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| 1 | Multiple genetic alterations and behavior of cellular biology in gastric cancer and other gastric mucosal lesions:H.pylori infection,histological types and staging显示文摘AIM To investigate the expression of multiplegenes and the behavior of cellular biology ingastric cancer(GC)and other gastric mucosallesions and their relations to Helicobacter pylori(H.pylori)infection,tumor staging andhistological subtypes.METHODS Three hundred and twenty-sevenspecimens of gastric mucosa obtained viaendoscopy or surgical resection,and ABCimmunohistochemical staining were used todetect the expression of p53,p16,Bcl-2 andCOX-2 proteins.H.pylori was determined byrapid urea test combined with pathologicalstaining or14C urea breath test.Cellular image analysis was performed in 66 patients withintestinal metaplasia(IM)and/or dysplasia(Dys).In 30 of them,both cancer and theparacancerous tissues were obtained at the timeof surgery.Histological pattern,tumor staging,lymph node metastasis,grading ofdifferentiation and other clinical data werestudied in the medical records.RESULTS p16 expression of IM or Dys wassignificantly lower in positive H.pylori chronicatrophic gastritis(CAG)than those withnegative H.pylori(CAG:54.8% vs 88.0%,IM:34.4% vs 69.6%,Dys:23.8% vs 53.6%,allP<0.05),Bcl-2 or COX-2 expression of IM orDys in positive H.pylori cases was significantlyhigher than that without H.pylori(Bcl-2:68.8%vs23.9%,90.5% vs 60.7%;COX-2:50.0% vs10.8%,61.8% vs 17.8%;all P<0.05).Themean number of most parameters of cellularimage analysis in positive H.pylori group wassignificantly higher than that in negative H.pylori group(Ellipser:53±14,40±12μm,Area1:748±572,302±202 μm2,Area2:3050±1661,1681±1990 μm2,all P<0.05;Ellipseb:79±23,58±15 μm,Ratio1:22%±5%,13%±4%,Ratio2:79%±17%,53%±20%,all P<0.01).There was significant correlation between Bcl-2and histologic pattern of gastric carcinoma,andbetween COX-2 and tumor staging or lymph nodemetastasis(Bcl-2:75.0% vs 16.7%;COX-2:76.0% vs 20.0%,79.2% vs 16.7%;allP<0.05).CONCLUSION p1l6, Bcl-2, and COX-2 but not p53 gene may play a role in the early