GST-π基因与胃癌病理类型及TNM分期的关系

目的探讨GST-π基因表达与胃癌病理类型及TNM分期之间的相关性及在胃癌早期诊断中的作用。方法采用免疫组化SP法，检测265例胃癌石蜡包埋的肿瘤蜡块中GST-π基因表达情况。结果正常胃黏膜中两种基因均无表达。GST-π基因表达阳性率为65．3％（173／265），与肿瘤病理学分型差异有显著性（P〈0．05），与TNM分期间差异无显著性（P〉0．05）。结论GST-π的阳性率为65．3％，在高分化胃癌组织中表达阳性率高于低分化癌、印戒细胞癌及黏液细胞癌，提示应注意临床化疗药物的敏感性。提高治疗效果。     

生存素在胃癌及其癌前病变中的表达和临床意义

背景:生存素(survivin)是凋亡抑制蛋白家族的成员,在胃癌和癌前病变中可能有一定程度的表达,对胃癌和癌前病变的诊断有相当重要的意义。目的:探讨生存素在不同胃黏膜病变中的表达,以及胃癌组织中生存素的表达与胃癌临床病理参数的关系,以阐明生存素在胃癌发生中的作用和临床意义。方法:分别应用逆转录聚合酶链反应(RT鄄PCR)和免疫组化法检测生存素mRNA和蛋白在慢性非萎缩性胃炎、胃癌前病变和胃癌组织中的表达,分析胃癌组织中生存素的表达与胃癌临床病理参数的关系。结果:慢性非萎缩性胃炎、胃癌前病变和胃癌组织中生存素mRNA的表达率分别为2.5%、25.0%和59.6%,生存素蛋白的表达率分别为0%、15.0%和51.9%,三组间差异有统计学意义(P<0.05)。肿瘤累及浆膜层、有局部淋巴结转移和TNM分期Ⅲ～Ⅳ期胃癌患者癌组织中生存素mRNA和蛋白的表达率分别显著高于肿瘤未累及浆膜层、无淋巴结转移和TNM分期Ⅰ～Ⅱ期者(P<0.05)。结论:生存素在胃癌中有较高的表达率,其表达与胃癌的浸润深度、局部淋巴结转移和TNM分期相关。生存素基因可能参与了正常胃黏膜、癌前病变至胃癌的转化过程,可作为胃癌的独立预后指标。     

凋亡抑制基因生存素在胃癌组织中的表达及意义

目的　研究凋亡抑制基因生存素在胃癌组织的表达及其与临床病理指标的关系 ,以探讨其在胃癌发生、发展中的作用。方法　应用免疫组化Envision法检测生存素在 6 5例胃癌中的表达情况 ,分析它们与胃癌临床病理指标的关系。结果　 (1) 6 5例胃癌组织中生存素总的阳性率为 5 3.85 %(35 / 6 5 ) ;2 0例胃良性溃疡无一例生存素表达阳性。 (2 )Ⅰ、Ⅱ、Ⅲ、Ⅳ期胃癌组织中生存素阳性率分别为 2 / 8例、2 6 .32 % (5 / 19)、74 .0 7% (2 0 / 2 7)、72 .73% (8/ 11) ,Ⅰ期 +Ⅱ期 /Ⅲ期 +Ⅳ期 =2 5 .93% (7/ 2 7)∶73.6 8% (2 8/ 38) ,差异有显著性 (P <0 .0 1)。 (3)淋巴结转移阳性 (N1)的胃癌组织中生存素阳性表达率为 6 2 .86 % (2 2 / 35 ) ,无淋巴结转移 (N0 )为 4 3.33% (13/ 30 ) ,差异有显著性 (P <0 .0 5 )。 (4)有远处转移 (M1)的胃癌组织中生存素阳性表达率为 7/ 9例 ,无远处转移 (M0 )的阳性率为 5 0 .0 0 % (2 8/ 5 6 ) ,差异有显著性 (P >0 .0 5 )。 (5 )高分化、中分化、低分化腺癌的胃癌组织中生存素的阳性率分别为 4 0 .0 0 %(8/ 12 )、5 5 .5 6 % (10 / 18)、6 2 .96 % (17/ 2 7) ,呈逐渐增高的趋势 ,但各组间两两比较均差异无显著性 (P >0 .0 5 )。结论　生存素基因在胃癌的发生发展中起重要作     

