胰腺双部位实性假乳头肿瘤1例

目的:总结1例胰腺双部位实性假乳头肿瘤(SPT)的临床病理特点,探讨其可能起源.方法:手术行标准胰十二指肠切除术和胰体尾及脾切除术,分析该病例SPT的临床病理特点,并行多个抗体的免疫组织化学检查.结果:患者术后血糖5.5-8.9 mmol/L,第5天开始恢复饮食.未发生胰漏、胆漏及腹腔感染等并发症.大体形态的囊实性比例不尽相同,但镜下肿瘤细胞形态学一致,均确诊为SPT,对各个免疫表型的表达具有异质性,其中VIM、S100、AAT、CyclinD1、PR及Nestin 均呈阳性.结论:SPT可能起源于胰腺干细胞及与其发育密切相关的胚胎神经嵴的神经前体细胞,由干细胞发育过程中分化不成熟所致.     

肺硬化性血管瘤临床病理诊断及鉴别诊断

目的:探讨肺硬化性血管瘤(SHL)的临床病理特点及免疫表型。方法:对5例SHL的临床和病理资料进行分析并进行12种免疫组化标记:甲状腺转录因子(TTF-1)、上皮膜抗原(EMA)、细胞角蛋白(AE1/AE3)、表面活性蛋白-B(SP-B)、波形蛋白(Vimentin)、内皮细胞(CD31)、Ⅷ因子相关抗原(Ⅷ因子)、S-100蛋白、嗜铬素(CgA)、突触素(Syn)、钙结合蛋白(Calretinin)、间皮细胞(MC)。结果:肿瘤主要由实性区、乳头状区、血管瘤样区和硬化区4种组织形态构成,瘤细胞主要由立方细胞和多角形细胞组成。2种细胞共同表达TTF-1和EMA,AEl/AE3、SP-B仅在立方细胞中表达。结论:SHL组织形态特征结合TTF-1、SP-B、EMA、Vimentin和AE1/AE3的免疫组化标记,有助于SHL的诊断和鉴别诊断。     

类肝素酶在胰腺癌组织中的表达意义

目的 探讨胰腺癌组织中类肝素酶(heparanase 1,Hpal)表达与胰腺癌侵袭性、临床病理等因素之间的关系.方法 采用逆转录-聚合酶链反应(RT-PCR)、免疫组化(SP)法检测37例胰腺癌患者痛组织、癌旁组织及正常胰腺组织中Hpal表达,并统计分析Hpal表达与胰腺癌侵袭性、临床病理等因素之间的相关性.结果 Hpal在胰腺癌组织、癌旁组织、正常胰腺组织中的表达阳性率分别为64.9%(24/37)、56.8%(21/37)和10.8%(4/37).胰腺癌组织中Hpal表达与胰腺癌TNM分期、侵及神经和血管情况、包膜完整情况以及淋巴转移明显相关(P＜0.05),但与患者年龄、性别、组织学分化程度、肿瘤大小无关(P＞0.05).结论 Hpal与胰腺癌发生、发展密切相关,Hpal表达与胰腺癌的侵袭性、局部浸润、临床分期以及区域淋巴结转移有密切关系,胰腺癌Hpal过表达可促进胰腺癌浸润生长与转移,其表达对评价胰腺癌预后亦有一定的价值.     

粘蛋白MUC1、MUC2、MUC4和MUC5AC在胰腺导管腺癌中的表达及意义

目的 研究胰腺导管腺癌(pancreatic ductal adenocarcinoma,PDA)组织中粘蛋白MUC1、MUC2、MUC4和MUC5AC的表达及其与临床病理参数间的关系.方法 应用SP免疫组织化学方法检测26例PDA、4例CP、16例正常胰腺组织、2例导管内乳头状黏液性肿瘤(IPMN)、4例实性假乳头状瘤(SPT)和1例浆液性囊性肿瘤(SCN)组织中MUC1、MUC2、MUC4、MUCSAC的表达.结果 正常胰腺和CP组织仅有MUC1表达,表达率均为100%;PDA中MUC1、MUC4和MUC5AC表达率分别为100%、88.5%(23/26)和76.9%(20/26);2例IPMN均见MUC2和MUC5AC表达;SPT和SCN中4种粘蛋白均无表达.MUC4和MUC5AC表达同PDA的临床病理参数之间无相关性(P＞0.05).结论 PDA时存在多种粘蛋白的表达,联合检测MUC1、MUC2、MUC4和MUC5AC的表达可能有助于对PDA的诊断和鉴别诊断.     

