口腔粘膜癌前病变和鳞癌组织凋亡相关蛋白Bcl-2和Fas的表达

目的 :研究凋亡相关蛋白Bcl 2、Fas在口腔异常增生上皮和鳞癌组织中表达。方法 :采用免疫组化SP法检测 10例正常粘膜 ,48例异常增生上皮 ,42例鳞癌石蜡包埋样本中Bcl 2和Fas的表达。结果 :Bcl 2在正常粘膜和异常增生上皮中少见表达 ,鳞癌组织中Bcl 2表达明显增强 (p <0 0 5 )。Fas在正常粘膜中广泛表达 ,在异常组和鳞癌组中表达明显下调 (p <0 0 5 )。结论 :Fas在异常增生上皮中表达下降 ,可能导致异常增生细胞累积 ;Bcl 2和Fas共同作用导致肿瘤的最终发生、发展     

口腔黏膜癌前病变及鳞癌中Fas/FasL的表达研究

目的 :研究凋亡相关基因Fas/FasL在口腔正常粘膜、上皮单纯增生、上皮异常增生和鳞癌中的表达及意义。方法 :采用SABC免疫组织化学方法检测正常口腔粘膜 ( 10例 ) ,上皮单纯增生 ( 8例 ) ,上皮异常增生 ( 2 0例 ) ,鳞癌 ( 32例 )中Fas/FasL的表达。结果 :在正常口腔粘膜中Fas表达于棘层和粒层细胞的胞膜 ;FasL局限于基底层细胞的胞膜和胞浆。上皮异常增生中随异常增生程度的增高 ,Fas表达降低 ;FasL表达增强 ,甚至遍布上皮全层。鳞癌组中Fas表达明显低于正常组 (P <0 .0 5 ) ,且与组织学分级呈正相关 ;FasL表达明显高于正常组 (P <0 .0 5 ) ,且与组织学分级呈负相关。结论 :Fas在调节鳞状上皮细胞自我更新中具有重要作用。Fas表达水平下调 ,FasL上调 ,可能是口腔上皮癌变过程中的一个早期事件。Fas/FasL是肿瘤细胞逃逸肿瘤反应T细胞攻击而获得免疫赦免的重要机制之一。     

口腔异常增生上皮及鳞癌组织细胞凋亡和增殖的研究

目的：了解细胞凋亡、增殖及p53、Bcl—2在口腔异常增生上皮及鳞癌组织中的变化规律。方法：采用TUNEL技术检测细胞凋亡，免疫组化SP法检测PCNA、p53和Bcl—2。结果：从单纯性增生、轻度异常增生、中度异常增生至原位癌、鳞癌，增殖指数逐渐上升；凋亡指数在前三个阶段和增殖指数同时上升，而从原位癌开始，凋亡指数开始下降，鳞癌时达最低峰。p53表达依次增高到鳞癌时出现高峰；Bcl—2在原位癌时表达升高。结论：细胞凋亡和增殖比例失调在口腔鳞癌发生过程中起着重要作用。Bcl—2、p53参与了口腔鳞癌的发生、发展，p53异常是早期且相对持续行为。     

口腔黏膜癌前病变和口腔鳞癌组织Fas/FasL的表达及其意义

目的：研究调亡相关基因Fas／FasL在正常口腔黏膜、上皮异常增生和口腔鳞癌组织中的表达及意义。方法：应用免疫组织化学方法检测10例正常口腔黏膜、26例上皮异常增生、38例口腔鳞癌组织及肿瘤浸润淋巴细胞（TIL）中Fas／FasL的表达。结果：Fas在正常口腔黏膜中广泛表达;上皮异常增生和鳞癌组织表达明显下调（P〈0．05）;Fas表达与口腔鳞癌分化程度有关;FasL在正常口腔黏膜不表达;上皮异常增生和鳞癌组织表达明显上调（P〈0．05）;FasL表达与口腔鳞癌分化程度无关（P〉0．05）;TIL细胞Fas、FasL阳性表达率为81．6％和84．2％。结论：Fas表达与口腔黏膜上皮细胞的自然分化成熟、衰老及口腔鳞癌的形成和肿瘤的恶性度有关;FasL的表达上调可能是口腔鳞癌组织免疫反攻击的体现;Fas、FasL可作为监测口腔上皮癌变的标记物。     

