75例胃肠间质瘤临床病理分析

对75例胃肠间质瘤（GIST）进行常规病理及免疫组化CD117、CD34、SNA、S-100、Ki-67等染色特点分析,胃肠间质瘤由梭形细胞和上皮样细胞组成．其中66例CD117和56例CD34标记阳性,阳性表达率分别为88％和74．7％。胃肠间质瘤缺乏定向分化．CD117和CD34标记阳性对胃肠间质瘸的诊断具有重要价值．检测Ki-67对预测GIST恶性潜能非常有用,Ki-67标记阳性病例更具有复发的倾向。     

胃肠道间质瘤28例临床病理分析

目的探讨胃肠道间质瘤(GIST)的临床病理特点,分析其生物学行为与形态学的关系。方法回顾性总结分析28例GIST患者的临床病理资料,并复习相关文献。结果本组28例GIST患者中,发生在胃13例,小肠8例,结肠3例,食管2例,肠系膜1例,腹腔1例;高度恶性GIST 20例,低度恶性GIST 8例。镜下肿瘤组织由梭形细胞及上皮样细胞以不同比例混合而成。高度恶性GIST上皮样细胞比较增多。免疫组化标记显示CD117均为阳性。高度恶性组Ki-67阳性指数30%,低度恶性组Ki-67阳性指数3%。S-100及Actin仅2例灶状阳性,其余均阴性。结论上皮样细胞型GIST可能侵袭性更强,转移率更高;免疫组化标记Ki-67可能会成为评价其转移潜能的一个重要指标。     

颈椎上皮样恶性外周神经鞘膜瘤的诊断

目的:探讨上皮样恶性外周神经鞘膜瘤(epitheloid malignant peripheral nerve sheath tumor,EMPNST)的临床病理学特征。方法:对1例上皮样恶性外周神经鞘膜瘤进行大体、组织病理学和免疫组化染色观察,并复习相关文献。结果:患者女性,49岁,病变发生于颈椎。镜下肿瘤细胞密集区与细胞稀疏区交替排列。免疫组化Vimentin(+++),S-100(+++),CgA(++),CD34(++),CK(-),EMA(-),HMB45(-),Actin(-),Desmin(-),Ki-67约10%阳性。结论:上皮样恶性外周神经鞘膜瘤是一种罕见的恶性软组织肿瘤,结合临床病理学特征及免疫组化,可作出正确诊断。     

肺上皮样血管内皮瘤一例临床病理观察

目的 探讨肺上皮样血管内皮瘤的临床病理特征,提高对该病的认识.方法 对1例肺上皮样血管内皮瘤进行组织学观察及免疫组织化学标记,并复习相关文献.结果 镜下见瘤组织在肺内呈小结节状肾小球样增生,充满肺泡腔,局灶区域可见圆形、梭形的上皮样细胞区,胞质空泡形成.免疫组织化学标记肿瘤细胞表达CD34、CD31、Vimentin、CEA,而CK7、CK20、TTF-1、CK、间皮细胞、EMA均为阴性.结论 上皮样血管内皮瘤是一种低度恶性肿瘤,发生在肺内可形成多个小结节,应注意与上皮样血管肉瘤、肺腺癌、间皮瘤相鉴别.     

食管基底样鳞状细胞癌17例临床病理分析

目的:观察食管基底样鳞状细胞癌的临床病理特点,为病理诊断和鉴别诊断提供依据.方法:采用组织病理学、组织化学及免疫组化SP法染色,对17例食管基底样鳞状细胞癌患者系统分析.结果:基底样鳞状细胞癌由密集的小细胞组成,该细胞类似于鳞状上皮的基底层细胞,其组织结构呈巢状、伴中央坏死的大分叶状、筛网状、一致小圆状未分化细胞构成的缎带状,9例合并中、高分化鳞状细胞癌,1例合并腺癌,2例粘膜重度不典型增生伴癌变,1例食管合并另两处独立鳞癌;瘤细胞CgA、Syn、S-100、Actin、CEA均阴性,AE1、AE3、CK34βE12局灶阳性,Ki-67阳性率为50%～80%,癌巢内基底样癌细胞间见丰富的Ⅳ型胶原.结论:基底样鳞状细胞癌是食管少见的鳞状细胞癌变异型,是具有独特形态特点、明显侵袭性的生物学行为和预后差的肿瘤,应与其他恶性肿瘤鉴别.     

