Patterns of antigenic expression of human glioma cells.
Patterns of antigenic expression of human glioma cells.
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发表时间：
1991
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通讯作者：
Paul E. McKeever;Davenport Rd;P. Shakui
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作者：
Paul E. McKeever;Davenport Rd;P. Shakui
已知神经胶质瘤表达超过100种抗原，毫无疑问，还会产生更多的未知抗原。神经胶质瘤细胞抗原的主要类别包括神经胶质抗原、ECM抗原、肌肉抗原、黑素瘤抗原、“肿瘤特异性”抗原和细胞增殖抗原。培养的胶质瘤表达胶质抗原的数量少得惊人。它们通常不仅表达外胚层，而且表达间充质ECM抗原。肿瘤特异性抗原一直是神经肿瘤学家难以实现的目标，但仍有光明的新前景需要进一步研究。这些方法包括在胶质瘤组织上直接筛选杂交瘤上清液和靶向糖脂、糖蛋白和癌基因产物。细胞增殖抗原在预测胶质瘤预后中将变得越来越重要。目前，对培养的胶质瘤的增殖抗原进行了严格的审查。胶质瘤中肿瘤细胞抗原异质性的程度和演变提出了具有深远临床影响的基本生物学问题。单个神经胶质瘤细胞系可产生30多种亚型的细胞，在抗原表达方面具有微小到主要的差异。这些包括代表多种不同细胞谱系的抗原的表达。间质漂移是胶质瘤逐渐失去胶质细胞并获得间质特征的趋势。体内间充质漂移模型发生在神经胶质瘤细胞培养中，其机制比原位更容易研究。外源性蛋白吸收和成纤维细胞过度生长都不能解释这种现象。间充质标记物纤维连接蛋白的细胞在胶质瘤中过度生长GFAP阳性细胞。许多纤维连接蛋白阳性细胞表达肿瘤的细胞学和生长特征。这些细胞的来源不明。这些肿瘤性纤连蛋白阳性细胞来源的主要候选者是胶质瘤组织的血管和间充质细胞成分的增殖，通常称为“内皮增殖”。然而，组织中的这些元素并不显示与培养中的纤连蛋白阳性细胞相同的瘤形成异常。理解这种“组织/外植体悖论”可能会解决间充质漂移的难题。在没有对应的组织中的这些肿瘤性纤维连接蛋白阳性细胞，所以丰富的神经胶质瘤细胞培养，机制的间充质漂移以外的过度生长的肿瘤间充质必须加以考虑。表达完全不同细胞谱系的抗原标志物的“双细胞”的出现表明肿瘤性胶质细胞通过改变基因表达产生间质漂移的可能性。各种研究表明，培养的胶质瘤改变其基因的表型表达的能力进行了严格的检查，并讨论其相关性间充质漂移。（400字处截断摘要）
Gliomas are known to express over a hundred antigens, and no doubt make many more unknown antigens. Major categories of glioma cell antigens include glial antigens, ECM antigens, muscle antigens, melanoma antigens, "tumor-specific" antigens, and cellular proliferation antigens. A strikingly low number of cultured gliomas express glial antigens. They commonly express not only ectodermal, but also mesenchymal ECM antigens. Tumor-specific antigens have been an elusive goal of neuro-oncologists, but there are bright new prospects in need of further study. These include direct screening of hybridoma supernatants on glioma tissue and targeting glycolipids, glycoproteins, and oncogene products. Cellular proliferation antigens will become increasingly important in predicting prognosis of gliomas. Proliferation antigens of cultured gliomas are under intense scrutiny at present. The extent and evolution of antigenic heterogeneity of neoplastic cells in gliomas raise basic biologic questions with profound clinical ramifications. Individual glioma cell lines may generate more than 30 subtypes of cells with minor to major differences in antigen expression. These include expression of antigens representing multiple different cell lineages. Mesenchymal drift is the tendency of gliomas to progressively lose glial and gain mesenchymal features. Models of in vivo mesenchymal drift occur in glioma cell culture where mechanisms are more easily investigated than in situ. Neither exogenous protein absorption nor fibroblast overgrowth explain the phenomenon. Cells with the mesenchymal marker, fibronectin, overgrow GFAP-positive cells during explanation of gliomas. Many of these fibronectin-positive cells express cytologic and growth characteristics of neoplasia. The source of these cells is unknown. A leading candidate for the source of these neoplastic fibronectin-positive cells is the proliferation of vascular and mesenchymal cell elements of glioma tissue commonly called "endothelial proliferations". However, these elements in tissue do not display the same abnormalities of neoplasia as the fibronectin-positive cells in culture. Understanding this "tissue/explant paradox" may solve the conundrum of mesenchymal drift. In the absence of a counterpart in tissue of these neoplastic fibronectin-positive cells so abundant in glioma cell cultures, mechanisms of mesenchymal drift other than overgrowth of neoplastic mesenchyme must be considered. The occurrence of "dual cells" which express antigenic markers of entirely different cellular lineages suggests the possibility that neoplastic glia generate mesenchymal drift by altered gene expression. Various studies which suggest the capacity of cultured gliomas to alter phenotypic expression of their genes are critically examined and their relevance to mesenchymal drift discussed.(ABSTRACT TRUNCATED AT 400 WORDS)