良性淋巴上皮病变及其恶性变中上皮性成分的免疫组化研究

采用抗肌动蛋白单克隆抗体HHF35和抗细胞角蛋白单克隆抗体AE1/AE3对10例良性淋巴上皮病变和3例恶性淋巴上皮病变中上皮性成分的构成细胞进行了免疫组织化学研究。结果发现：良性淋巴上皮病变中上皮岛构成细胞在部分HHF35呈阴性，仅在外周可见少许HHF35阳性细胞。AE1／AE3抗体在上皮岛构成细胞中大部分呈阳性。恶性淋巴上皮病变中癌巢内AE1／AE3抗体呈弥漫阳性，HHF35抗体主要分布在癌巢外周细胞。讨论了良性淋巴上皮的发生、发展、诊断及鉴别诊断方面存在的问题。     

36例良、恶性淋巴上皮病临床病理分析

目的：分析恶性淋巴上皮病（MLEL）、良性淋巴上皮病（BLEL）及与之相联系的黏膜相关淋巴组织型结外边缘区B细胞淋巴瘤（MALToma）的临床特点、病理学特征、发病机制、诊断、治疗及转归。方法：对13例MLEL、20例BLEL及3例MT进行免疫组化染色和HE染色观察，复习相关临床资料并随访。结果：MLEL的病理学特征为大量增生的淋巴组织中见成簇或条索状分布的肿瘤细胞，界限不清，核分裂像多见；免疫组化示CKpan全部阳性（13／13），Vim部分阳性（3／13），SMA部分阳性（2／13）；8例MLEL可随访资料中，术后1例死于复发，1例死于其他疾病，1例局部复发，5例未见复发或转移，随访3．5个月-4a。BLEL的病理学特点为腺实质萎缩，间质淋巴细胞浸润及形态温和的腺肌上皮岛；免疫组化示CKpan19例阳性，LCA17例阳性。UCHL-1、L2616例阳性。CK10 10例阳性．S-1002例阳性；12例可随访的BIEL中，2例术后复发诊断为MLEL，其余健在，随访3个月～6a不等。3例MT中。1例术后6个月复发，经再次手术并化疗后缓解；免疫组化L26、LCA、CD79、CD43均阳性；UCHL-1、CKpan、EMA均有2例阳性。结论：MLEL好发于腮腺，且女性多见，来源于唾液腺导管上皮。对已发生颈淋巴结转移的患者行原发灶一颈联合根治，术后放疗，少数MLEL可在BLEL基础上发生，故BLEL局部切除后应长期随访；MT为B细胞淋巴瘤，手术切除辅以适当化疗可获较好疗效。术中冷冻切片是本病目前最可靠的术中诊断手段。     

Ki-67、 PI3K、 Beclin1在口腔鳞癌组织中的表达及意义

目的：检测Ki-67、磷酸肌醇-3-激酶（PI3K）、Beclin1在口腔鳞癌组织中的表达及意义。方法：选取2017年1月—2018年12月南京市口腔医院收治的口腔鳞癌患者30例,取所有手术切除癌组织及癌旁组织标本,进行免疫组织化学染色处理,并检测Ki-67、PI3K、Beclin1的表达,采用Pearson分析TMSG-1、Ki-67、Pgp1之间的相关性。采用SPSS 20.0软件包对数据进行统计学分析。结果：口腔鳞癌癌组织中Ki-67、PI3K阳性表达率显著高于癌旁组织,Beclin1阳性表达率显著低于癌旁组织（P<0.05）。Ki-67、PI3K、Beclin1在高分化口腔鳞癌中的阳性表达率显著高于中分化、低分化口腔鳞癌（P<0.05）。Ki-67、PI3K在有淋巴结转移的口腔鳞癌中的阳性表达率显著高于无淋巴结转移的口腔鳞癌,Beclin1在有淋巴结转移的口腔鳞癌中的阳性表达率显著低于无淋巴结转移的口腔鳞癌（P<0.05）。Ki-67、PI3K、Beclin1在Ⅰ+Ⅱ期、Ⅲ+Ⅳ期口腔鳞癌中的阳性表达率无统计学差异（P>0.05）。Ki-67与PI3K的表达呈正相关（r=0.391,P=0.032）,Ki-67与Beclin1的表达呈负相关（r=-0.525,P=0.02）,Beclin1与PI3K的表达呈负相关（r=-0.367,P=0.045）。结论：Ki-67、PI3K、Beclin1的表达具有相关性,与患者有无淋巴结转移、病理分期有关,可能参与口腔鳞癌发生与发展。     