表皮生长因子及其受体在口腔黏膜上皮异常增生和口腔鳞癌中的表达

目的 探讨表皮生长因子(epidermal growth factor,EGF)及其受体(epidermal growth factor receptor,EGFR)与口腔黏膜癌变的关系.方法 ①以30例健康成年人唾液样本为对照,通过放射免疫法对12例上皮异常增生患者、40例口腔鳞癌(oral squamous cell carcinoma,OSCC)患者唾液EGF含量进行测定分析.②采用免疫组化法检测10例正常口腔黏膜,16例上皮异常增生,30例OSCC上皮组织中EGFR的表达水平.结果 ①上皮异常增生组唾液EGF含量[(5.12±4.30)μg/L]显著高于口腔鳞癌[(2.35±1.00)μg/L]和正常对照组[(2.18±1.02)μg/L](P<0.01),OSCC和正常对照组无显著性差异.②上皮异常增生组织中EGFR的表达高于正常黏膜(P<0.05).OSCC中EGFR的表达显著高于正常黏膜(P<0.01).OSCC组和上皮异常增生组织中EGFR的表达无显著性差异.结论 EGF和EGFR可能参与口腔黏膜癌变的早期阶段.     

口腔粘膜上皮异常增生和鳞癌组织中凋亡蛋白Bax的表达研究

目的 研究凋亡相关蛋白Ｂａｘ在口腔正常粘膜、上皮异常增生和鳞癌组织中表达及意义。方法 采用免疫组化方法检测１０例正常粘膜、１０例单纯性增生上皮、３２例异常增生上皮１９例高分化鳞癌、９例低分化鳞癌石蜡包理样本中Ｂａｘ的表达。结果 正常粘膜中见Ｂａｘ弱表达局限于角化层。上皮单纯增生时Ｂａｘ表达较正常组增强,轻度异常增生时反面较单纯增生下降,随异常增生程度加重,Ｂａｘ明显增加。癌变时Ｂａｘ表达较正常组增     

Fas/FasL凋亡途径与口腔肿瘤

凋亡(apoptosis)又称程序性细胞死亡(programmed cell death,PCD),是不同于坏死的生理性细胞死亡方式,对维持机体自身稳定具有重要意义。研究发现,人体多种疾病的发生都与机体细     

口腔鳞癌中Bax,Bcl-2和Survivin 蛋白表达与预后相关性研究

目的:研究凋亡相关蛋白Bax,Bcl-2及Survivin的表达与口腔鳞癌预后的相关性,确定预后判断的有效标志物。方法:采用免疫组织化学方法,检测110例口腔鳞癌患者术后石蜡切片组织中Bax、Bcl-2及Survivin蛋白的表达。通过目标蛋白阳性染色细胞比例和阳性细胞中蛋白的染色强度判定各种蛋白的表达水平;应用SAS 9.0软件中的Kaplan-Meier及Cox回归分析Bax、Bcl-2及Survivin蛋白表达与口腔鳞癌预后的相关性。结果:110例标本检测和统计分析结果表明,Bax、Bcl-2和Survivin蛋白单独表达水平与口腔鳞癌术后生存时间并无显著的相关性;Bcl-2/Bax的比值与口腔鳞癌的术后生存时间呈显著相关(P<0.05)。结论:口腔鳞癌患者组织标本中的Bcl-2/Bax值是影响预后的重要指标,提示该指标在临床上可作为口腔鳞癌患者预后判断的有效标志物。     