genesis/ progression of gastric carcinoma and are associated with H. pylori infection. p53 gene is relatively late event in gastric tumorigenesis and mainly relates to its progression. There is more cellular-biological behavior of malignant tumor in gastric mucosal lesions with H. pylori infection. Aberrant Bcl-2 protein expression appears to be preferentially associated with the intestinal type cancer. COX-2 seems to be related to tumor staging and lymph node metastasis. | Heng Jun Gao Lian Zhen Yu Jian Feng Bai Yan Shen Peng Gu Sun Han Lin Zhao Kun Miu Xiu Zhen Lü Xiao Yong Zhang Zhi Quan Zhao | 2000 | World Journal of Gastroenterology2000，6，6： | 52 |
| 2 | Expression,deleton and mnutation of ρ16 gene in human gastric cancer显示文摘AIM To investigate the relationship between the expression of p16 gene and the gastric carcinogenesis,depth of invasion and lymph node metastases, and to evaluate the deletion and mutation of exon 2 in p16 gene in gastric carcinoma.METHODS The expression of P16 protein was examined by streptavidin-peroxidase conjugated method (S-P); the deletion and mutation of p16 gene were respectively examined by polymerase chain reaction (PCR) and polymerase chain reaction single-strand conformation polymorphism analysis (PCR-SSCP) in gastric carcinoma.RESULTS Expression of P16 protein was detected in 96.25% (77/80) of the normal gastric mucosa, in 92.00% (45/50) of the dysplastic gastric mucosa and in 47.54% (58/122) of the gastric carcinoma. The positive rate of P16 protein expression in gastric carcinoma was significantly lower than that in normal gastric mucosa and dysplastic gastric mucosa (P<0.05). The positive rate of P16 protein expression in mucoid carcinoma 10.00% (1/ 10) was significantly lower than that in poorly differentiated carcinoma 51.22% ( 21/ 41 ),undifferentiated carcinoma 57.69% (15/26) and signet ring cell carcinoma 62.50% (10/ 16) (P<0.05). The positive rate of p16 protein in 30 cases paired primary and lymph node metastatic gastric carcinoma: There was 46.67% (14/30) in primary gastric carcinoma, 16.67% (5/30) in lymph node metastatic gastric carcinoma. The positive rate