胰腺腺泡细胞癌的临床特点和病理特征及基因突变分析

目的:分析胰腺腺泡细胞癌(PACC)的临床特点、病理特征和基因突变情况。方法:回顾性分析2009年12月至2018年7月间海军军医大学第一附属医院胰腺外科收治的34例PACC患者的临床资料,总结其临床特点,采用免疫组织化学法检测胰腺肿瘤组织α1抗凝乳蛋白酶(α1-ACT)、极低分子量细胞角蛋白(CAM5.2)、突触素(...     

胰腺癌中RECK和MMP-9蛋白的表达及临床病理意义

目的 观察RECK和MMP-9在胰腺癌组织中的表达,探讨其与胰腺癌临床病理特征的关系.方法 采用免疫组化PV6000法检测28例胰腺癌及10例正常胰腺组织中RECK、MMP-9的表达,应用SPSS13.0软件对RECK、MMP-9的表达与肿瘤临床病理特征的关系进行统计学分析.结果 RECK在胰腺癌组织中的阳性表达率为46.4%(13/28),显著低于它在正常胰腺组织中90.0%(9/10)的阳性表达率.胰腺癌临床分期为Ⅰ+Ⅱ期组的RECK阳性表达率(75.0%,9/12)明显高于Ⅲ+Ⅳ期组(25.0%,4/16,P＜0.05),无远处转移组的RECK阳性表达率(60.0%,12/20)明显高于有远处转移组(12.5%,1/8,P＜0.05).MMP-9在胰腺癌组织中的阳性表达率为75.0%(21/28),显著高于正常胰腺组织中的20.0%(2/10)阳性表达率(P＜0.01).胰腺癌临床分期为Ⅰ+Ⅱ期组的MMP-9阳性表达率(50.0%,6/12)明显低于Ⅲ+Ⅳ期组(93.8%,15/16,P＜0.05),肿瘤高分化组的MMP-9阳性表达率(33.3%,1/3)明显低于低分化组(100%,12/12,P＜0.01).胰腺癌组织中RECK与MMP-9的表达呈负相关(r=-0.536,P＜0.01).结论 胰腺癌组织中RECK呈低表达,MMP-9呈高表达,RECK、MMP-9联合检测可以作为胰腺癌临床分期评估的指标.     

胰腺腺泡细胞癌八例临床病理及免疫组化分析

目的 分析胰腺腺泡细胞癌的临床病理特征及蛋白表型.方法 收集2001年1月至2011年1月收治的8例胰腺腺泡细胞癌病例,分析其临床病理特征,采用免疫组化法检测肿瘤的蛋白表型,并进行随访.结果 8例胰腺腺泡细胞癌病例均为男性,中位年龄47岁.肿瘤位于胰头部和胰体尾部各4例,大小平均为4.5 cm×4.0 cm ×3.2 cm,切面灰黄、灰红色,呈实性或囊实性,体积较大者常伴有出血、坏死.镜下见肿瘤细胞排列呈腺泡状、梁索状或实性片巢状,胞质丰富、嗜酸性,核圆形、卵圆形,轻度异型.免疫组化显示癌细胞低分子量细胞角蛋白(CAM5.2)、α1-抗胰蛋白酶(α1-AT)、抗胰糜蛋白酶(α1-ACT)蛋白表达呈弥漫阳性,CA19-9、CEA,上皮型钙粘蛋白(E-cad)、β-连环素(β-cat)和粘蛋白-1( MUC-1)呈灶性阳性,AFP、神经特异性烯醇化酶(NSE)、突触素(Syn)和铬粒素A(CgA)仅少数瘤细胞呈阳性表达.7例获得随访,1例因术后胰漏伴腹腔感染病死,发生肝转移4例,其中2例病死.结论 胰腺腺泡细胞癌是一种少见的胰腺上皮源性恶性肿瘤,有其特征性的蛋白表型.     