细胞角蛋白在牙龈鳞癌颈淋巴结中的表达及临床意义

目的　研究细胞角蛋白（CK-AE1/AE3）在牙龈鳞状细胞癌颈淋巴结 中的表达及临床意义。方法　将17例牙龈鳞癌患者病理报告为阳性的28枚淋巴结及139枚阴性淋巴结重新切片,应用广谱细胞角蛋白单克隆抗体（AE1/AE3）作为免疫标志物,采用免疫组织化学（SP法）检测抗体在淋巴结中的表达。结果　167枚淋巴结中,28枚HE染色阳性的淋巴结CK表达均为阳性;另有11枚HE染色阴性淋巴结CK表达为阳性,其位于Ⅰ区6枚,Ⅱ区5枚,共分布在9例患者中。结论　采用CK（AE1/AE3）作为免疫标志物的免疫组化法检测牙龈鳞状细胞癌的淋巴结,较传统HE染色法更为准确,有利于早期发现微转移灶,从而为牙龈癌的治疗及预后判断提供依据。     

P27kipl��Ki-67�ڿڵ���״ϸ�����еı�Ｐ����

目的    探讨P27kipl和Ki-67在口底鳞状细胞癌中的表达水平及其与肿瘤分化程度、淋巴结转移、预后的关系。方法    收集枣庄矿业集团中心医院病理科1998年1月至2004年12月的口底鳞状细胞癌手术根治标本蜡块及其相应的癌旁正常黏膜组织（距肿物1.5 cm）蜡块各45例，应用免疫组织化学染色S-P方法进行P27kipl、Ki-67基因蛋白的检测。结果    癌旁正常黏膜中，P27kipl高表达率为75.56%、Ki-67阳性表达率为8.89%，口底鳞状细胞癌中P27kipl高表达率为22.22%、Ki-67阳性表达率为35.56%，经比较两组间差异均有统计学意义（均P＜0.01）。口底鳞状细胞癌分化较好者，P27kipl高表达率（26.92%）高于分化较差者（15.79%），但差异无统计学意义（P＞0.05）；Ki-67阳性表达率在分化较好者（23.08%）与较差者（52.63%）间差异有统计学意义（P＜0.05）。P27kipl高表达率、Ki-67阳性表达率在有、无淋巴结转移中比较，差异均有统计学意义（均P＜0.05）。P27kipl高表达率、Ki-67阳性表达率在术后存活期中比较，差异亦均有统计学意义（均P＜0.05）。结论    P27kipl、Ki-67在口底鳞状细胞癌中起重要的调控作用，并是判断其预后的重要参考指标。     

CD44与CD33在77例口腔黏膜良性淋巴组织增生病中的表达及临床意义

目的：探讨CD44与CD33在口腔黏膜良性淋巴组织增生病（benign lymphoadenosis of oral mucosa,BLOM）中的表达及临床意义。方法：选择2017年1月—2020年3月青岛市中医医院病理科77例BLOM蜡块作为实验组，另取同时间段63例正常口腔黏膜组织蜡块作为对照组。采用免疫组织化学法检测2组CD44、CD33阳性表达情况，采用Spearman分析BLOM患者病变组织中CD33与CD44阳性表达的相关性。收集患者一般资料，分析BLOM患者病变组织中CD33、CD44表达与临床病理特征的关系。采用SPSS 21.0软件包对数据进行统计学分析。结果：对照组、实验组CD33阳性表达率分别为95.24%、63.64%，差异有统计学意义（P<0.05）;CD44阳性表达率分别为93.65%、67.53%，差异有统计学意义（P<0.05）。Spearman分析结果显示，BLOM患者病变组织中CD33与CD44阳性表达呈正相关（r=0.834,P=0.002）;CD33、CD44表达与临床分型、炎症程度、有无淋巴滤泡、淋巴细胞浸润有关（P<0.05...     