of lymph node metastatic carcinoma was significantly lower than that of primary carcinoma (P<0.05). There was of p16 gene mutation in exon 2, but 5 cases displayed deletion of p16 gene in exon 2 in the 25 primary gastric carcinomas.CONCLUSIONS The expression loss of P16 protein related to the gastric carcinogenesis, gastric carcinoma histopathological subtypes and lymph metastasis. The mutation of p16 gene in exon 2 may not be involved in gastric carcinogenesis. But the deletion of p16 gene in exon 2 may be involved in gastric carcinogenesis. | Xiu-Sheng He Qi Su Zhu-Chu Chen Xiu-Tao He Zhi-Feng Long Hui Ling Liang-Run Zhang Oncology Institute,Nanhua University,Hengyang 421001,Hunan Province,ChinaOncology Institute,Center South University,Changsha 410078,Hunan Province,China Department of Gastroenterology,First People’s Hospital of Changde City,Changde 415003,Hunan Province,China | 2001 | World Journal of Gastroenterology2001，7，4： | 40 |
| 3 | 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 |
| 4 | 健脾中药复方胃肠安对人胃癌裸小鼠原位移植瘤生长和转移的影响显示文摘目的:观察以健脾为基础的中药复方胃肠安对人胃癌裸小鼠原位移植瘤生长和转移的抑制作用。方法:采用人胃癌细胞SGC-7901,裸小鼠66只,其中41只制作原位移植瘤模型,另25只制作皮下移植瘤模型。两种模型的裸小鼠分别随机分为3组:胃肠安组,5-FU组和生理盐水对照组。胃肠安组予以含生药0.12g/ml的胃肠安煎剂0.5ml灌胃,1次/d;5-FU组以5-FU50mg/kg行腹腔化疗,1次/周;生理盐水对照组予以生理盐水0.5ml/d灌胃。原位移植瘤裸小鼠于造模后第64天处死;皮下移植瘤裸小鼠于造模后第41天处死。观察各组的抑瘤率,原位移植瘤各组肿瘤的转移情况,皮下移植瘤各组增殖细胞核抗原(pro-liferatingcellnuclearantigen,PCNA)和细胞凋亡情况。结果:原位移植瘤模型中,胃肠安组和5-FU组抑瘤率分别为40.82%和37.92%;皮下移植瘤模型中两组的抑瘤率则分别为48.70%和60.10%。原位移植瘤模型中,胃肠安组和5-FU组裸小鼠胃周淋巴结转移、肝转移、肝门淋巴结转移、横膈转移和腹膜转移比生理盐水对照组明显减少,3组的总转移率分别为30.77%、28.57%和71.43%(P<0.()5)。皮下移植瘤模型中,胃肠安组和5-FU组的PCNA总阳性率低于生理盐水对照组,细胞凋亡指数高于生理盐水对照组,差异有统计学意义(P<0.05或P<0.01)。胃肠安组和5-FU组瘤重、总转移率和PCNA总阳性率比较,差异无统计学意义,但胃肠安组细胞凋亡指数明显高于5-FU组(P<0.05)。结论:健脾中药复方胃肠安具有抑制人胃癌裸小鼠原位移植瘤生长和转移的作用。胃肠安对胃癌细胞的体内抑制作用可能通过抑制增殖、诱导肿瘤细胞凋亡而实现,对其抑制转移的机制尚需作进一步的研究。 | 赵海磊 赵爱光 尤圣富 顾缨 唐莱娣 杨金坤 | 2005 | 中西医结合学报2005，3，5： | 24 |
| 5 | 胃癌及癌前病变ras P21,P53的表达意义显示文摘近年来的研究结果揭示,胃癌的发生是一个涉及多种癌基因、抑癌基因及多阶段累积的复杂过程,其中癌基因rasp21及抑癌基因p53是与胃癌发生有关的癌相关基因。我们采用SP免疫组化法,同步检测ras p21及p53,观察二种基因蛋白产物在胃癌及癌前病变中的表达情况,以探讨ras癌基因及p53基因在胃癌发生中的作用及意义。 1 材料和方法 1.1 材料胃粘膜活检组织经病理诊断的胃癌42例,不典型增生23例,肠上皮化生26例,慢性萎缩性胃炎14例,慢性浅表性胃炎24例,用100mL·L^(-1)福尔马林液固定,常规组织脱水,石蜡包埋,4μm连续切片。鼠抗人ran P21单克隆抗体及鼠抗人P53单克隆抗体均为美国Maxim Biotech公司产品,试剂盒购自福州迈新生物技术开发公司。 1.2 方法应用免疫组化(SP法)染色,测定方法按试剂盒说明书进行。ras P21蛋白阳性表现为细胞质染色呈棕黄色;P53蛋白阳性表现为细胞核染色呈棕黄色至深棕黄色。 | 费素娟 陈玉林 林志发 陈淑敏 刘广珍 | 2001 | 世界华人消化杂志2001，9，4： | 13 |