TGF-β/Smads信号通路相关蛋白在胰腺上皮内瘤变和胰腺癌组织中的表达

目的探讨转化生长因子(TGF)-β/Smads信号转导通路中Smads相关蛋白、TGF-β1及其Ⅰ、Ⅱ型受体在胰腺上皮内瘤变(PanIN)和胰腺癌组织中表达的意义.方法用EnVision和SP免疫组化技术检测266灶不同级别PanINs和121例胰腺癌组织中Smads相关蛋白、TGF-β1及其Ⅰ、Ⅱ型受体的表达并联系临床病理学指标进行相关分析.结果高级别PanINs病灶Smad4表达率(60.6%,20/33)显著低于低级别PanINs Smad4表达率(79.8%,186/233)(P<0.05);而高级别PanINs中Smad7、TGF-β1、TGF-βRⅡ表达率明显高于低级别PanINs(P<0.05).胰腺癌组织中,Smad4蛋白表达率在淋巴结转移组和神经受累组显著低于各自对照组(P<0.05);Smad7、TGF-β1及其Ⅰ、Ⅱ型受体的表达率在淋巴结转移组和神经受累组则分别显著高于各自对照组(P<0.05).胰腺上皮内瘤变和胰腺癌组织中Smad2、4、7蛋白,TGF-β1及其Ⅰ、Ⅱ型受体表达率的差异具有非常显著性(P<0.01).结论从低级别PanINs到高级别PanINs再到胰腺癌中,Smad4蛋白表达率逐渐降低,而Smad7、TGF-β1及其Ⅰ、Ⅱ型受体表达率逐渐升高,支持胰腺癌形成的分子模型.     

Mucin4在胰腺癌组织中的表达及其临床意义

目的研究胰腺癌组织中Mucin 4(MUC4)的表达及其与临床病理参数间的关系.方法 (1)采用ABC免疫组织化学方法检测35例胰腺癌、12例胰腺良性肿瘤及5例慢性胰腺炎组织MUC4的表达.(2)通过RT-PCR方法检测12例胰腺癌组织、癌旁胰腺组织以及2株胰腺癌细胞株MUC4 mRNA的表达.结果 (1)35例胰腺癌组织中MUC4蛋白阳性表达24例,12例胰腺良性肿瘤中MUC4蛋白阳性表达2例,5例慢性胰腺炎组织中MUC4蛋白均为阴性.MUC4蛋白胰腺癌组织中阳性表达率显著高于胰腺良性肿瘤及慢性胰腺炎组织(P ＜ 0.05).MUC 4在胰腺癌组织中阳性表达率与肿瘤的部位、淋巴结转移、临床分期无关(P ＞ 0.05).(2)12例胰腺癌组织中MUC4 mRNA表达阳性有6例,癌旁组织中无阳性表达,2株胰腺癌细胞株均呈阳性表达.MUC4 mRNA在胰腺癌组织中阳性表达率显著高于癌旁组织(P ＜ 0.05).结论 MUC4在胰腺癌中有较高的表达率,检测其表达可能有助于胰腺癌的诊断,并可作为鉴别胰腺癌和慢性胰腺炎一个重要参考指标.     