牙源性角化囊性瘤Ki-67抗原表达与其影像学特征的相关性研究

目的研究Ki-67抗原在颌骨牙源性角化囊性瘤（keratocystic odontogenic tumor,KOT）上皮的表达与其临床病理特征及影像学特征有无相关性。方法选取40例经病理检查证实为KOT的患者,按影像学特征将所有患者进行分类,并对其手术切除标本之存档石蜡块分别行Ki-67抗原免疫组织化学染色。观察每张切片,有明显的细胞核棕黄色着色者视为Ki-67抗原阳性。将每张切片按等距抽样原则随机摄取10个视野输入计算机,采用IMAGE PRO PLUS图像分析软件测定阳性面积率、平均光密度及积分光密度。结果 Ki-67抗原的表达与KOT大小及患者性别无明显相关性。青少年KOT患者上皮的Ki-67抗原表达与成人及老年患者有差异,多囊性KOT的Ki-67抗原表达强度与单囊性KOT及基底细胞痣综合征者有差异,基底细胞痣综合征者与多发性KOT者的Ki-67抗原表达有差异。结论 KOT的影像学特征与Ki-67抗原在上皮的表达存在相关性,不同影像学特征对KOT的细胞增殖活性有一定提示意义。     

原发咽旁滑膜肉瘤1例

本文报告1例咽旁滑膜肉瘤,患者男,15岁,以左咽旁无痛性逐渐增生包块1月就诊。专科检查发现左侧咽旁有一大小约8 cm×4 cm×3 cm肿物,蒂部位于左扁桃体上隐窝。影像学检查见左侧口咽不规则肿块,与左舌根后份分界不清,增强扫描明显不均匀强化。免疫组织化学检查：上皮细胞膜抗原（+）,细胞角蛋白（CK）19（+）,CD7（+）,波形蛋白（+）,CK10（-）,钙黏蛋白（+）,B淋巴细胞瘤-2（-）,CD2（-）,CD10（-）,CD138（+）,CD99（+）,白细胞共同抗原（+）,Ki-67（20%+）。病理诊断为咽旁滑膜肉瘤。     

量子点荧光探针检测人舌鳞状细胞癌荷瘤裸鼠模型早期下颌下淋巴结转移的研究

目的 利用量子点标记的特异性细胞角蛋白抗体QDs605-CK（AE1/AE3）免疫荧光探针检测人舌鳞状细胞癌荷瘤裸鼠早期下颌下淋巴结转移率及微转移率,并与传统的免疫组织化学（IHC）染色及苏木精-伊红（HE）染色方法进行比较,为舌鳞状细胞癌的早期诊断与治疗提供一种新的检测方法。方法 传代培养人舌鳞状细胞癌Tca8113 细胞,接种于18只裸鼠舌体内（不过中线）,建立人舌癌荷瘤裸鼠下颌下淋巴结转移模型。接种6周后,处死裸鼠,解剖下颌下淋巴结,将同一淋巴结分为两份。一份作石蜡包埋半连续切片,行HE染色和IHC检测;另一份即刻液氮冷冻,制作冰冻切片行QDs605-CK（AE1/AE3）荧光探针检测。分别计算3种方法检测出的淋巴结转移率和微转移率。结果 量子点标记的免疫荧光染色检测出裸鼠下颌下淋巴结转移率为66.7%,其中微转移率为38.9%;IHC染色检测的淋巴结转移率为61.1%,其中微转移率为33.3%;HE染色检测的淋巴结转移率为27.8%。经统计学分析,3种方法的差异有统计学意义（χ2=6.379,P<0.05）,量子点标记的免疫荧光染色和IHC检测都优于HE染色,但是量子点标记的免疫荧光染色和IHC染色间的差异无统计学意义（χ2=0.120,P>0.05）。结论 量子点标记的QDs605-CK（AE1/AE3）免疫荧光探针能准确定位于下颌下淋巴结转移的肿瘤细胞的细胞质内,发出红色荧光,其特异性强,分辨率高,背景清晰,能够用于淋巴结转移灶及微转移灶的检测。     

