摘要
目的探讨肺硬化性血管瘤的组织来源。方法回顾性总结49例肺硬化性血管瘤的临床和病理组织学特征，应用组织芯片及免疫组织化学SP法检测49例硬化性血管瘤中广谱细胞角蛋白（CKpan）、上皮细胞膜抗原（EMA）、波形蛋白、甲状腺转录因子（TTF）-1、napsinA、突触素、嗜铬粒素A（CgA）、CD56、E—cadherin、β-catenin、CD117、CD68及转化生长因子（TGF）-β1的表达。结果肿瘤组织中表面立方细胞表达CKpan、EMA、TTF-1、napsinA；多角形细胞表达EMA、TTF-1，不表达CKpan，napsinA的阳性率为16．3％（8／49）。突触素、CgA、CD56两型细胞均呈阴性表达。E-cadherin、B—catenin在49例硬化性血管瘤的表面立方细胞均呈强阳性表达，E-cadherin呈胞膜阳性表达，β-catenin呈胞膜及胞质阳性表达。而多角形细胞E—cadherin不表达（32／49）或弱阳性表达（17／49），且大部分不表达B—catenin，仅部分呈胞质表达。波形蛋白在所有49例硬化性血管瘤的多角形细胞中均见强阳性表达，其中立方细胞仅见少量细胞阳性表达。CD117及CD68阳性的炎性细胞散在分布于多角形细胞间，TGF-β1阳性表达细胞的分布与CD117及CD68阳性者-致。结论肺硬化性血管瘤起源于原始呼吸上皮，多角形间质细胞可能来源于立方细胞的转化。TGF-β1可能在硬化性血管瘤上皮细胞间质转化中起着重要的作用。
Objective To investigate the histogenesis of pulmonary sclerosing hemangioma （PSH）. Methods Tissue microarray and immunohistochemical technique were used to detect the expression of pan- cytokeratin, epithelial membrane antigen（EMA）, vimentin, thyroid transcription factor（TTF）-1, napsin A, synaptophysin, chromogranin A, CD56, E-eadherin, β-catenin, CD117, CD68 and transforming growth factor（TGF） -β1 in 49 cases of PSH. Results Immunohistochemistry revealed that all cuboidal surface cells expressed pan-eytokeratin, EMA, TTF-1 and napsin A. The polygonal cells expressed EMA, TTF-1, napsin A （positive rate 16. 3%, 8/49 ）, but not pan-cytokeratin. Both types of cells were negative for synaptophysin, chromogranin A and CD56. Strong positive staining for E-cadherin and β-catenin appeared on the membrane of euboidal cells in all PSH, with cytoplasm staining for β-eatenin as well. The expression levels of these adhesion molecules decreased in the polygonal cells, with the staining localized to the cytoplasm. E-eadherin staining was not detected or was weak. β-eatenin staining was not detected on the cell membrane but partially in the cytoplasm. The polygonal cells stained strongly for vimentin, while only a few cuhoidal cells were positive. CDll7 and CD68 positive inflammatory cells were scattered between the polygonal ceils, which was consistent with the distribution of TGF-β1 positive cells. Conclusions PSH originates from the primitive respiratory epithelium, and polygonal stromal cells may be derived from epithelial-mesenchymal transformation of the cuboidal cells. TGF-β1 may play an important role in the formation of selerosing hemangioma.
出处
《中华病理学杂志》
CAS
CSCD
北大核心
2012年第4期239-242,共4页
Chinese Journal of Pathology
基金
基金项目：北京市科技新星计划项目（2009BG-02）
关键词
肺肿瘤
肺硬化性血管瘤
免疫组织化学
Lung neoplasms
Pulmonary sclerosing hemangioma
Immunohistoehemistry