乳腺腺样囊性癌病理及免疫组化特点研究

目的探讨乳腺腺样囊性癌临床病理和免疫组化特点。方法回顾总结2006年2月至2016年2月安阳市肿瘤医院收治并行手术治疗的18例乳腺腺样囊性癌患者的临床资料,分析病理和免疫组化特点。结果大体标本切面呈实性,质地中等,灰白或灰黄色。肿瘤切片镜检下13例(72.22%)见呈管状、梁索状、筛状或实体性结构混合型;2例(11.11%)肿瘤以小管/梁索状结构为主(90%);1例(5.56%)肿瘤团巢呈筛状;2例(11.11%)肿瘤为具有基底样特征的实体型乳腺腺样囊性癌。18例免疫组化表型相似,腺上皮细胞CK5、CK7、Cam5.2、CK5/6、EMA和CD117均(+);肌上皮-基底样细胞CK5、CK14、CK5/6、CK34βE12及肌上皮标志物SM-MHC、p63、S-100和calponin均(+)。1例ER呈(+);10例PR(-),8例弱(+);5例Her-2(++)、4例(+);Ⅰ级乳腺腺样囊性癌Ki-67阳性率3%~10%;Ⅱ级乳腺腺样囊性癌筛状区及小管状区Ki-67阳性率为5%,实性区为25%~30%;Ⅲ级乳腺腺样囊性癌性及其他Ki-67阳性率均25%。结论乳腺腺样囊性癌具有独特的组织病理学特征和免疫表型,需与乳腺良性及其他恶性病变相鉴别。     

胃肠道间质瘤53例临床病理及免疫组化分析

目的探讨胃肠道间质瘤的临床病理及免疫组化特点.方法结合免疫组化和病理形态学观察,对53例胃肠道间质瘤进行分析.结果胃肠道间质瘤最常见于胃,其次为回肠、直肠.其中胃31例伴其中肝转移1例,空肠1例,十二指肠、空肠多发1例,回肠14例,直肠6例.镜下瘤组织主要由梭形细胞和或上皮样细胞构成.CD 34、CD 117有很高的阳性表达率,SMA、S-100、NSE在向平滑肌、神经各自的分化有一定的表达率.结论胃肠道间质瘤由非上皮性梭形细胞和(或)上皮样细胞构成,免疫组化CD 34、CD 117有助于做出正确的病理诊断.     

宫颈上皮内瘤变p16~(INK4a)和p53及Ki-67表达及其诊断价值探讨

目的:探讨用p16和p53及Ki-67等免疫组化标记作为宫颈上皮内瘤变(CIN)诊断的辅助指标。方法:选取我院档案CIN患者133例,年龄20～86岁,中位年龄46岁。经3位高年资病理医师复查确认,其中CIN 1级31例、CIN 2级37例和CIN 3级65例。另选同期我院宫颈慢性炎患者19例,浸润性鳞状细胞癌患者20例作为对照。采用SP法进行p16、p53和Ki-67免疫组化染色,结果独立评分。各级别CIN与免疫组化表达的关系采用单变量χ2检验和Spearman等级相关分析。结果:p16阳性表达位于细胞核或胞核伴胞质,p53和Ki-67定位于细胞核。p16、p53和Ki-67表达阳性率随着CIN的加重而升高,均与CIN级别呈正相关,r值分别为0.789、0.554和0.749,P<0.001。153例CIN 1+标本中p16、p53和Ki-67与组织学诊断符合率分别为96.7%(148/153)、71.9%(110/153)和88.2%(135/153)。在102例CIN 2+标本中,p16、p53和Ki-67免疫组化染色的敏感性分别为97.1%(99/102)、74.5%(76/102)和97.1%(99...     