中文文摘

1．量子点荧光探针检测人舌鳞状细胞癌荷瘤裸鼠模型早期下颌下淋巴结转移的研究 传代培养人舌鳞状细胞癌 Tca8113细胞，接种于18只裸鼠舌体内（不过中线），建立人舌癌荷瘤裸鼠下颌下淋巴结转移模型。接种6周后，处死裸鼠，解剖下颌下淋巴结，将同一淋巴结分为两份。一份作石蜡包埋半连续切片，行 HE染色和 IHC 检测；另一份即刻液氮冷冻，制作冰冻切片行QDs605-CK（AE1／AE3）荧光探针检测。分别计算3种方法检测出的淋巴结转移率和微转移率。结果：量子点标记的免疫荧光染色检测出裸鼠下颌下淋巴结转移率为66．7％，其中微转移率为38．9％；IHC 染色检测的淋巴结转移率为61．1％，其中微转移率为33．3％；HE 染色检测的淋巴结转移率为27．8％。经统计学分析，3种方法的差异有统计学意义（P ＜0．05），量子点标记的免疫荧光染色和 IHC 检测都优于 HE 染色，但是量子点标记的免疫荧光染色和 IHC 染色间的差异无统计学意义（P ＞0．05）。结论：量子点标记的QDs605-CK（AE1／AE3）免疫荧光探针能准确定位于下颌下淋巴结转移的肿瘤细胞的细胞质内，发出红色荧光，其特异性强，分辨率高，背景清晰，能够用于淋巴结转移灶及微转移灶的检测。     

Basal cell adenocarcinoma of the salivary gland: an ultrastructural and immunohistochemical study

OBJECTIVE: The purpose of this study was to examine the ultrastructural and immunohistochemical characteristics of basal cell adenocarcinoma. STUDY DESIGN: Three cases of basal cell adenocarcinoma of the salivary glands were studied by means of light microscopy, electron microscopy, and immunohistochemistry. RESULTS: Some of the architectural tumor patterns encountered were solid, some were trabecular, and some were mixed. Ultrastructurally, solid areas were composed of nonluminal cells, some of which contained tonofilaments and well-formed desmosomes; tubulo-trabecular areas differentiated into both luminal and nonluminal cells. Both growth patterns were associated with the formation of excess basal lamina, marginally and between nonluminal cells. Myofilaments were infrequent in nonluminal cells of solid or trabecular areas. Cytokeratin (AE1/AE3) stained all 3 tumors, more peripherally in the solid pattern and usually centrally in the trabecular areas; vimentin stained all 3 tumors diffusely; smooth muscle actin (IA4) stained all 3 tumors but was mainly confined to peripheral tumor cells in both the solid and the trabecular growth patterns; epithelial membrane antigen and carcinoembryonic antigen stained 1 of the 3 tumors, predominantly in the luminal cells; p53 oncoprotein was focally positive in 2 of the 3 tumors; Ki-67 stained less than 5% of the tumor cells in all cases; and c-erb-B2 was uniformly negative in all cases. Staining patterns of cytokeratin and actin varied with the architecture of the tumor. CONCLUSIONS: Neither ultrastructural characteristics nor immunohistochemistry findings appear to distinguish basal cell adenocarcinoma from basal cell adenoma.     

CD147和Ki-67在口腔黏膜白斑和鳞癌组织中的表达及意义

目的：观察CD147和ki-67在口腔正常黏膜、白斑和鳞癌组织中表达的变化,阐明CD147在口腔癌发病机制中的作用。方法：采用免疫组织化学法检测10例正常口腔黏膜、20例白斑伴上皮异常增生上皮和40例鳞癌组织中CD147及Ki-67的表达变化。结果：CD147在正常黏膜阴性表达,白斑和鳞癌组上皮均显著表达CD147;正常组Ki-67表达主要位于上皮棘层,鳞癌组织中Ki-67阳性细胞分布广泛,有大部分侵入固有层中。结论：口腔黏膜发生癌前病变时,即出现CD147表达阳性,随着Ki-67阳性细胞数的增多,癌变细胞增殖不断加强,两者共同作用促进鳞癌的发展。     

