Takeuchi Hiroaki, Sato Kazufumi, Ido Kazunori, Kubota Toshihiko
Department of Neurosurgery, Faculty of Medical Sciences, University of Fukui, 23-3 Shimoaizuki, 910-1193, Matsuoka, Fukui, Japan.
J Neurooncol. 2006 May;78(1):15-8. doi: 10.1007/s11060-005-9067-z. Epub 2006 Apr 25.
To investigate the mitotic activity of multinucleated giant cells (MNGCs) with glial fibrillary acidic protein (GFAP) in glioblastomas, double immunohistochemical staining for GFAP and Ki67 was performed in formalin-fixed and paraffin-embedded specimens obtained from 12 primary glioblastomas with MNGCs including three giant cell glioblastomas. The Ki67 labeling index (LI:%) of GFAP+ tumor cells ranged from 0 to 5.6 (2.5+/-1.7, mean+/-standard deviation). The Ki67 LI of GFAP- tumor cells ranged from 18.6 to 35.9 (24.7+/-6.6). The Ki67 LI of GFAP+ cells was significantly lower than that of GFAP- cells (P<0.0001). The number of Ki67+ GFAP- MNGCs ranged from 0 to 23 (8.6+/-8.2). The number of Ki67- GFAP+ MNGCs ranged from 0 to 15 (6.2+/-5.1). There was no significant difference between them (P=0.42). The Ki67 LI of GFAP+ MNGCs was 10.4+/-12.6. The Ki67 LI of GFAP- MNGCs was 45.9+/-29.9. The Ki67 LI of GFAP+ MNGCs was significantly lower than that of GFAP- MNGCs (P<0.01). Our study suggested that MNGCs with mitotic capacity were not dominant and that GFAP+ MNGCs had little mitotic activity in glioblastomas. MNGCs identified in glioblastomas may develop via not only the proliferation of abnormal nuclei in a single tumor cell but also other processes.
为研究胶质母细胞瘤中多核巨细胞(MNGCs)与胶质纤维酸性蛋白(GFAP)的有丝分裂活性,对取自12例伴有MNGCs的原发性胶质母细胞瘤(包括3例巨细胞胶质母细胞瘤)的福尔马林固定石蜡包埋标本进行了GFAP和Ki67的双重免疫组化染色。GFAP+肿瘤细胞的Ki67标记指数(LI:%)为0至5.6(2.5±1.7,平均值±标准差)。GFAP-肿瘤细胞的Ki67 LI为18.6至35.9(24.7±6.6)。GFAP+细胞的Ki67 LI显著低于GFAP-细胞(P<0.0001)。Ki67+ GFAP- MNGCs的数量为0至23(8.6±8.2)。Ki67- GFAP+ MNGCs的数量为0至15(6.2±5.1)。两者之间无显著差异(P=0.42)。GFAP+ MNGCs的Ki67 LI为10.4±12.6。GFAP- MNGCs的Ki67 LI为45.9±29.9。GFAP+ MNGCs的Ki67 LI显著低于GFAP- MNGCs(P<0.01)。我们的研究表明,具有有丝分裂能力的MNGCs并非占主导地位,且GFAP+ MNGCs在胶质母细胞瘤中的有丝分裂活性很低。在胶质母细胞瘤中鉴定出的MNGCs可能不仅通过单个肿瘤细胞中异常核的增殖,还通过其他过程形成。