ANXA1，Ki-67抗原在宫颈上皮内瘤变和宫颈癌中的表达及其相互关系

目的：探讨膜联蛋白A1（Annexin A1,ANXA1）和细胞核相关抗原Ki-67在正常宫颈上皮、宫颈上皮内瘤变和宫颈鳞状细胞癌组织中的表达及其相关性。方法：应用免疫组化法检测56例宫颈上皮内瘤变（ CIN）,39例早期宫颈鳞状细胞癌（ SCC）和26例正常宫颈鳞状上皮组织中ANXA1和Ki-67的表达,分析两者之间表达的相关性。应用免疫印迹法检测正常宫颈组织、宫颈上皮内瘤变及宫颈鳞状细胞癌组织中ANXA1的蛋白表达情况。结果：在正常宫颈上皮中 ANXA1蛋白呈高阳性表达,随着宫颈病变的进展, ANXA1蛋白表达呈明显下降趋势。在正常宫颈上皮、宫颈上皮内瘤变和宫颈癌组织中ANXA1蛋白表达具有显著性差异（ P＜0.05）。在正常宫颈上皮和CIN组织中Ki-67抗原表达与ANXA1蛋白表达呈负相关（ P＜0.01）。结论：ANXA1蛋白在宫颈癌中低表达,并与抗原表达明显负相关,与宫颈癌发生、发展过程中凋亡抑制和增殖能力增强有关,可以作为预测宫颈鳞癌不良预后因素之一。     

化生性胸腺瘤的临床病理特征及免疫组化表型

目的:了解化生性胸腺瘤的临床病理特征.方法:收集2例化生性胸腺瘤的临床资料,手术切除组织光镜切片观察,另作10项免疫组织化学标记,CKp,EMA,Vimentin,SMA, Ki-67,CD3和CD5,TdT,CD20.结果:2例化生性胸腺瘤均为女性,前上纵膈包膜完整的肿瘤,由上皮细胞岛和梭形细胞束构成.上皮细胞岛CKp 阳性,Vimentin 阴性,梭形细胞Vimentin阳性,CKp和EMA阴性.瘤组织CD3,CD5,TdT和CD20阴性.Ki-67核阳性细胞指数<5%,肿瘤无坏死. 结论:化生性胸腺瘤是一种罕见的胸腺肿瘤,诊断靠病理组织学和免疫组织化学标记,手术切除为主要的治疗方法.     

中国乳腺癌患者生活质量研究进展

生活质量（qualityoflife,QOL）又译作生命质量、生存质量,它是在世界卫生组织提倡的健康新概念“人们在躯体上、精神上及社会生活中处于一种完好的状态,而不仅仅是没有患病和衰弱”的基础上构建的,是医学模式由生物医学模式向生物一心理一社会医学模式转变的体现。西方发达国家已将此概念广泛应用于临床试验、卫生政策制定和卫生资源效益评价等众多领域。生存质量已作为评价肿瘤患者术后状况的首选指标。     

外泌体在肿瘤发展中的研究进展

外泌体是细胞经过"内吞-融合-外排"等一系列调控过程而形成的细胞外纳米级小囊泡。外泌体可以携带蛋白,运送RNA,在细胞间物质和信息转导中起重要作用。外泌体可能通过调控免疫功能,促进肿瘤血管新生和肿瘤转移,以及直接作用于肿瘤细胞等途径,影响肿瘤的进展。外泌体可应用于肿瘤的诊断。本文总结了近年来有关外泌体在肿瘤发展中作用的研究进展。     