涎腺良性淋巴上皮病变中上皮岛的免疫组织化学和电镜研究

采用抗肌动蛋白单克隆抗体ＨＨＦ３５和抗细胞角蛋白抗体ＡＥ１／ＡＥ３对１０例涎腺良性淋巴上皮病变（ＢＬＥＬ）中上皮岛的构成细胞进行免疫组织化学研究，同时对３例ＢＬＥＬ进行电镜研究。结果发现：涎腺ＢＬＥＬ中构成上皮岛的细胞大部分呈ＨＨＦ３５阴性，仅在外周可见少许ＨＨＦ３５阳性细胞，而ＡＥ１／ＡＥ３在上皮岛构成细胞中大部分呈阳性。超微结构发现上皮岛大部分由含张力原纤维束的细胞构成，这些细胞结构与残存导管上皮细胞相似，细胞之间散在分布着淋巴细胞和浆细胞。上皮岛外周有时可见含肌微丝的肌上皮样细胞。此结果表明，涎腺ＢＬＥＬ中上皮岛起源于增生的导管上皮，构成细胞主要为导管上皮细胞     

Comparison of proliferation,apoptosis and expression of syndecan-1 and α-SMA in edentulous ridge oral mucosa of successful and early failed submerged dental implants—An immunohistochemical study

AimsPathogenic mechanisms involved in early submerged implant failure are poorly understood. In this study we immunohistochemically analyse differences in proliferation, apoptosis and inflammation in edentulous ridge oral mucosa (ERM) of successful and early failed submerged implants.Materials and methods30 samples of ERM covering successful and early failed submerged implants were obtained at the end of osseointegration period along with control samples of healthy ERM. Sections were stained with Ki-67 (proliferation), caspase-3 (apoptosis) and syndecan-1 (epithelial marker). Percentage of positive cells was analysed by Kruskal-Wallis test and Dunn’s post hoc test. Co-localization of Ki-67 and caspase-3 with α-SMA, CD68 and TGF-β was done by double immunofluorescence.ResultsThere was no significant difference in number of Ki-67 positive cells within surface epithelium (SE) in all groups. Proliferation was significantly higher in underlying connective tissue (UCT) of ERM of early failed submerged implants (26%) compared to ERM of successful submerged implants (3%) and controls (4%). More apoptotic cells appeared in UCT of early failed submerged implants (8%) compared to UCT of successful submerged implants (4%) and UCT of control ERM (3%). Co-localization of Ki-67 and α-SMA in ERM of early failed submerged implants disclosed proliferating fibroblasts and pericytes of blood vessels. Macrophages and cells expressing TGF-β appeared in UCT of failed implants. Expression of syndecan-1 was significantly weaker in SE of early failed submerged implants.ConclusionsImbalance between proliferation and apoptosis, changes in syndecan-1 expression and inflammation are histopathological features of ERM of early failed submerged implants.     

Multiple parotid lymphoepithelial cysts in patients with HIV-infection: report of two cases

OBJECTIVE: Bilateral and multiple lymphoepithelial cysts (LECs) of major salivary glands, in particular of parotid glands, are quite rare and have been reported in human immunodeficiency virus (HIV) infected patients with an incidence of about 3-6%. These lesions represent an early manifestation of HIV infection and are rarely found in patients with advanced acquired immunodeficiency syndrome. MATERIALS: Two cases of parotid LECs, the first occurring in a middle-age white woman and the second in a young white boy, both in advanced phases of HIV infection, are reported. RESULTS: Clinical, cytological, histological and immunohistochemical (cytokeratin AE1/AE3, CD20, CD45RA, CD8, kappa and lambda immunoglobulin light chains, S-100, MLA and Ki67) features are described. CONCLUSIONS: Fine needle aspiration (FNA), a relatively non-traumatic procedure, could represent both a diagnostic and a therapeutic tool in parotid LECs. No surgical therapy is usually required for these lesions and aspiration of cystic fluid with FNA is quite resolutive, although evidence of further relapses does exist. Surgical excision may become necessary when pain, because of persistent and progressive swelling of the parotid gland, occurs.     