| 6 | 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 |
| 7 | The therapeutic effects of recombinant adenovirus RA538 on human gastric carcinoma cells in vitro and in vivo显示文摘AIM To evaluate the potential of RA-538 genetherapy for gastric carcinoma.METHODS Human gastric carcinoma cell lineSGC7901 treated with Ad-RA538 or Ad-LacZ wereanalysed by X-gal stain,MTT,DNA ladder,Tunel,flow cytometric analysis,PCR,andWestern Blot in vitro.The tumorigenicity andexperimental therapy in nude mice model wereassessed in vivo.RESULTS Ad-LacZ could efficiently transferthe LacZ gene into SGC7901 cells.X-gal-positivecells at MOI 25,50,100,and 200 were 90%,100%,100%,and 100% respectively.Ad-RA538could strongly inhibit cell growth and inducedapoptosis in SGC7901 cells.The proliferation ofthe Ad-RA538-infected SGC7901 cells wasreduced by 76.3%.The mechanism of killing ofgastric carcinoma cells by Ad-RA538 was foundto be apoptosis by DNA ladder,Tunel and flowcytometric analysis.The tumorigenicity in nudemice using Ad-RA538 showed that all three micefailed to form tumor from 7 to 30 days comparedwith Ad-LacZ and parent SGC7901 cells.Experimental therapy on the nude mice modelbearing subcutaneous tumor of SGC790| cells showed that intratumor instillation of Ad-RA538inhibited the growth of the tumors.Ad-RA538-treated tumors were inhibited by 60.66 %,compared with that of the tumor injected withAd-LacZ and mock.CONCLUSION The expression of Ad-RA538 can inhibit growth and induce apoptosis of gastric cancer cell in vitro and in vivo. Ad-RA538 can be used potentially in gene therapy for gastric carcinoma. | Jie Ping Chen Chen Lin Cai Pu Xu Xue Yan Zhang Ming Wu | 2000 | World Journal of Gastroenterology2000，6，6： | 12 |
