Tuber and subependymal giant cell astrocytoma associated with tuberous sclerosis: an immunohistochemical, ultrastructural, and immunoelectron microscopic study

Tuber and subependymal giant cell astrocytoma associated with tuberous sclerosis: an immunohistochemical, ultrastructural, and immunoelectron microscopic study
复制标题

与结节性硬化症相关的结节和室管膜下巨细胞星形细胞瘤:免疫组织化学、超微结构和免疫电子显微镜研究

DOI:
--
复制
发表时间:
2004
影响因子:
12.7
通讯作者:
J. C. Charlesworth
J. C. Charlesworth
中科院分区:
医学1区
文献类型:
--
作者:
Takanori Hirose;B. W. Scheithauer;M. Lopes;H. Gerber;H. Altermatt;M. Hukee;Scott R Vandenberg;J. C. Charlesworth

文献摘要

参考文献

被引文献

相似文献

结节性硬化症(TS)中结节的巨细胞嗜酸性细胞和室管膜下巨细胞星形细胞瘤(SEGA)的细胞性质尚不清楚。为了评估这些病变的特点,对13个结节和6个SEGA进行了神经胶质和神经元相关抗原的免疫组织化学研究。除常规超微结构外,6块块茎和8块SEGA为纤维酸性蛋白(GFAP)和生长抑素。嗜酸性巨细胞呈波形蛋白(100%)、胶质纤维酸性蛋白(77%)和S-100蛋白(92%)阳性反应,并有不同程度的神经元相关抗原反应,包括神经丝(NF)蛋白(38%)或III类β-微管蛋白(77%)。SEGA对胶质纤维酸性蛋白(50%)或S-100蛋白(100%)呈不同程度的免疫反应,其中2例(33%)、5例(83%)和4例(67%)表达了核因子表位、Ⅲ类β微管蛋白和钙结合蛋白28-kD。生长抑素(50%)、甲硫氨酸脑啡肽(50%)、6-羟色胺(33%)、β-内啡肽(33%)和神经肽Y(17%)在SEGA中有胞质表达,而在块茎中未见表达。在超微结构上,块茎的巨细胞和SEGA的细胞含有大量的中间丝、频繁的溶酶体和偶尔出现的长方形或菱形的膜结合晶体,表现出片层周期性和向溶酶体的结构转变。一些SEGA细胞表现出神经元分化的特征,包括成堆的粗面内质网,偶见微管和少数致密核颗粒。此外,在块茎的一个案例中,可以看到单个大细胞的突起参与突触的形成。用金颗粒标记的GFAP抗血清修饰两种病变的少数细胞内的中间纤维。在SEGA的肿瘤细胞中,不规则的、非膜结合的、电子透亮的区域经常含有生长抑素免疫反应颗粒,而后者在结节中检测不到。本研究提供了块茎巨细胞和SEGA细胞分化分化神经胶质细胞分化的进一步证据。在不同部位,包括室管膜下区、白质(“异位”)和皮质的相似细胞的发现间接支持了TS的这些损害是移行异常所致的观点。
The cellular nature of the giant eosinophilic cells of tuber and of the cells comprising subependymal giant cell astrocytoma (SEGA) in tuberous sclerosis (TS) remains unclear. To assess the characteristics of these lesions, 13 tubers and 6 SEGA were immunohistochemically studied with glial and neuron-associated antigens. In addition to conventional ultrastructure, 6 tubers and 8 SEGA were fibrillary acidic protein (GFAP) and somatostatin. Eosinophilic giant cells of tubers were positive for vimentin (100%), GFAP (77%) and S-100 protein (92%); such cells were also found to a various extent to be reactive for neuron-associated antigens, including neurofilament (NF) proteins (38%) or class III β-tubulin (77%). SEGA also showed variable immunoreactivity for GFAP (50%) or for S-100 protein (100%); NF epitopes, class III β-tubulin, and calbindin 28-kD were expressed in 2 (33%), 5 (83%) and 4 (67%) cases, respectively. Cytoplasmic staining for somatostatin (50%), met-enkephalin (50%), 6-hydroxytryptamine (33%), β-endorphin (33%) and neuropeptide Y (17%) was noted in SEGA, but not in tubers. Ultrastructurally, the giant cells of tubers and the cells of SEGA contained numerous intermediate filaments, frequent lysosomes and occasional rectangular or rhomboid membrane-bound crystalloids exhibiting lamellar periodicity and structural transition to lysosomes. Some SEGA cells showed features suggestive of neuronal differentiation, including stacks of rough endoplasmic reticulum, occasional microtubules and a few dense-core granules. Furthermore, in one case of tuber, a process of a single large cell was seen to be engaged in synapse formation. Intermediate filaments within a few cells of both lesions were decorated by gold particle-labeled GFAP antiserum. Within the tumor cells of SEGA, irregular, non-membrane-bound, electron-lucent areas often contained somatostatin-immunoreactive particles, whereas the latter could not be detected in tuber. The present study provides further evidence of divergent glioneuronal differentiation, both in the giant cells of tubers and the cells of SEGA. The findings of similar cells at different sites, including the subependymal zone, white matter (“heterotopias”), and cortex indirectly supports the idea that these lesions of TS result from a migration abnormality.
DOI: --
发表时间: 1989-11
期刊: The American journal of pathology
影响因子: --
作者:
D. Caccamo;Mary M. Herman;A. Frankfurter;Christos D. Katsetos;V. Collins;L. J. Rubinstein
通讯作者: D. Caccamo;Mary M. Herman;A. Frankfurter;Christos D. Katsetos;V. Collins;L. J. Rubinstein
DOI: 10.1007/bf00691851
发表时间: 1984
影响因子: 12.7
作者:
Bonnin,JM;Rubinstein,LJ;Papasozomenos,SC;Marangos,PJ
通讯作者: Marangos,PJ
DOI: 10.1002/cm.970170207
发表时间: 1990-01-01
影响因子: --
作者:
LEE, MK;TUTTLE, JB;FRANKFURTER, A
通讯作者: FRANKFURTER, A