Analysis of the Ki-67 antigen at the invasive tumour front of human oral squamous cell carcinoma

BACKGROUND: It is hypothesised that cell proliferation, as measured by the Ki-67 labelling index (LI) at the invasive tumour front (ITF) was directly related to the histological grade in human oral squamous cell carcinomas (SCCs). METHODS: Tissues from 42 human oral SCCs were collected and stained with an antibody directed against the Ki-67 antigen using an advanced polymer staining system. Quantitation of the immunopositive cells was performed on two parallel sections at the invasive tumour front (ITF), using an image analyser. The Ki-67 LI was expressed as the number of positive nuclei/mm2 of epithelium. The control tissue used was normal epithelium at the excision margin. RESULTS: The mean Ki-67 LI for oral SCCs at the ITF was significantly greater than that for the excision margin tissue (P < 0.0001). There was a positive association between increasing Ki-67 LI and increasing Broders' grade (P < 0.05), with a well-differentiated tumour having the lowest mean Ki-67 LI (1549 +/- 806) and a poorly differentiated tumour having the highest value (2232 +/- 771). A similar trend was observed between the mean Ki-67 LI and Bryne's multifactorial grading system. CONCLUSIONS: It was concluded from this study that cell proliferation (as measured by the Ki-67 antigen) at the ITF had a strong positive relationship with histological grading in human oral SCC.     

Nuclear DNA content, an adjunct to p53 and Ki-67 as a marker of resistance to radiation therapy in oral cavity and pharyngeal squamous cell carcinoma

Factors of prognosis and radioresistance in oral cavity and pharyngeal squamous cell carcinoma (OCPSCC) are limited. In the present study, the usefulness of tumor DNA content in predicting radioresistance in patients with OCPSCC has been investigated. Radioresistance has been defined as local recurrence or tumor persistence after radiation therapy. DNA-ploidy analysis was performed by static cytometry on smears of cell suspensions obtained from formalin-fixed paraffin-embedded material and stained with Feulgen. DNA-ploidy was correlated with the proliferation rate (Ki-67) and p53 protein accumulation obtained by immunohistochemistry. The follow-up of patients ranged from 8 to 62 months. Radioresistance was more common in non-diploid tumors; 14/28 (50%) non-diploid tumors recurred, whereas only 3 (10.7%) out of 28 diploid tumors had local failure (P=0.0019). Proliferation rate and p53 accumulation, evaluated by immunohistochemistry, also added prognostic information. Twelve out of 14 failures were from non-diploid tumors with a low proliferation rate (Ki-67<20%), whereas none of 20 p53-negative diploid tumors developed recurrences. This study showed that non-diploid tumors responded poorly to radiotherapy. DNA content appeared, therefore, as a significant prognostic marker for the evaluation of OCPSCC in patients receiving radiation therapy. This study also showed that DNA content adds information to p53 accumulation and the proliferation rate (Ki-67) for the purposes of determining patient management.     

Co-expression of Ki-67 and p53 protein in ameloblastoma and keratocystic odontogenic tumor

Abstract Objectives. The purpose of this study was to evaluate the cell proliferation and p53 protein expression in ameloblastomas (ABs), keratocystic odontogenic tumor (KCOT) and dentigerous cyst (DC). Method. The immunohistochemistry were carried out for Ki-67 and p53 protein expression by using MIB-1 clone and DO-7 clone, respectively, in ABs (n = 23), KCOT (n = 32), DC (n = 30), normal oral mucosa (NOM) (n = 12) and fetal oral mucosa (FOM) (n = 10). Results. Both the Ki-67 LI Labeling index (LI) and p53 LI was significantly higher in ABs than KCOT, DC, NOM and FOM. The Ki-67 LI and p53 LI was significantly higher in KCOT as compared to DC. Ki-67 LI and p53 LI was observed in descending order in ABs, KOCT, FOM, NOM and DC. There was significant correlation between Ki-67 expression and p53 expression in ABs, KCOT, DC and NOM. The densely stained p53 positive cells were noted higher in ABs than KCOT. The very few densely p53 positive cells were noted in DC, NOM and FOM. Conclusion. The results suggest that the p53 protein expression does not necessarily imply an association with malignant disease and/or p53 gene mutation, but a tendency to be expressed in an increasing quantitative and qualitative manner, as the biologic behavior of odontogenic cyst or tumors becomes more aggressive. p53 over-expression may promote cell proliferation in odontogenic lesions. Thus, it can be stipulated that Ki-67 and p53 protein expression can be used as a prognostic marker in odontogenic lesions.     

