Hirano H, Lopes M B, Laws E R, Asakura T, Goto M, Carpenter J E, Karns L R, VandenBerg S R
Department of Neurosurgery, Kagoshima University, Kagoshima, Japan 890-8520.
Neuro Oncol. 1999 Apr;1(2):109-19. doi: 10.1093/neuonc/1.2.109.
Studies of experimental tumorigenesis have strongly implicated signaling of the insulin-like growth factor 1 (IGF-1) as a key component in astrocytic neoplasia; however, its role in the growth of low-grade and malignant human tumors is not well understood. Correlative analyses of IGF-1, p53, and Ki-67 (MIB-1) immunohistochemistry and IGF-1 receptor (IGF-1R) mRNA expression were performed to examine the cellular pattern of IGF-1 signaling in 39 cases of astrocytoma (World Health Organization grades II-IV). Tumor cells expressing IGF-1 and IGF-1R were present in all tumor grades. The proportion of tumor cells that expressed IGF-1 correlated with both histopathologic grade and Ki-67 labeling indices, while expression of IGF-1R mRNA correlated with Ki-67 indices. In cases where stereotactic tissue sampling could be identified with a specific tumor area by neuroimaging features, the numbers of IGF-1 immunoreactive cells correlated with the tumor zones of highest cellularity and Ki-67 labeling. In glioblastomas, the localization of IGF-1 immunoreactivity was notable for several features: frequent accentuation in the perivascular tumor cells surrounding microvascular hyperplasia; increased levels in reactive astrocytes at the margins of tumor infiltration; and selective expression in microvascular cells exhibiting endothelial/pericytic hyperplasia. IGF-1R expression was particularly prominent in tumor cells adjacent to both microvascular hyperplasia and palisading necrosis. These data suggest that IGF-1 signaling occurs early in astroglial tumorigenesis in the setting of cell proliferation. The distinctive correlative patterns of IGF-1 and IGF-1R expression in glioblastomas also suggest that IGF-1 signaling has an association with the development of malignant phenotypes related to aberrant angiogenesis and invasive tumor interactions with reactive brain.
实验性肿瘤发生的研究强烈表明,胰岛素样生长因子1(IGF-1)信号传导是星形细胞瘤形成的关键组成部分;然而,其在低度和恶性人类肿瘤生长中的作用尚未得到充分了解。对39例星形细胞瘤(世界卫生组织II-IV级)进行了IGF-1、p53和Ki-67(MIB-1)免疫组织化学及IGF-1受体(IGF-1R)mRNA表达的相关性分析,以研究IGF-1信号传导的细胞模式。所有肿瘤分级中均存在表达IGF-1和IGF-1R的肿瘤细胞。表达IGF-1的肿瘤细胞比例与组织病理学分级和Ki-67标记指数均相关,而IGF-1R mRNA表达与Ki-67指数相关。在通过神经影像学特征可将立体定向组织采样与特定肿瘤区域识别出来的病例中,IGF-1免疫反应性细胞数量与细胞密度最高的肿瘤区域及Ki-67标记相关。在胶质母细胞瘤中,IGF-1免疫反应性的定位有几个显著特征:在微血管增生周围的血管周肿瘤细胞中频繁增强;在肿瘤浸润边缘的反应性星形胶质细胞中水平升高;在表现出内皮/周细胞增生的微血管细胞中选择性表达。IGF-1R表达在紧邻微血管增生和栅栏状坏死的肿瘤细胞中尤为突出。这些数据表明,在细胞增殖的情况下,IGF-1信号传导在星形胶质细胞肿瘤发生的早期就已出现。胶质母细胞瘤中IGF-1和IGF-1R表达的独特相关模式也表明,IGF-1信号传导与异常血管生成和肿瘤与反应性脑的侵袭性相互作用相关的恶性表型的发展有关。