| 8 | P53过度表达及细胞外基质与胃癌分化、浸润和转移的关系显示文摘目的观察 P53蛋白表达及细胞外基质(ECM)在胃癌组织中的表达及其与胃癌分化、浸润和转移的关系.方法采用免疫组化 S-P 法观察胃癌51例及正常胃组织12例中 P53的表达及 ECM 成分-层粘连蛋白(LN)、Ⅳ型胶原和纤维连接蛋白(FN)的分布.结果胃癌组织中 P53阳性表达率为45.1%(23/51),正常胃组织中无1例阳性,P53过度表达与胃癌的分化程度、浸润深度无明显关系,但与淋巴结转移有密切关系(X^2-5.368,P<0.05).LN 和Ⅳ型胶原分布在血管和上皮基底膜(BM)内,FN 在上皮细胞、基底膜及间质内均有分布.正常胃组织中LN,Ⅳ型胶原和基膜 FN 呈连续线状完整地分布.胃癌组织中LN 和Ⅳ型胶原的阳性率分别为41.2%(21/51)和43.1%(22/51).呈连续线状型、间断线状型、碎片状型及完全缺失型四种方式分布。胃癌分化越高,基底膜样物质表达的完整率越高,并与胃癌的浸润深度、淋巴结转移有明显关系.细胞 FN 和基膜 FN 在胃癌组织中的阳性率为47.1%(24/51),37.3%(19/51).且与胃癌的分化和淋巴结转移有关.间质 FN 的分布与胃癌生物学行为无关.结论 P53过度表达和 ECM 缺失在胃癌分化、浸润中各自起着独立的作用,但 P53过度表达同时伴 ECM 缺失的患者,具有较高的淋巴结转移率. | 张林 付红梅 金树珍 黄润 周成刚 | 2001 | 世界华人消化杂志2001，9，9： | 11 |
| 9 | 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 |
| 10 | 胃癌组织中转化生长因子和血小板源生长因子表达的意义显示文摘目的:研究转化生长因子(TGF-β_1)、血小板源生长因子(PDGF-A)在胃癌中表达及其与预后的关系。 方法:应用免疫组织化学方法和分子原位杂交方法检测有随访资料的101例胃癌手术切除标本中的TGF-β_1蛋白、PDGF-A蛋白及mRNA表达。 结果:在101例胃癌手术切除标本中TGF-β_1阳性表达者48例(47.5%)。TGF-β_1表达阳性率:有淋巴结转移者明显高于无淋巴结转移者(x^2=4.4431,p<0.05);脉管内有癌栓者明显高于无癌栓者(x^2=9.8568 p<0.01);癌组织浸润程度:粘膜及粘膜下、肌层、浆膜下及浆膜,三者比较有显著性差异(x^2=7.4799,p<0.05);组织学分级之间比较有显著性差异(x^2=9.1160,p<0.05).PDGF-A阳性表达者43例(42.6%)。PDGF-A表达阳性率:有淋巴结转移者明显高于无淋巴结转移者(x^2=5.5702,p<0.05);脉管内有癌栓者明显高于无癌栓者(x^2=8.8080,p<0.01);癌组织浸润程度:粘膜及粘膜下、肌层、浆膜下及浆膜,三者比较有显著性差异(x^2=14.0504,p<0.01)。PDGF-A阳性表达者5a及10a生存率明显低于阴性表达者5a及10a生存率(p=0.0174,p=0.0038),说明PDGF-A阳性表达者预后较差,阴性表达者预后较好。PDGF-A mRNA表达(61.5%)与PDGF-A蛋白表达(42.6%)一致。PDGF-A阳性表达与TGF-β_1阳性表达之间无关(p>0.01),但他们阳性表达? | 万顺梅 孙少华 邓明德 葛勤利 杨玉捷 | 2002 | 世界华人消化杂志2002，10，1： | 8 |
| 11 | P^53突变与VEGF在大鼠胃癌中的表达及中药胃康宁的防治作用显示文摘目的:了解P53基因突变与VEGF在大鼠实验性胃癌中的表达及中药胃康宁的防治作用.方法:Wistar ♂大白鼠,2-3月龄,体重120-140 g,用MNNG限期饲饮法诱导大鼠发生胃腺癌,设对照组,胃康宁1组、2组,用光镜、电镜观察大鼠胃黏膜细胞形态,用免疫组化法检测突变型P53及VEGF表达.结果:与对照组比较,胃康宁组大鼠胃黏膜细胞异形性、核浓染、核浆比增大等恶性表型轻微,能降低突变型P53蛋白表达(3.4905±1.5225),和VEGF表达(3.519±2.204),(P<0.001).结论:以MNNG诱导大鼠实验性胃癌的发生与P53基因突变及VEGF高表达有关,中药胃康宁具有良好的防治作用,能显著抑制P53蛋白和VEGF表达. | 李庆明 余谦 闵存云 | 2003 | 世界华人消化杂志2003，11，7： | 7 |
| 12 | 人胃癌细胞与血管内皮细胞间的相互作用显示文摘目的实体瘤内多种细胞间存在着复杂的相互关系,为明确人胃癌血管系统的建立、维持及其血行转移中的一些机制,研究人胃癌细胞与血管内皮细胞间的相互作用关系。方法分别制备人胃癌细胞和血管内皮细胞的不同细胞融合状态、不同制备时间的条件培养液,以不同的体积分数作用于对方细胞不同的时间,以四唑盐MTT法测定细胞的增殖状态;通过条件培养液的酸化碱化实验激活TGF-β后,再测条件培养液的活性。用ELISA-ABC法测定条件培养液中人VEGF的水平。结果人胃癌细胞(HGCC)的条件培养液(CM)能刺激人血管内皮细胞(HVEC)的增殖,最高可使HVEC的MTT吸光度A值为原来的(2.70±0.01)倍(P<0.05)。该刺激作用与CM的体积分数、细胞融合状态、制备时间及作用时间有关,并且他不是通过激活TGF-β途径发挥作用。亚融态HGCC的CM中可检测到人VEGF的水平为(92.06±16.9)ng·L^(-1);任何融合状态、任何制备时间的人血管内皮细胞的条件培养液都能抑制人胃癌细胞的增殖。最大增殖抑制率可达(52.97±0.01)%(P<0.05)。结论人胃癌细胞能促进人血管内皮细胞的增殖,该刺激作用不是通过激活TGF-β途径.HGCC可分泌一定量的人VEGF。刺激作用是否与VEGF有关,还须进一步研究。人血管内皮细胞能抑制人胃癌细胞的增殖.具体作用机制尚需进一步探讨。 | 任娟 董蕾 潘伯荣 徐仓宝 李明众 | 2001 | 世界华人消化杂志2001，9，11： | 7 |