磷酸化p38促分裂原活化的蛋白激酶、尿激酶型纤溶酶原激活物及Ki-67在牙源性上皮性肿瘤中的表达

目的 检测磷酸化p38促分裂原活化的蛋白激酶(phosphorylated-p38 mitogen-activated protein kinase,p-p38MAPK)、尿激酶型纤溶酶原激活物(urokinase plasminogen activator,uPA)及Ki-67在牙源性上皮性肿瘤中的表达,探讨p-p38MAPK对牙源性上皮性肿瘤细胞增殖活性及侵袭性的影响.方法 根据2005年WHO关于牙源性肿瘤的分类标准,应用免疫组化方法检测p-p38MAPK、uPA和Ki-67在成釉细胞瘤(ameloblastoma,AB)、牙源性角化囊性瘤(keratocystic odontogenic tumour,KCOT)、牙源性钙化上皮瘤(calcifying epithelial odontogenic tumor,CEOT)、牙源性腺样瘤(adenomatoid odontogenic tumour,AOT)及牙源性钙化囊性瘤(calcifying cystic odontogenic tumour,CCOT)(以上为肿瘤组)和5例牙胚(对照组)中的表达.结果 p-p38MAPK在肿瘤组的阳性表达率为26%(17/65),在肿瘤细胞胞质和胞核均可见着色;uPA在肿瘤组的阳性表达率为78%(51/65),主要表现为肿瘤细胞胞质着色;Ki-67在肿瘤组的阳性表达率为95%(62/65),为弥散的肿瘤细胞胞核着色.p-p38MAPK、uPA和Ki-67在牙源性上皮性肿瘤的阳性表达率显著高于对照组(P＜0.05),三者的阳性表达呈正相关(P＜0.05).结论 p-p38MAPK信号传导通路可能以正性调节的方式调控uPA从而促进牙源性上皮性肿瘤的发生,可能是肿瘤发生、侵袭和增殖的重要途径之一.     

The expression of apoptotic proteins and matrix metalloproteinases in odontogenic myxomas

PURPOSE: The odontogenic myxoma is a rare benign tumor affecting the jaws. We hypothesize that odontogenic myxomas have dysregulated antiapoptotic mechanisms to assist in neoplastic growth. We believe that antiapoptotic proteins of the Bcl-2 family are over expressed and that tumor cells must generate some form of matrix proteinase. The aim of this study was to evaluate odontogenic myxomas for the expression of cell cycle protein Ki-67, apoptosis-regulating proteins Bcl-2, Bcl-XL, Bak, and Bax, and matrix metalloproteinases MMP-2, MMP-3, and MMP-9. MATERIALS AND METHODS: Odontogenic myxomas submitted to oral pathology between 1974 and 1998 were evaluated. Twenty-six paraffin-embedded tissue sections were used in a standard immunohistochemistry protocol and incubated with one of the following antibodies: Bcl-2, Bcl-XL, Bak, Bax, or Ki-67. The sections were then incubated with anti-immunoglobulin conjugated to peroxidase-labeled dextran polymer in a Tris-HCl buffer. Counts of positive (staining) cells were completed in 5 high-power fields for each specimen. Each slide was reviewed by 2 investigators, and final data were pooled and averaged. RESULTS: Specimen slides showed an increase in cells staining positively for anti-apoptotic proteins Bcl-2 and Bcl-X. An average of 6.5% of specimen cells were positive for Bcl-2 and 10.4% for Bcl-X. Control tissue showed only 1.1% of cells to be positive for Bcl-2 and 1.2% for Bcl-X. Less than 1% of both specimen and control cells stained positively for Ki-67. Proapoptotic proteins (Bak and Bax) were not detected in tumor cells. Ninety percent of tumor cells stained positively for MMP-2 compared with 10% of controls. Specimen and controls were negative for MMP-3 and MMP-9. CONCLUSION: Odontogenic myxoma tumor cells did not show an increase in cell division. Less than 1% of tumor and control cells were positive for Ki-67. Odontogenic myxoma tumor cells showed increased expression of antiapoptotic proteins (Bcl-2 and Bcl-X) and the matrix metalloproteinase MMP-2. This study suggests that 2 mechanisms of disease progression used by the odontogenic myxoma are the production of antiapoptotic proteins and the secretion of matrix metalloproteinases.