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经典型和细胞型神经鞘瘤的克隆性染色体异常及体外生长特征

Clonal chromosome abnormalities and in vitro growth characteristics of classical and cellular schwannomas.

作者信息

Stenman G, Kindblom L G, Johansson M, Angervall L

机构信息

Department of Oral Pathology, University of Göteborg, Sweden.

出版信息

Cancer Genet Cytogenet. 1991 Nov;57(1):121-31. doi: 10.1016/0165-4608(91)90197-3.

DOI:10.1016/0165-4608(91)90197-3
PMID:1756478
Abstract

Cytogenetic analysis was performed on 12 schwannomas, 10 classical and two of the cellular type. Electron microscopic examination of cultured cells from two classical and two cellular schwannomas revealed features compatible with a Schwann cell differentiation. Immunohistochemical analysis of the cultures demonstrated immunoreactivity for S-100 protein in 6 of 6 cases and for vimentin in 2 of 2 cases of classical schwannoma, thus further supporting the authenticity of the cultured cells. Cultured cells from one cellular schwannoma also exhibited immunoreactivity for glial fibrillary acid protein (GFAP). Cytogenetic analysis of the 12 tumors revealed clonal abnormalities in 10 of the cases. In the majority of tumors, cells with a normal karyotype coexisted with different abnormal clones and sporadic deviations. Numerical changes predominated and were found in all tumors, while structural rearrangements were detected in eight tumors. The most common abnormality was clonal or sporadic loss of chromosome 22, which was found in all cases. Other clonal abnormalities included loss of one sex chromosome found in five cases, -15 found in three cases, and -12, +5, +7, +20 found in two cases each. These results provide further evidence in support of a role for loss of chromosome 22 in the pathogenesis of schwannomas. Our findings also indicate that there exist several different evolutionary pathways for schwannomas, and that some of these are shared by several other types of benign and malignant tumors of the nervous system.

摘要

对12例神经鞘瘤进行了细胞遗传学分析,其中10例为经典型,2例为细胞型。对2例经典型和2例细胞型神经鞘瘤的培养细胞进行电子显微镜检查,发现其特征与施万细胞分化相符。对这些培养物进行免疫组织化学分析,结果显示,6例经典型神经鞘瘤中有6例对S-100蛋白呈免疫反应,2例中有2例对波形蛋白呈免疫反应,从而进一步支持了培养细胞的真实性。1例细胞型神经鞘瘤的培养细胞对胶质纤维酸性蛋白(GFAP)也呈免疫反应。对这12例肿瘤进行细胞遗传学分析,发现10例存在克隆性异常。在大多数肿瘤中,核型正常的细胞与不同的异常克隆及散在的变异共存。以数目改变为主,所有肿瘤均有发现,而8例肿瘤检测到结构重排。最常见的异常是22号染色体的克隆性或散在性缺失,所有病例均有发现。其他克隆性异常包括5例出现一条性染色体缺失,3例出现-15,2例分别出现-12、+5、+7、+20。这些结果为22号染色体缺失在神经鞘瘤发病机制中的作用提供了进一步证据。我们的研究结果还表明,神经鞘瘤存在几种不同的进化途径,其中一些途径与其他几种神经系统良性和恶性肿瘤相同。

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