生存素转录变异体在胃癌中的表达及其与细胞增殖、凋亡的关系

目的　研究生存素各转录变异体表达及其与胃癌细胞增殖和凋亡的关系。方法　采用实时荧光定量RT PCR技术 ,对 77例胃恶性肿瘤患者的肿瘤组织和正常胃黏膜的成对冰冻标本进行mRNA定量检测。对相同病例的石蜡标本 ,采用DNA缺口原位末端标记 (TUNEL)技术检测肿瘤细胞凋亡 ,免疫组化 (Ki 6 7)检测细胞增殖。结果　与患者正常胃黏膜比较 ,肿瘤组中 3个转录变异体表达水平显著上调 (P <0 .0 0 0 1)。野生型生存素在胃癌中的表达率为 10 0 .0 % (77/77) ,生存素 2B表达率是 79.2 % (6 1/77) ,并且高表达组为早期胃癌 (P =0 .0 0 1)、分化型胃癌 (P =0 .0 0 7)以及浸润浅的胃癌组织 (P =0 .0 31) ;生存素△Ex3在胃癌中的表达率为 6 4 .9% (5 0 /77) ,并且高表达组的凋亡指数显著降低(P =0 .0 19,r =0 .2 6 7)。本实验未发现生存素的 3个转录变异体表达水平与肿瘤细胞增殖指数相关。结论　生存素 2B的表达与肿瘤的分期、分化和肿瘤浸润深度相关 ,表明生存素 2B可能是野生型生存素和生存素 △Ex3的天然拮抗物 ;同时还发现生存素 △Ex3在胃癌组织中的表达与凋亡指数负相关。     

胃癌中HER-2/neu基因扩增和蛋白表达的多中心研究

目的 观察中国人胃癌HER-2／neu基因扩增和蛋白表达状况，探讨两者间关系及与患者临床病理参数间的关系。方法 前瞻性研究中挑选胃腺癌蜡块270例，回顾性研究中挑选蜡块277例，分别用显色原位杂交（CISH）和免疫组化法（IHC）检测HER-2／neu基因扩增和蛋白表达状况。结果 胃癌前瞻性病例中HER-2／neu基因扩增率为14．8％，蛋白过表达率为11．9％。肠型胃癌HER-2／neu基因扩增率和蛋白过表达率分别为25．4％和18．8％，明显高于弥漫型胃癌的4．7％和5．5％（P值均〈0．01）。高、中度分化胃癌HER-2／neu基因扩增率和蛋白过表达率均明显高于低分化胃癌（P值均〈0．01）。回顾性、前瞻性研究及汇总后的总结果中HER-2／neu蛋白CISH和IHC检测结果符合率分别为77．0％、89．2％、83．2％，两者显著相关（P值均〈0．01）。结论 HER-2／neu基因扩增、蛋白过表达可能与中国人胃癌发生有关，基因扩增可能是其蛋白过表达的主要分子机制，HER-2／neu基因扩增和蛋白过表达与肠型胃癌和高中度分化胃癌相关。     

胃癌组织中miR-451与MIF的表达及与临床病理的关系

目的探讨胃癌组织中microRNA-451(miR-451)与巨噬细胞游走抑制因子(MIF)的表达及与临床病理的关系。方法收集2013年3月至2014年3月该院接受治疗的30例胃癌患者,取其肿瘤及肿瘤旁相关组织,采用RT-PCR法检测组织内的miR-451与MIF的表达水平,并分析其与胃癌临床病理的关系。结果肿瘤组织中的miR-451相对表达为(0.287±0.143),显著低于肿瘤旁组织的(0.520±0.257)(t=-4.021,P0.05);肿瘤组织中的MIF相对表达为(1.542±0.023),显著高于肿瘤旁组织的(0.631±0.027)(t=-23.183,P0.05);miR-451与MIF的相对表达呈现显著负相关性(t=-0.721,P0.05);肿瘤组织中miR-451及MIF与胃癌的组织类型(高、中、低分化)、TNM分期(Ⅰ+Ⅱ、Ⅲ+Ⅳ)、浸润深度(T1+T2、T3+T4)及淋巴结转移(有、无)相关(均P0.05)。结论胃癌组织中miR-451及MIF的表达与胃癌的组织类型、TNM分期、浸润深度及有无淋巴结转移相关,推测miR-451反向抑制MIF,进一步调控胃癌在人体内的发生及发展。     