| 13 | 结肠肿瘤cFLIP基因表达与p53突变的关系显示文摘目的:检测 cFIP_(short/long)在结肠肿瘤和癌旁组织的表达状况及其与p53基因突变的关系,初步探讨cFLIp在结肠肿瘤发生发展中的意义及p53对其调控作用。 方法:采用免疫组织化学法检测cnLIP在45例结肠腺癌、癌旁组织和42例结肠腺瘤组织中的表达,同时对以上45例结肠腺癌组织行免疫组化染色检测突变p53的表达状况。 cFLIP_(short/long)在结肠腺癌、癌旁组织和腺瘤中的表达差异采用多个样本两两比较的秩和检验(Nemenyi法),cFLIP_(short/long)和突变p53的表达关系采用t检验分析。 结果:cFLIP_(short/long)在结肠腺癌、癌旁组织和腺瘤中都有阳性表达,其染色记分均数分别为3.28±0.37、1.25±0.64和1.13±0.64。结肠腺癌组织的表达强度明显高于癌旁正常组织(3.28±0.37 vs 1.25±0.64,p<0.01)和腺瘤组织(3.28±0.37 vs 1.13±0.64,P<0.01)。60%结肠腺癌突变型p53呈阳性表达,cFLIP_(short/long)在突变型p53阳性组结肠腺癌中的表达水平明显高于突变型p53阴性组(3.74±0.35 vs 2.58±0.59,P<0.01)。 结论:cFLIP_(short/long)特异性高表达于结肠腺癌组织且在结肠肿瘤转化过程中是一较晚期事件,可能与肿瘤的进展有关。P53突变可使结肠腺癌cFLIP_(short/long)表达水平升高。 | 周晓东 于皆平 冉宗学 罗和生 余保平 | 2002 | 世界华人消化杂志2002，10，5： | 6 |
| 14 | 胃癌组织端粒酶hTRT与抑癌基因p53和p16表达的关系显示文摘目的:探讨胃癌中端粒酶基因hTRT及抑癌基因p53和p16mR-NA表达与临床参数的关系,评价hTRT表达检测在胃癌诊断中的价值,探讨hTRT基因与p53和p16基因表达的关系。 方法:用核酸探针和原位杂交的方法分别检测端粒酶基因hTRT及抑癌基因p53和p16mRNA在57例胃癌、57例癌旁组织和69例胃良性病变中的表达和分布情况。 结果:57例胃癌中hTRT基因表达阳性率为94.7%(54/57);57例癌旁组织中hTRT基因表达阳性率为0%(0/57);69例胃良性病变中hTRT基因表达阳性率为2.9%(2/69)。胃癌组织中hTRT基因的表达与癌旁组织、胃良性病变比较差异有显著性(P均<0.001)。胃癌组织中hTRT的表达与肿瘤分化程度、淋巴结转移相关(P均<0.05),与肿瘤分期无相关性(P>0.05)。p53仅在胃癌组织中表达,胃黏膜良性病变中未见表达。胃癌组与后者比较有显著差异(X^2=35.889,P<0.01)。p16仅在胃癌组织中表达,胃黏膜良性病变中未见表达。胃癌组与后者比较有显著差异(X^2=34.059,P<0.01)。统计学分析,胃癌中hTRT基因表达和p53基因表达无相关性(X^2=0.100,P>0.05)。胃癌中hTRT基因表达和p16基因表达无相关性(X^2=0.065,P>0.05)。 结论:端粒酶基因hTRT表达检测在胃癌诊断中可能有一定的价值。研究结果还不能证明hTRT基因表达和抑癌基因p53、p16的表达有? | 李贵新 李国庆 赵常在 徐功立 | 2002 | 世界华人消化杂志2002，10，5： | 6 |
| 15 | 胃癌细胞p16蛋白表达与DNA定量分析的相关性研究显示文摘目的 探讨胃癌细胞p16蛋白表达情况及其与DNA含量的相关性及意义。方法 应用流式细胞仪 (FCM)和图像分析仪 (ICM)检测 41例胃癌细胞p16蛋白表达量和DNA含量 ,10例正常胃组织也用FCM测p16蛋白表达量。结果 41例胃癌p16蛋白表达量明显低于正常胃组织 (荧光指数分别为 0 .81± 0 .0 9和 1.0 0± 0 .11,P <0 .0 1) ,p16蛋白表达量与胃癌病理分级有关 ,随病理分级增高而降低 (P <0 .0 5 ) ,与胃癌患者的性别、年龄无关。胃癌DNA相对倍体均值 (U值 )范围为 1.14~2 98,U值随病理分级增高而升高 (P <0 .0 1)。同时 ,胃癌p16蛋白表达量与DNA含量呈负的直线相关 (P <0 .0 1)。结论 p16蛋白的异常表达与胃癌的发生发展、恶性程度有关 ,并具有较重要临床意义。 | 高美霞 张乃珍 冀春萱 | 2001 | 中华病理学杂志2001，30，3： | 6 |