Inhibitory effect of suramin in rat models of angiogenesis in vitro and in vivo

The aim of the present study was to test the ability of the chemotherapeutic agent suramin to inhibit angiogenesis in experimental models in vitro and in vivo. In the culture of rat aortic rings on fibronectin, suramin dose-dependently inhibited vascular cell growth, achieving the maximal effect (mean − 88% versus controls, P < 0.05) at 400 μg/ml. Image analysis showed that suramin could inhibit microvessel sprouting in fibrin from rat aortic rings as evaluated by the ratio between the cellular area and the mean gray value of the sample (sprouting index); suramin at 50 μg/ml significantly reduced the sprouting index from the control value of 0.35 ± 0.04 to 0.14 ± 0.02 mm²/gray level (P < 0.05). Likewise, the area occupied by cells was 19.2 ± 1.8 mm² as compared with 41.8 ± 4.2 mm² in controls (P < 0.05). In the rat model of neovascularization induced in the cornea by chemical injury, suramin at 1.6 mg/eye per day reduced the length of blood vessels (0.7 ± 0.1 mm as compared with 1.5 ± 0.1 mm in controls, P < 0.05). In the same model the ratio between the area of blood vessels and the total area of the cornea (area fraction score) was decreased by suramin from 0.19 ± 0.02 in controls to 0.03 ± 0.003 (P < 0.05). Suramin given i.p. at 30 mg/kg per day markedly inhibited the neovascularization induced in the rat mesentery by compound 48/80 or conditioned medium from cells secreting the angiogenic protein fibroblast growth factor-3 (FGF-3). The area fraction score in control rats treated with compound 48/80 was 0.31 ± 0.03, and this was reduced to 0.07 ± 0.01 by suramin (P < 0.05). After i.p. administration of FGF-3 the area fraction score was reduced by suramin from 0.29 ± 0.03 to 0.05 ± 0.01 (P < 0.05). These results provide evidence that suramin exerts inhibitory effects on angiogenesis in both in vitro and in vivo models. Received: 9 January 1998 / Accepted: 29 June 1998     

Dicer在肿瘤中的研究进展

Dicer是miRNA剪切成熟的关键酶,在肿瘤中扮演单倍体不足抑癌基因的角色.Dicer基因突变携带者易发生家族性肺胸膜母细胞瘤;Dicer在各种肿瘤的发生发展过程中发挥重要作用,基因低表达肿瘤更常表现出恶性程度高和预后差的特点;同时也能介导对药物治疗的敏感性;另外Dicer与miRNA之间复杂的调控体系是其参与肿瘤发生发展的根本所在,可为肿瘤的靶向治疗提供研究基础.     

The role of ultrasonography in diagnosis of cryptorchidism in children

Complex preoperative ultrasonic investigation of the inguinoscrotal area and abdominal cavity was made in 265 patients with cryptorchidism aged 1 to 14 years. The data of this investigation allowed development of an original technique of differential diagnosis of testicular retention and ectopy. Informative value of ultrasonic investigation in diagnosis of testicular ectopy and retention reached 100%. Examination of 44 children with unpalpable testes diagnosed abdominal cryptorchidism in 42 (65.6%) patients. In 10 (15.6%) patients testicular visualization failed. Testicular aplasia was diagnosed in 12 (18.8%) patients. Assessment of morphofunctional condition of the retained gonade showed that all the children had deficiency of testicular volume and abnormal intratesticular blood circulation.     

Role of MutSalpha in the recognition of iododeoxyuridine in DNA

We have previously demonstrated that both the MLH1 and MSH2 status impact the DNA levels of the halogenated thymidine (dThd) analogues iododeoxyuridine (IdUrd) and bromodeoxyuridine (BrdUrd), and thereby radiosensitization induced by these analogues, indirectly implicating both mismatch repair (MMR) proteins in the removal of these bases from DNA. More recent data from our group demonstrate that base excision repair (BER) also impacts IdUrd-DNA levels, supporting a role for the BER pathway in IdUrd removal as well. In this study, we have examined more direct interactions between the MSH2 protein and the processing of IdUrd incorporated in DNA. Our data demonstrate that the MutSalpha (MSH2/MSH6) complex binds specifically to DNA containing an IdUrd-G mismatch, using both purified human MutSalpha as well as nuclear extracts from Msh2-proficient and-deficient mouse cell lines. MutSalpha binding to a IdUrd-G is better recognized than a G-T mismatch in the same sequence context. In addition, MSH2 protein can be found colocalized with IdUrd-DNA using confocal microscopy in G(1) synchronized cells after treatment with IdUrd. Consistent with our recent publication, coadministration of IdUrd and a chemical inhibitor of BER, methoxyamine (MX), also increases the extent of MSH2 nuclear colocalization with IdUrd. Furthermore, we show that the extent of MSH2 colocalization with IdUrd in G(1)-synchronized human tumor cells varies with MLH1 status, suggesting a role for the MLH1 protein in stabilizing the interaction between the MSH2 protein and DNA containing IdUrd. These data, both in vitro and in vivo, suggest direct involvement of MSH2 in processing IdUrd in DNA.