胃癌组织p21基因表达及基因改变的研究

目的研究胃癌组织P21蛋白表达和p21基因改变的意义．方法32例胃癌石蜡标本，其中乳头状腺癌6例，管状腺癌9例，粘液腺癌8例，低分化腺癌7例，未分化癌2例，存在淋巴结转移的标本23例，32例癌旁正常胃粘膜组织作对照．应用ABC免疫组化方法检测P21蛋白表达，单链构象多态性分析（SSCP）检测p21基因改变．参照文献确定p21蛋白表达的阳性标准及SSCCP检测p21基因异常标准，并对结果进行统计学分析．结果胃癌组织P21蛋白表达阳性率56．3％（18／32），其中管状腺癌77．8％（7／9），乳头状腺癌83．3％（5／6），粘液腺癌37．5％（3／8），低分化腺癌42．9％（3／7），未分化癌0％（0／2），存在淋巴结转移组为43．5％（10／23），无淋巴结转移组为88．9％（8／9），癌旁组织为90．6％（29／32）．P21蛋白表达阳性率胃癌组织较癌旁组织明显降低（P＜0．05），与胃癌伴淋巴结转移呈负相关（P＜0．05），不同病理类型间未见差异显著（P＞0．05）．PCR－SSCR分析18．8％（6／32）胃癌组织存在p21基因改变．结论p21基因以异常表达及基因改变的方式参与胃癌发生、发展．     

SLP-76基因在消化道肿瘤中的表达差异分析

目的 分析SLP-76基因在食管癌、贲门癌、胃癌、结肠癌及其癌旁组织中的差异表达。方法 依据微阵列技术筛选出SLP-76基因在食管癌组织中高表达的结果，应用逆转录-聚合酶链式反应(RT-PCR)，对上述消化道肿瘤组织及其癌旁组织中的SLP-76基因表达进行检测。结果 SLP-76在73．3％(22／30)的食管癌组织中高表达(P=0．005)：在75％(9／12)的贲门癌组织中高表达(P=0．014)；在75％(12／16)胃癌组织中高表达(P=0．005)；在72．2％(13／18)结肠癌组织中高表达(P=0．008)。结论 在RNA水平，SLP-76基因在上述肿瘤之间的表达无显著性差异(P=0．9684)。但该基因在消化道肿瘤中高表达，SLP-76与上述消化道肿瘤生长关系密切；可能具有潜在的致癌性。     

胃癌组织中PTEN,MMP-9和Caspase-3表达的关系

目的:研究PTEN,MMP-9和Caspase-3在胃癌及正常胃组织中的表达,探讨他们在胃癌的发生、发展、浸润和转移中的作用．方法:选择临床病理资料齐全的胃癌蜡块标本54例,另取正常胃黏膜标本15例作对照．采用SP免疫组化方法检测PTEN,MMP-9和 Caspase-3在其中的表达．结果:胃癌中PTEN低表达(28/54,51．9％),且肿瘤浸润深(P=0．004)、有淋巴(P=0．003) 和远隔转移(P=0．01 5)、临床分期高(P= 0．001)、病理分化低(P=0．008)时降低．胃癌中MMP-9高表达(41／54,75．9％),且肿瘤浸润深(P=0．040)、有淋巴转移(P=0．025)、临床分期高(P=0．039)、病理分化低(P=0．009)时增高．胃癌中Caspase-3低表达(12／54,22．2％), 且有淋巴转移(P=0．045)、临床分期高(P= 0．015)、病理分化低(P=0．035)时降低．胃癌中PTEN与MMP-9(r=-0．543,P=0．001), Caspase-3与MMP-9的表达负相关(r=0．741, P=0.001),PTEN与Caspase-3的表达正相关(r =0．515,P=0．001)．结论:胃癌中PTEN,Caspase-3低表达,MMP-9 高表达;PTEN、MMP-9和Caspase-3可作为胃癌诊断和预后判断的指标．     

利用组织芯片技术研究PTEN和VEGF在胃癌中的表达及意义

目的研究PTEN和血管内皮生长因子（vascular endothelial growth factor，VEGF）在胃癌中的表达及临床意义。方法应用组织微阵列仪制作97孔胃癌组织芯片（tissue microarray）。用免疫组织化学S—P法检测PTEN、VEGF在72例胃癌和25例正常胃黏膜中的表达。结果胃癌组织中PTEN蛋白阳性表达率显著低于正常胃黏膜（45．8％ VS 100％，P〈0．01）；VEGF的阳性表达率显著高于正常胃黏膜（75％VSl2％，P〈0．01），PTEN在胃癌中的表达与VEGF呈负相关（P〈0．01）。PTEN、VEGF的表达在中高分化腺癌分别为68．8％、62．5％（P〉0．05），在低分化及未分化腺癌分别为27．5％、85．0％（P〈0．05）；伴淋巴结转移者分别为31．6％、86．9％（P〈0．05），无淋巴结转移者分别为61．8％、61。8％（P〉0．05）；临床病理分期Ⅰ＋Ⅱ期分别为57．1％、61．9％（P〉0．05），Ⅲ＋Ⅳ期分别为30．0％、93．3％（P〈0．05）；与性别、年龄、肿瘤大小和组织分型无显著差异（P〉0．05）。结论PTEN失活或蛋白表达降低、VEGF的高表达与胃癌临床病理特征和生物学行为有密切关系。PTEN在低分化或未分化以及伴淋巴结转移和临床Ⅲ＋Ⅳ期胃癌中的表达与VEGF呈负相关。联合检测PTEN、VEGF对胃癌的恶性程度及预后判断具有一定的临床参考意义。应用组织芯片大规模高效检测临床组织样本是可行的，具有快速、准确、方便经济的特点。     