| 16 | 胃癌组织中细胞凋亡及PCNA表达的意义显示文摘细胞凋亡(Apoptosis,apo)是机体进行生理性细胞代谢,清除细胞的重要途径,在淋巴细胞发育分化成熟过程中扮演重要角色,通过 apo 使可能导致自身免疫疾病的细胞凋亡而加以清除.PCNA 存在于细胞核内,是 DNA 聚合酶的辅助因子,参与DNA 的合成,并在细胞周期中起着重要的调控作用.PCNA 的周期性变化与细胞增殖过程有关. | 申兴斌 赵晓明 胡建功 金小平 王军 | 2000 | 世界华人消化杂志2000，8，9： | 6 |
| 17 | 胃癌及癌旁组织p73基因的表达显示文摘p53基因是人类肿瘤中发生变异频率最高的抑癌基因,在多种肿瘤的生物学行为中具有重要的作用[1-10].p73基因是近来发现的p53基因家族中新成员,其产物与P53蛋白具有非常相似的结构和功能,被认为是一个候选的抑癌基因[11-16];目前国内外虽有少数对胃癌及癌旁组织中p73基因表达的研究,但意见极不一致.为了解该基因在胃癌发生发展中的作用,我们应用RT-PCR技术对胃癌、癌旁及正常组织标本中p73mRNA表达水平进行了分析. | 李伟 王东旭 房殿春 王建文 黄壕 刘为纹 | 2001 | 世界华人消化杂志2001，9，5： | 5 |
| 18 | 肝外胆管癌中p73与p53蛋白表达的相关性显示文摘目的讨论基因 p73和 p53在肝外胆管癌(ECHC)中的表达情况、相互关系及其临床病理意义.方法采用免疫组织化学(SABC 法)对41例肝外胆管癌(男27例,女14例,年龄43岁-69岁)及10例胆总管囊肿病例(男7例,女3例,年龄23岁-54岁)中 p73和 p53表达进行研究.结果肝外胆管癌中 p73基因阳性表达率为41%(17/41),而在胆总管囊肿 p73未见表达,二者相比有显著性差异(P<0.05);经统计学分析 p73的表达与 ECHC 的临床病理分级分期肿瘤大小均无关(P>0.05).p53基因在肝外胆管癌中阳性表达率为34%(14/41),在胆总管囊肿未见表达,二者相比有显著性差异(P<0.05);p53的表达与 ECHC 的病理分级显著相关(P<0.05).在14例 p53表达阳性的 ECHC 病例中有10例 p73表达亦为阳性,在27例未发现 p53突变的标本中,有7例 p73表达阳性,经分析 p73和 p53表达显著相关(P<0.05).结论 p73、p53基因在肝外胆管癌的发生发展过程中起重要作用,二者的表达有一定的相关性,在体内二者的作用可能存在互补性. | 张智勇 窦科峰 刘正才 | 2001 | 世界华人消化杂志2001，9，10： | 4 |
| 19 | 胃癌中Autotaxin基因、CD44v6分子、DNA含量的相关性研究显示文摘Autotaxin (ATX)是一种肿瘤细胞自分泌运动因子,与肿瘤浸润转移关系密切[1].CD44v6是粘附分子家族成员之一,也与肿瘤浸润转移复发有关[2-7].细胞核DNA含量是反映细胞增殖状态的一个良好指标,而细胞无限增殖与肿瘤的发生、发展及预后密切相关[8-10].胃癌在我国常见[11-19],我们拟检测胃癌组织中ATX,CD44v6的表达特征及细胞核DNA含量分析,对三者之间进行相关性分析,探讨以ATX,CD44v6,DNA含量分析联合来判断胃癌浸润、转移能力的可能性和方法. | 张军 孙士其 林惠华 孙丹莉 王自正 王书奎 | 2001 | 世界华人消化杂志2001，9，7： | 3 |
| 20 | Bcl-2、Bax、P21-WAF1、P16-MTS1蛋白在胃腺癌演化系列中的表达显示文摘目的 通过对胃腺癌演化系列胃粘膜中Bcl 2、Bax、P2 1 WAF1、P16 MTS1蛋白的检测 ,探讨胃腺癌发生的机制及四种蛋白表达与胃腺癌生物学行为的关系。方法 1、利用免疫组化S P法检测胃癌演化系列胃粘膜中Bcl 2、Bax、P2 1 WAF1、P16 MTS1蛋白的表达 ;2、利用SPSS统计软件包作统计学分析处理。结果 在CSG、CAG、IM系列胃粘膜中Bax、Bcl 2表达先高后低 ,而P16 MTS1、P2 1 WAF1表达先低后高 ,(P <0 .0 5 )。高分化胃腺癌中Bcl 2、Bax、P2 1 WAF1、P16 MTS1表达较低分化者高 ;P16 MTS1表达在非贲门癌中比贲门癌中高 ,P2 1 WAF1表达在有淋巴结转移的胃腺癌中较低 (P<0 .0 5 )。结论 Bax、Bcl 2的高表达及P2 1 WAF1、P16 MTS1的表达受抑可能参与胃腺癌发生 ;四种蛋白异常表达均与胃腺癌分化呈正相关 ;P16 MTS1、P2 1 WAF1的表达异常与胃腺癌的发生部位及淋巴结转移相关。 | 陈奕贵 郑天荣 郑雄伟 谢佑福 | 1999 | 胃肠病学和肝病学杂志1999，8，4： | 3 |
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