Ha-fas的阳性表达细胞,而Ki-ras阳性的细胞数则很少,且反应强度弱;而诱癌后期,各癌基因mRNA阳性表达细胞均减少;至17 wk,所有癌组织内均显示3种癌基因表达阴性,或仅见个别小癌巢内少数癌细胞呈弱阳性.而癌旁肝组织内却可见三种癌基因的大量表达.结论:c-myc与Ha-fas被激活是肝癌发生过程中的早期事件,且二者之间具有协同作用,而这种协同作用在肝癌的启动上可能具有重要意义;Ki-ras的激活则发生较晚,可能与促进细胞恶性转化有关. | 薛玲 廖冰 赵国强 胡瑞德 车丽洪 董郡 | 2003 | 世界华人消化杂志2003，11，7： | 2 |
| 12 | AgNORs计数DNA含量及PCNA与肝硬化增生结节和肝癌的关系显示文摘目的:探讨肝硬化(LC)、增生结节与肝细胞癌(HCC)之间的关系. 方法:分别应用银染色技术、图像分析技术及免疫组织化学技术检测LC、增生结节及HCC中AgNORs计数、DNA 含量及增生细胞核抗原(PCNA)的表达. 结果:增生结节中,其AgNORs计数、DNA含量及.PCNA 的表达均与正常肝组织和LC组织有明显差异(P分别<0.01, 0.05,0.05);其中AgNORs计数与I级HCC相近(P>0.05), DNA含量与HCC相近(P>0.05).LC组织和正常肝组织间的AgNORs计数、DNA含量及PCNA的表达差异均无显著性(P均>0.05). 结论:增生结节与LC是两种不同性质的细胞群体,前者属于活跃增生性病变,是HCC的癌前期病变,后者仍为成熟的细胞,与HCC的发生没有直接关系. | 牛兆山 张昭成 | 2004 | 世界华人消化杂志2004，12，3： | 2 |
| 13 | 抑癌基因p27^(Kip1)及其Ser^(10)突变体对HepG_2细胞周期和增生的影响显示文摘目的:p27kip1氨基端第10号位置的丝氨酸(Ser10)磷酸化位点是该蛋白分子中最重要的磷酸化位点,探讨人工诱变该位点丝氨酸为丙氨酸(S10A)后对肝癌细胞株HepG2细胞周期以及细胞增生的影响.同时比较野生型p27kip1和Ser10突变型p27kip1基因转染对肝癌细胞株HepG2细胞周期和增生的影响. 方法:应用脂质体转染法将含人野生型和突变型p27kip1质粒DNA瞬时转染HepG2细胞,免疫细胞化学检测p27kip1蛋白的表达和细胞内分布,流式细胞计数仪分析细胞周期变化. 结果:野生型和突变p27kip1蛋白转基因后HepG2细胞均可以G0期阻滞,且突变型的阻滞作用强于野生型(P<0.05),细胞生长受到抑制.无血清培养96 h同步化于G0期,野生型和突变型p27kip1均分布于细胞核;而在20mL/L血清继续培养8 h后野生型向细胞质转运而主要分布于细胞质, 突变型仍然滞留于细胞核. 结论:p27kip1的过度表达可明显抑制HepG2细胞的增生, p27kip1Ser10磷酸可能介导其细胞核外转运的重要分子机制. | 管晓翔 陈龙邦 张爱华 王靖华 德伟 | 2004 | 世界华人消化杂志2004，12，9： | 2 |
| 14 | 胃癌MGMT基因启动子CpG岛甲基化与蛋白表达缺失显示文摘目的:探讨6-氧-甲基鸟嘌呤-DNA甲基转移酶基因启动子甲基化状况在胃癌发生、发展中的作用. 方法:用甲基特异性聚合酶扩增链式反应检测20例正常胃黏膜组织、38例胃癌组织及癌旁正常组织DNA中MGMT 基因启动子的甲基化状况,用免疫组化方法检测MGMT 蛋白的表达隋况. 结果:19.1%(9/47)的肿瘤组织和10.6%(5/47)的癌旁正常组织存在MGMT基因启动子甲基化,正常胃黏膜组织均不存在甲基化.免疫组化发现有21.3%(10/47)的肿瘤组织MGMT蛋白失表达,其中7例(70.0%)存在启动子甲基化. 胃癌中MGMT基因启动子高甲基化与MGMT蛋白表达缺失存在显著联系(P<0.001). 结论:胃癌组织中存在一定程度的MGMT基因启动子高甲基化和MGMT蛋白表达缺失.胃癌发生过程中MGMT基因高甲基化可导致MGMT蛋白表达缺失,可能是胃癌发生的重要途径之一. | 齐健 朱尤庆 杨冬 张友才 张蔚英 刘军 魏芸 | 2004 | 世界华人消化杂志2004，12，3： | 2 |
| 15 | DNA甲基化与肿瘤显示文摘表观遗传学
恶性肿瘤的发生涉及多种基因功能的异常,导致异常的除了以往我们研究得很多的基因突变、基因缺失等遗传改变外,近年来表观遗传学成为了研究热点。1999年Jones等在Nature上撰文“Cancer epigenetics comes of age”,表明肿瘤研究进入了新的时期。表观遗传是指DNA序列不发生变化,但基因表达却发生了改变,并且此种变化在发育和细胞增殖过程中能稳定传递。 | 翟亮 王丹 沈志豪(校审) | 2012 | 健康必读(下)2012，，1： | 0 |
| 16 | Springbio蛋白芯片技术研究气虚质及鼻咽癌气虚癌变差异蛋白表达显示文摘目的利用蛋白芯片技术研究气虚质及鼻咽癌气虚癌变差异蛋白的表达。方法选择具有典型气虚质的鼻咽癌及鼻咽炎各4例作为研究对象,采用可同时检测722个蛋白的Springbio蛋白芯片技术及协方差分析方法,检测气虚质差异蛋白、鼻咽癌差异蛋白以及鼻咽癌气虚癌变差异蛋白的表达情况,探索其特征蛋白。结果相比于正常质,气虚质蛋白主要以下调表达为主,下调蛋白19个(P<0.05),气虚质下调的蛋白主要包括角蛋白及细胞周期蛋白依赖激酶;相比于鼻咽炎,鼻咽癌蛋白既可上调表达亦可下调表达,上调表达有13个蛋白,下调表达有9个蛋白;CD115/CSF-1R和角蛋白既在气虚质下调,又在鼻咽癌下调,Cdk1/p34cdc2和p170/MDR-1蛋白在气虚质下调,在鼻咽癌却上调。结论气虚质存在着特定的蛋白表达特征,表现为角蛋白及细胞周期蛋白依赖激酶的低表达,集落刺激因子1受体及角蛋白低表达为鼻咽癌气虚癌变特征蛋白。 | 周小军 张丽娟 陈江华 汪芸 | 2015 | 北京中医药大学学报2015，38，10： | 0 |
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