胃肠道神经内分泌肿瘤的内镜表现及病理学特征

目的分析内镜检查胃肠道神经内分泌肿瘤(NEN)的表现及病理学诊断特点。方法对南京市浦口区中心医院及南京市第一医院病理科2011年5月至2017年5月收集的经内镜检出并经病理活检证实为胃肠道NEN的29例患者进行回顾性分析。通过内镜检查和光学显微镜对组织形态学变化进行综合分析,采用免疫组织化学方法检测细胞广谱角蛋白(AE1/AE3)、细胞角蛋白(CK8/18)、嗜铬粒素(Cg A)、突触素(Syn)、神经元特异性烯醇化酶(NSE)、神经细胞黏附分子(CD56)及核抗原(Ki-67)在肿瘤细胞中的表达情况。结果胃肠道NEN患者均为单发,胃肠道神经内分泌癌(NEC)和胃肠道混合性腺神经内分泌癌(MANEC)为溃疡型肿物。AE1/AE3、CK8/18、Cg A、Syn、NSE、CD56的阳性率分别为96.77%、80.65%、77.42%、88.71%、53.23%、79.03%。胃肠道高分化神经内分泌肿瘤(NET)核抗原(Ki-67)阳性指数≤20%,NEC、MANEC核抗原(Ki-67)阳性指数20%。结论 NEN缺乏典型的临床表现,通过内镜不能对其进行确切诊断,但其病理组织学特异性较为明显,AE1/AE3、CK8/18、Cg A、Syn等免疫组化检测对病理诊断起到重要作用。     

Heterogenous expression of nestin in human pancreatic tissue precludes its use as an islet precursor marker

The discovery of a pancreatic adult stem cell would have significant implications for cell-based replacement therapies for type 1 diabetes mellitus. Nestin, a marker for neural precursor cells, has been suggested as a possible marker for islet progenitor cells. We have characterized the expression and localization of nestin in both the intact human pancreas and clinical human pancreatic islet grafts. Nestin was found to be expressed at different levels in the acinar component of human pancreatic biopsies depending on donor, as well as in ductal structures and islets to some degree. In islets, insulin-producing beta-cells rarely co-expressed the protein, and in the ducts a small percentage (1-2%) of cells co-expressed nestin and cytokeratin 19 (CK19) while most expressed only CK19 (90%) or nestin (5-10%) alone. Assessment of nestin expression in neonatal pancreatic sections revealed an increased number of islet-associated positive cells as compared with adult islets. Nestin immunoreactivity was also found in cells of the pancreatic vasculature and mesenchyme as evidenced by co-localization with smooth muscle actin and vimentin. Samples from post-islet isolation clinical islet grafts revealed a pronounced heterogeneity in the proportion of nestin-positive cells (<1-72%). Co-localization studies in these grafts showed that nestin is not co-expressed in endocrine cells and rarely (<5%) with cytokeratin-positive ductal cells. However, relatively high levels of co-expression were found with acinar cells and cells expressing the mesenchymal marker vimentin. In conclusion we have shown a diffuse and variable expression of nestin in human pancreas that may be due to a number of different processes, including post-mortem tissue remodeling and cellular differentiation. For this reason nestin may not be a suitable marker solely for the identification of endocrine precursor cells in the pancreas.     

肺硬化性血管瘤5例报道及文献复习

目的分析肺硬化性血管瘤(sclerosing hemangioma of lung,SHL)组织成分及免疫组织化学表型,探讨其病理形态学特征、免疫组化在诊断中的价值。方法用免疫组化SP法对5例SHL组织标本的CK、CEA、EMA、CD34、SMA、MC、Vim、NSE、CgA进行标记,观察其表达情况。结果 SHL主要表现为乳头区、实性细胞区、血管瘤样区及硬化区等四种结构,乳头、实性区裂隙及血管瘤样区表面衬覆有立方状上皮细胞,乳头间隙及实性细胞区为圆形多角形胞质浅染的细胞。免疫组化显示乳头、实性区裂隙及血管瘤样区表面衬覆细胞阳性表达CK、CEA、EMA,圆形或多角形细胞阳性表达Vim和CgA,NSE和EMA在圆形或多角形细胞灶性表达阳性,CD34仅在肿瘤组织中的血管内皮细胞呈阳性表达,MC和SMA在两种细胞均为阴性表达。结论 SHL的组织成分包括表面的立方状上皮细胞、圆形多角形胞质浅染的细胞、肺泡腔内出血和硬化性变化,四种组织结构至少存在三种,免疫组化对SHL的诊断有帮助。     