口腔鳞癌中p53、Bcl-2、E-Cadherin以及Ki-67表达与临床病理参数及预后的关系

目的:探讨p53、Bcl-2、E-Cadherin以及Ki-67蛋白在口腔鳞癌中的表达情况,与临床病理相关关系及其预后意义。方法:收集116例手术切除的口腔鳞癌组织,采用免疫组化法检测肿瘤组织中p53、Bcl-2、E-Cadherin、Ki-67蛋白的表达。分析各蛋白的表达以及临床病理特征的相关性,Kaplan-Meier、Cox回归分析患者预后。结果:P53、Bcl-2、E-Cadherin蛋白在肿瘤中的表达率分别为75%(87/116)、19.8%(23/116)、91.4%(106/116);Ki-67蛋白在肿瘤中阳性表达率<50%为31.0%(36/116),≥50%为69.0%(80/116)。P53的表达与肿瘤原发部位、神经浸润情况密切相关(P<0.05),E-Cadherin的表达与肿瘤原发部位、神经浸润情况密切相关(P<0.05),Ki-67的表达与浸润前沿的情况、神经侵犯密切相关(P<0.05)。Kaplan-Meier分析结果显示,p53、E-Cadherin阳性组OSCC患者3年总生存率低于阴性组,且差异具有统计学意义(P<0.05)...     

Elevated serum levels of the apoptosis related molecules TNF-α, Fas/Apo-1 and Bcl-2 in oral lichen planus

BACKGROUND: The serum circulatory levels of apoptosis related molecules measured in patients with oral lichen planus (OLP) and healthy individuals in order to investigate possible alterations associated with the clinical forms of OLP. METHODS: Serum levels of tumor necrosis factor (TNF)-alpha, soluble Fas (sFas) and Bcl-2 studied by enzyme-linked immunosorbent assay in whole blood samples in 13 OLP reticular, 13 OLP atrophic-erosive form patients and 26 healthy subjects. RESULTS: Significantly elevated levels of TNF-alpha and sFas detected in OLP patients as compared with controls. Serum concentrations of Bcl-2 although increased in 17/26 patients, they were not statistically significant. Reticular OLP exhibited slightly elevated TNF-alpha and significantly elevated Bcl-2 serum levels, compared with erosive OLP. CONCLUSIONS: These data suggest that a putative dysfunction in the Fas/FasL mediated apoptosis might be involved in the OLP pathogenesis. A downregulation of Bcl-2 serum levels in the atrophic-erosive OLP may be associated with promotion of the disease activity.     

Suppression of Fas receptor and negative correlation of Fas ligand with differentiation and apoptosis in oral squamous cell carcinoma

Apoptosis and the expression of Fas receptor (Fas) and Fas ligand (FasL) were studied in 8 samples of normal oral mucosa (OM) and in 19 oral squamous cell carcinomas (OSCC) by immunohistochemistry and the TUNEL method. Fas was detected in less than 2% of cells of OSCC compared with 84.3 ± 9.0% of cells in the basal layer in OM. FasL was found to be highly expressed in poorly differentiated lesions (90.9 ± 3.6%), and in cells of both the basal (88.3 ± 4.3%) and central (85.3 ± 5.7%) parts of moderately differentiated lesions, whereas in well-differentiated (WD) lessions expression was considerably lower in both basal (42.7 ± 4.1%) and central (11.5 ± 2.4%) parts. In normal OM FasL was primarily detected in cells of the basal layer, but in a high proportion of cells (84.9 ± 4.3%). Apototic cell death was greater in OSCC (1.6 ± 0.6%) than in OM (0.6 ± 0.2%, P <0.05) and was most pronounced in the central part of WD OSCC (2.3 ± 0.5%). Our results show that Fas is expressed in low quantities in OSCC and that FasL expression correlates negatively with degree of differentiation and apoptosis in OSCC.     

伴放线放线杆菌诱导T淋巴细胞通过Fas-FasL途径的细胞凋亡的研究

目的 :检测与Aa诱导T淋巴细胞凋亡有关的Fas(CD95 )介导的细胞凋亡途径。方法 :选取 10名全身及牙周组织健康受试者 ,分离外周血单核细胞 (PBMC) ,Aa体外刺激PBMC ,用特殊的单克隆抗体 (Fas、FasL)标记 ,并进行流式细胞仪检测。结果 :Fas和FasL的表达量明显上调。实验组Fas:2 4h - 2 7.2 2 %± 4 .10 ,96h - 6 8.2 6 %± 3.14 ;FasL :2 4h 6 .18%± 1.37,96h - 2 2 .6 4 %± 2 .82。用抗Fas单克隆抗体阻滞Fas-FasL相互作用导致明显的T细胞凋亡减少 ,百分比为 2 2 .72 %± 3.5 4 ,未加抗体的为 5 1.4 7%± 3.75。 (P <0 .0 0 0 5 ,但残余的细胞凋亡活动比阴性对照仍高。结论 :Aa诱导T淋巴细胞主要通过Fas -FasL途径凋亡 ,在细胞凋亡的分子机制上得到了数据证明 ,且有时间依赖性     