From gastric inflammation to gastric cancer

The majority of gastric adenocarcinomas are related to chronic inflammation induced by Helicobacter pylori infection. For intestinal-type gastric cancer, a multistep process of mucosal alterations leading from gastritis via glandular atrophy, intestinal metaplasia and dysplasia to invasive carcinoma is well recognized. Ongoing clinical studies focus on a 'point of no return'. It is defined as a situation when certain alterations are no longer reversible by H. pylori eradication and progression to gastric cancer may continue. H. pylori affects the mucosal as well as the systemic immune response by secretion of cytokines and the recruitment of distinct inflammatory cells. The immune response is characterized by a balance between a Th1-dominated response and the recruitment of antigen-specific regulatory T cells that allow the bacteria to persist in human gastric mucosa. Besides immune-mediated effects, H. pylori induces cellular alterations as well as genetic alterations in genes that are essential for the epigenetic integrity and mucosal homeostasis. These genetic alterations during gastric cancer development are in focus of intensive research and should ultimately allow the identification of risk factors involved in gastric carcinogenesis. The detection of individuals at high risk for gastric cancer would help to design appropriate strategies for prevention and surveillance.     

Control of gastric emptying by gastric tone

During ingestion of food, the stomach relaxes to accommodate the meal and, subsequently, a progressive gastric contraction parallels gastric emptying. Intestinal nutrients trigger feedback relaxatory mechanisms that regulate gastric tone and, hence, the nutrient load delivered into the small intestine. This regulation of gastric tone is mediated, at least in part, via the vagus. Defective gastric tone is associated with impaired gastric emptying, as seen in patients with postsurgical gastroparesis. However, increased intragastric pressure, corresponding with defective gastric accommodation, induces abdominal symptoms, but does not alter the gastric emptying pattern. These data indicate that gastric emptying is controlled by complementary mechanisms: gastric tone exerts an emptying force, but gastric outlet resistance is also an important regulator.     

胃起搏对胃动力紊乱犬胃排空及胃肌电活动的影响

目的　研究胃起搏对胃动力紊乱犬胃排空及胃电参数的影响。方法　采用双侧迷走神经干切断术联合应用胰高血糖素建立胃动力紊乱犬模型 ;采用 4导联胃肠电系统微机分析仪记录胃肠浆膜肌电活动 ;99mTc 植酸钠标记的半固体试餐 ,单光子计算机断层显像技术 (SPECT)检测胃半排空时间(GEt1/ 2 ) ;采用适宜起搏参数从胃体、胃窦在腹部投影部位输入起搏信号驱动胃电节律。结果　迷走神经干切断术后犬的GEt1/ 2 为 (79.4 2± 1.91)min ,较术前 (5 6 .35± 2 .99)min明显延迟 (P <0 .0 0 1) ,但行胃起搏治疗后GEt1/ 2 为 (6 4 .94± 1.75 )min ,较治疗前明显加快 (P <0 .0 0 1) ;胃起搏治疗前迷走神经干切断犬餐后的胃电频率为 (0 .0 81± 0 .0 0 7)Hz、胃电幅度为 (2 .32± 0 .35 )mV、慢波的传播速度为 (4 .0 6± 0 .4 0 )cm/s ,均较正常对照犬显著降低 [(0 .0 90± 0 .0 0 6 )Hz ,(4 .2 5± 0 .12 )mV ,(6 .92± 0 .2 4 )cm/s,(P <0 .0 5 ) ],治疗后其餐后胃电频率 (0 .0 92± 0 .0 0 5 )Hz、胃电幅度 (3.97± 0 .19)mV和慢波的传播速度 (5 .5 7± 0 .4 8)cm/s均明显高于治疗前 (P <0 .0 5 )。结论　采用适宜起搏参数输入起搏信号可完全触发胃电慢波 ,改善胃电参数 ,纠正药物导致的异常胃电节律 ,加速胃排空 ,恢     

