Subependymal giant cell astrocytoma. Significance and possible cytogenetic implications of an immunohistochemical study.
Subependymal giant cell astrocytoma. Significance and possible cytogenetic implications of an immunohistochemical study.
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室管膜下巨细胞星形细胞瘤。
DOI：
10.1007/bf00691851
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发表时间：
1984
影响因子：
12.7
通讯作者：
Marangos,PJ
中科院分区：
文献类型：
--
作者：
Bonnin,JM;Rubinstein,LJ;Papasozomenos,SC;Marangos,PJ
对 22 例室管膜下巨细胞星形细胞瘤 (SGCA) 病例（其中 5 例与结节性硬化症相关）进行了常规神经组织学染色和过氧化物酶抗过氧化物酶 (PAP) 免疫组织化学检查，以检测胶质纤维酸性 (GFA) 蛋白、68 Kd 神经丝亚基 (68 Kd-NF) 和神经元特异性烯醇化酶 (NSE)。神经组织学染色证实存在 PTAH 阳性原纤维，并且不存在尼氏体和源自肿瘤细胞的神经突。 GFA 蛋白阳性细胞存在于与结节性硬化症无关的所有肿瘤中。然而，每个肿瘤中的阳性细胞数量差异很大。 GFA 蛋白阳性细胞在伴有结节性硬化症的 2 例 SGCA 中很少见，而在其余 3 例中则不存在。神经组织学染色显示 GFA 蛋白阳性和阴性细胞之间没有差异。在 6 个肿瘤中发现了 68 个 Kd-NF 阳性细胞。在一种与结节性硬化症相关的肿瘤中，它仅存在于大神经节样细胞中。在检查的 18 个肿瘤中，有 13 个肿瘤中发现了 NSE 阳性细胞，其中包括与结节性硬化症相关的 5 个 SGCA 中的 4 个。中枢神经上皮肿瘤中 NSE 阳性对其可能的神经元起源的意义仍然悬而未决。这项研究表明，SGCA，尤其是与结节性硬化症相关的细胞，包括明显无法表达 GFA 蛋白的细胞。部分肿瘤细胞表达68 Kd-NF，但这种表达达不到神经元分化的完全表达。 SGCA 独特的形态学外观以及电子显微镜和免疫组织化学研究中报告的差异表明，这些肿瘤的起源细胞是早期发育中发育不良事件的产物。结果，该细胞星形细胞或神经元分化的潜力可能不完全或异常表达，特别是当结节性硬化症的斑头也存在时。从目前的组织化学结果中无法得出明显的神经节分化的证据，也无法推断出 SGCA 中肿瘤细胞的神经元起源。这项研究支持将这些肿瘤作为星形细胞瘤的一种变体的一般解释。
Twenty-two cases of subependymal giant cell astrocytoma (SGCA), five of which associated with tuberous sclerosis, were reviewed by conventional neurohistological stains and by peroxidase-antiperoxidase (PAP) immunohistochemistry for glial fibrillary acidic (GFA) protein, the 68 Kd neurofilament subunit (68 Kd-NF), and neuron-specific enolase (NSE). Neurohistological stains confirmed the presence of PTAH-positive fibrils and the absence of Nissl bodies and of neurites originating from the tumor cells. GFA protein-positive cells were present in all tumors not associated with tuberous sclerosis. However, the number of positive cells in each tumor was highly variable. GFA protein-positive cells were rare in the two SGCA accompanying tuberous sclerosis and absent in the remaining three. Neurohistological stains showed no differences between GFA protein-positive and negative cells. 68 Kd-NF-positive cells were found in six tumors. In one tumor, associated with tuberous sclerosis, it was present in the large ganglion-like cells only. NSE-positive cells were found in 13 of 18 tumors examined, including four of the five SGCA associated with tuberous sclerosis. The significance of NSE-positivity in central neuroepithelial neoplasms in respect of their possible neuronal origin remains open.This study suggests that the SGCA, especially those associated with tuberous sclerosis, include cells that are apparently unable to express GFA protein. Some of the tumor cells express the 68 Kd-NF, but this expression falls short of the complete expression of neuronal differentiation. The unique morphological appearances of the SGCA and the discrepancies reported in electron-microscopic and immunohistochemical studies suggest that the cell of origin of these tumors is the product of a dysgenetic event in early development. As a result, the potential of that cell for astrocytic or neuronal differentiation may be incompletely or aberrantly expressed, in particular when the stigmata of tuberous sclerosis are also present. No evidence of obvious ganglionic differentiation and no inference of a neuronal origin of the tumor cells in SGCA could be adduced from the present histochemical findings. This study supports the general interpretation of these tumors as a variant of astrocytoma.