Toombak-associated oral mucosal lesions in Sudanese show a low prevalence of epithelial dysplasia

Clinical ( n =281) and histopathological ( n =141) characteristics of toombak-associated oral mucosal lesions detected in an epidemiological study in northern Sudan in 1992/93 are described. The lesional site in the majority of toombak users was the anterior lower labial groove and the lower labial mucosa. 4 degrees (1–4) of clinical severity of lesions, similar to those used to characterise Swedish snuff-dipper's lesion, were applied. An association between the severity of mucosal lesions and a longer lifetime duration (>10 years) of toombak use was found, but the severity was not related to the daily frequency of the habit. Parakeratosis, pale surface staining of the epithelium and basal cell hyperplasia were commonly observed, but epithelial dysplasia was infrequent (10/141). The most significant observation was a PAS-positive amorphous deposit between the lamina propria and the submucosa, found in 25/141 biopsies. The clinical and histopathological features of toombak lesions are closely similar to Swedish moist snuff-dipper's lesions and this may reflect the high alkalinity of these products, resulting in an alkaline burn on the oral mucosa following chronic exposure. The low prevalence of epithelial dysplasia implies a low risk of malignant transformation. Nevertheless, the high concentrations of tobacco-specific nitrosamines present in toombak, and the high prevalence of oral cancer in Sudan, mandate biopsy and careful histopathological analysis of any such lesions detected in habitues.     

口腔白斑和癌组织中Smad4、Bel-2的表达及其相关性研究

目的：检测口腔白斑和癌组织中Smad4和Bcl-2的表达情况，探讨二者在口腔白斑的癌变过程中的变化及其相互关系。方法：免疫组织化学SABC法检测Smad4蛋白表达情况及Polymer法检测Bcl-2蛋白的表达情况。结果：Smad4蛋白在正常组织、白斑及癌组织中阳性表达率分别是100.0％、92.3％和33.3％，阳性表达差异有统计学意义（P〈0.01）；Bcl-2蛋白在正常组织中、白斑及癌组织中阳性表达率分别是30.0％、53.8％和100.0％，阳性表达差异有统计学意义（P〈0.01）；Smad4蛋白表达与Bcl-2蛋白表达呈负相关（r=-0.854，P〈0.01）。结论：Smad4和Bcl-2可能参与了口腔癌变的过程：在鳞癌的发生发展过程中，Smadd缺失表达和Bcl-2的过表达两者可能单独或协同参与。     

Content and distribution of glycogen in oral epithelial dysplasia

Abstract— Forty-four oral lesions with epithelial dysplasia and 25 other benign and malignant lesionsof the oarl mucosa were examined after ataining with hematoxylin-eosin and diastase controlled PAS. The intensity of the PAS-Positivity for glycogen, The grade of dysplasia, the type of keratinization and the degreeof subepithelial inflmmation were recored. Histologically normal epithelium at the margins of the lesions were used as controls. The presence and amount of glycogen in normal epithlium varied with the Form of keratinization in that non-orparakeratinized epithelium was rich in glycogen where as there was a negative glycogen-reaction in orthokeratinized epithelium. The most striking feature was and abrupt limitation of the glycogen at the junction between nondysplastic and dysplastic epithlium. The difference in the amount of glycogen in normal and dysplastic epithlium as assessed semiquantitativbely, was statistically significant. The diastase controlled PAS-staining may therefore be a useful method of distinguishing dysplastic form nondysplastic epithlium in doubtjurl cases. Pseudoepitheliomatous hyperplastic epithelium covering granular cell myoblastoma did not contain any glycogen. Five of six squamous cell acrcinomas nand four verrucous carcinomas contained no demosstrable glycogen. Glycogen was present in the epithelium of the cases of lichen planus and "denture hyperplasia" investigated.