甲状腺转录因子1和表面活性蛋白在肺硬化性血管瘤中表达的意义

目的　探讨甲状腺转录因子 1(TTF 1)和表面活性蛋白A、B(SP A ,SP B)在肺硬化性血管瘤 (PSH)中表达的生物学意义。方法　用免疫组织化学的方法 ,检测 4 2例经外科手术切除、病理诊断的PSH标本中TTF 1、SP A、SP B和上皮膜抗原 (EMA)、波形蛋白 (vimentin)、广谱角蛋白(pancytokeratin)、角蛋白 7(CK7)、CK5 / 6、钙结合蛋白 (calretinin)、S 10 0蛋白、神经元特异性烯醇化酶(NSE)、突触素 (Syn)、嗜铬素A(CgA)、CD3 4 、Ⅷ因子相关抗原 (F Ⅷ )、平滑肌肌动蛋白 (SMA)的表达状况 ,其中 10例进行透射电镜观察。结果　病理组织学上肿瘤主要由多角形细胞和立方细胞组成 ;免疫组织化学显示 95 % (4 0 / 4 2 )患者立方细胞和多角形细胞共同表达TTF 1、88% (37/ 4 2 )表达EMA、5 7% (2 4 / 4 2 )表达vimentin ,93% (39/ 4 2 )患者立方细胞表达SP A、81% (34/ 4 2 )表达SP B、10 0 %(4 2 / 4 2 )表达 pancytokeratin ;2 4 % (10 / 4 2 )患者多角形细胞散在表达Syn、14 % (6 / 4 2 )表达NSE、12 %(5 / 4 2 )表达S 10 0和 12 % (5 / 4 2 )表达CgA ;TTF 1和EMA在这两种细胞之间的表达状况差异无显著性 (χ2 分别为 0 0 0 0和 3 4 0 3,P >0 0 5 ) ,vimentin在这两种细胞之间的表达差异有显著性 (χ2 =10 118,P <     

大鼠胰腺干细胞的分离纯化、鉴定及定向分化

目的 探讨大鼠胰腺干细胞体外分离、纯化的实验条件及其定向分化潜能.方法 应用胰腺原位灌注V型胶原酶消化大鼠胰腺组织,100目滤网滤过,Ficoll 400浓度梯度离心法分离胰腺干细胞,采用添加表皮生长因子(EGF)、成纤维细胞生长因子(bFGF)的培养基行体外培养.运用荧光免疫染色法检测细胞表面CK-19、Pdx-1、Nestin、Insulin和Glucagon蛋白,计算阳性细胞率.双硫腙(DTZ)染色鉴定诱导分化后的细胞,光电酶标记法ELISA检测胰岛素分泌功能.结果 本实验获取的胰腺干细胞,体外培养可稳定传代培养8代以上.细胞表面CK-19、Pdx-1和Nestin蛋白均呈阳性,阳性细胞率分别为(88.6±6.2)%、(84.6±8.6)%和(81.3±7.5)%.诱导分化后细胞经DTZ染色呈棕红色.在高糖刺激下,培养上清液中胰岛素含量增高.结论本法可获取高纯度、多数量的胰腺干细胞,在人工诱导下可定向分化为具有胰岛素分泌功能的胰岛样细胞团,为临床胰岛移植获得足量细胞来源提供实验基础.     

Nestin in gastrointestinal and other cancers: effects on cells and tumor angiogenesis

Nestin is a class Ⅵ intermediate filament protein that was originally described as a neuronal stem cell marker during central nervous system (CNS) development, and is currently widely used in that capacity. Nestin is also expressed in non-neuronal immature or progenitor cells in normal tissues. Under pathological conditions, nestin is expressed in repair processes in the CNS, muscle, liver, and infarcted myocardium. Furthermore, increased nestin expression has been reported in various tumor cells, including...     