胃微生态与胃癌的研究进展

胃微生态平衡是人体健康的重要前提,幽门螺杆菌(Helicobacter pylori,Hp)是目前已发现的与胃癌相关的关键病原体之一,普遍存在于人胃黏膜上皮。Hp感染可引起胃内其他菌群的改变,还可引起长期慢性的胃黏膜损伤,导致一系列胃黏膜上皮恶性进展和胃癌的发生。本文就胃微生态与Hp感染的关系、Hp感染在胃癌发生中的作用、胃内其他菌群在胃癌发生中的作用及微生态制剂在胃癌治疗的作用进行综述。进一步揭示Hp感染对胃微生态平衡的影响,胃微生态平衡和Hp感染在胃癌发生发展中的作用及微生态制剂在胃癌治疗中的意义。     

The relationship between gastric microbiota and gastric disease

Traditionally, the stomach was believed to be a sterile organ unsuitable for microbiota growth. However, the discovery of H. pylori subverted this conception. With the development of molecular techniques, an abundance of microbiota of great diversity was found in the stomach. In addition, various lines of evidence suggest that the gastric microbiota plays a critical role in the development and progression of the gastric disease.The gastrointestinal microbiome plays an important role in various physiologic and pathologic processes.     

Endoscopy,gastric ulcer,and gastric cancer

The practice of following benign-appearing gastric ulcers until healing was critically evaluated in a retrospective manner by reviewing all gastric ulcers that were followed with serial endoscopy and all gastric cancers diagnosed at the University of Alabama at Birmingham. The stated purpose of following ulcers to healing is to detect those gastric cancers that may be masquerading as benign ulcer and were not correctly diagnosed at initial endoscopy. Over a five-year period, 148 gastric ulcers were followed with serial endoscopy and in no case was an unsuspected carcinoma found at follow-up endoscopy. In addition, of 67 gastric cancers diagnosed between 1979 and 1986, 62 were suspected of being malignant by the endoscopist at initial examination for an accuracy of 92%. The accuracy rate based solely on biopsy and/or brush cytology was 94%. When endoscopic and biopsy and/or cytology impressions were combined, only one case of gastric carcinoma was not suspected. The overall accuracy was 99%. These results suggest that if either the endoscopic impression or the biopsy and cytology is suspicious for malignancy, then follow-up endoscopy until healing should be done. On the other hand, if, at the initial examination, the ulcer appears benign and biopsy plus cytology are negative, then serial endoscopy has a low benefit relative to its cost.     

The role of gastric microbiota in gastric cancer

ABSTRACT

Gastric cancer represents one of the leading causes of cancer deaths worldwide. Helicobacter pylori (H. pylori) infection is the strongest risk factor associated with gastric cancer. Due to new molecular techniques allowing greater identification of stomach microbes, investigators are beginning to examine the role that bacteria other than H. pylori play in gastric cancer development. Recently, researchers have investigated how the composition of the gastric microbiota varies among individuals with various stages of gastric disease. Specific microbes residing in the stomach have been preferentially associated with gastric cancer patients compared to individuals with a healthy gastric mucosa. Studies conducted on the insulin-gastrin (INS-GAS) transgenic mouse model have provided additional insight into the association between the gastric microbiota and gastric cancer. The purpose of this article is to review the current state of literature on the relationship between the gastric microbiota and gastric cancer based on clinical studies performed to date.     

Relationship between gastric mucosal hemodynamics and gastric motility

Continuous measurement of gastric mucosal hemodynamics (the index of mucosal hemoglobin concentration, the index of oxygen saturation and blood flow) in rats showed oscillatory changes. The mechanism of the oscillations was investigated using a probe specially designed for simultaneous measurement of hemodynamics and intragastric pressure. A hemodynamics-measuring probe for either reflectance spectrophotometry or laser-Doppler flowmetry was tied to a pressure microtransducer, inserted through an incision in the forestomach, and brought into gentle contact with the corpus mucosa. Synchronous oscillatory changes (4-6 cycles/min) in hemodynamics and motility were observed in the resting state (mean blood pressure: 120 mmHg). During moderate hemorrhagic hypotension (mean: 81 mmHg), oscillations in the hemodynamics increased in both amplitude and frequency, while motility remained constant. Oscillations in the hemodynamics were also affected by fluctuations in blood pressure and by topical application of norepinephrine to the corpus serosa. In water-immersion restraint rats, changes in the oscillations in the hemodynamics and motility were virtually synchronous; frequency decreased and amplitude increased. These findings suggest that oscillatory changes in gastric mucosal hemodynamics are regulated not only by gastric motility but also by arteriolar vasomotion of the gastric wall.