Projected focal nodular hyperplasia of the liver with pronounced atypical ductular reaction resembling ductal plate and expressing KIT

A 26‐year‐old woman was found to have a left abdominal tumor in the space among the hepatic left lobe, stomach and spleen. A laparoscopic examination revealed that the tumor was a projected liver tumor, and resection of the tumor was performed. Grossly, the tumor was not encapsulated and measured 4 cm × 4 cm × 5 cm. Microscopically, the tumor was composed of mature hepatocytes, fibrous septae, abnormal vessels and ductular reaction (DR). A pathological diagnosis of projected focal nodular hyperplasia (FNH) was made. Characteristically, the cells of the DR showed atypical features such as small cells and hyperchromatic nuclei. The DR assumed the features of ductal plate‐like structures and immunohistochemically expressed KIT, suggesting that the cells of DR are stem cells and that when the stem cells proliferate they take a form of ductal plate‐like structures, similar to fetal bile duct development. Immunohistochemically, the cells of DR were positive for cytokeratin (CK) AE1/3, CK CAM5.2, CK7, CK8, CK18, CK19, carcinoembryonic antigen (CEA), CA19‐9, Ki‐67 (labeling = 3%) and KIT, but negative for CK20, p53, TTF‐1, CDX2, MUC1, MUC2, MUC5AC and MUC6. The hepatocytes were positive for CK CAM5.2, CK8, CK18 and Ki‐67 (labeling = 4%), but negative for CK AE1/3, CK7, CK19, CK20, CEA, CA19‐9, p53, KIT, TTF‐1, CDX2, MUC1, MUC2, MUC5AC and MUC6. In conclusion, the author reported a projected FNH. The DR of the FNH showed atypical features such as small cells and hyperchromatic nuclei. The DR assumed features of ductal plate‐like structures. KIT was positive in the DR in the FNH, suggesting that the cells of DR are liver stem cells, and proliferation of these cells take features of ductal plate‐like structures, similar to embryonic biliary development. MUC apomucins are negative in the DR.     

Imaging features of solid pseudopapillary tumor of the pancreas on multi-detector row computed tomography

AIM： To retrospectively analyze the imaging features of solid-pseudopapillary tumors （SPTs） of the pancreas on multi-detector row computed tomography （MDCT） and define the imaging findings suggestive of malignant potential. METHODS： A total of 24 consecutive cases with surgically and pathologically confirmed SPTs of the pancreas underwent preoperative abdominal MDCT studies in our hospital. All axial CT images, CT angiographic images, and coronally and sagittally reformed images were obtained. The images were retrospectively reviewed at interactive picture archiving and communication system workstations. RESULTS： Of the 24 cases of SPTs, 11 cases （45.8%） occurred in the pancreatic head and seven （29.1%） in the tail. Eighteen were pathologically diagnosed as benign and six as malignant. MDCT diagnosis of SPTs was well correlated with the surgical and pathological results （Kappa = 0.6, P 〈 0.05）. The size of SPTs ranged from 3 to 15 cm （mean, 5.8 cm）. When the size of the tumor was greater than 6 cm （including 6 cm）, the possibilities of vascular （8 vs 1） and capsular invasion （9 vs 0） increased significantly （P 〈 0.05）.Two pathologically benign cases with vascular invasion and disrupted capsule on MDCT presented with local recurrence and hepatic metastases during follow-up about 1 year after the resection of the primary tumors. CONCLUSION： Vascular and capsular invasion with superimposed spread into the adjacent pancreatic parenchyrna and nearby structures in SPTs of the pancreas can be accurately revealed by MDCT preoperatively. These imaging findings are predictive of the malignant potential associated with the aggressive behavior of the tumor, even in the pathologically benign cases.