Atypical teratoid/rhabdoid tumor of the CNS: cytopathology and immunohistochemistry of insulin-like growth factor-II, insulin-like growth factor receptor type 1, cathepsin D, and Ki-67.
Atypical teratoid/rhabdoid tumor of the CNS: cytopathology and immunohistochemistry of insulin-like growth factor-II, insulin-like growth factor receptor type 1, cathepsin D, and Ki-67.
复制标题
中枢神经系统非典型畸胎瘤/横纹肌样瘤：胰岛素样生长因子-II、胰岛素样生长因子受体 1 型、组织蛋白酶 D 和 Ki-67 的细胞病理学和免疫组织化学。
作者：
Shuji Ogino;Mark L. Cohen;F. W. Abdul
胰岛素样生长因子（IGF）-II是一种有效的生长因子，通常由许多其他因子控制，包括IGF结合蛋白和IGF结合蛋白蛋白酶。一般来说，后者通过切割IGF结合蛋白来增加IGF的生物利用度。组织蛋白酶D（IGF结合蛋白蛋白酶）也与肿瘤侵袭有关。虽然IGF-II与各种儿童肿瘤的发病机制有关，但其在中枢神经系统非典型畸胎样/横纹肌样肿瘤（ATRT-CNS）发病机制中的意义迄今尚未研究。我们目前的临床病理特征的两个案件ATRT-CNS。此外，对福尔马林固定、石蜡包埋的组织切片进行IGF-II、IGF受体1型、组织蛋白酶D和Ki-67的化学染色。两种肿瘤均表现出IGF-II的弥漫性强胞浆阳性，IGF受体I型的弥漫性胞浆和局灶性膜阳性，以及组织蛋白酶D的弥漫性胞浆阳性。Ki-67标记指数分别为10.0%和1.4%。我们的结论是，ATRT-CNS细胞表达IGF-II和IGF受体1型，支持的假设，自分泌/旁分泌刺激细胞生长的IGF-II可能是一种机制参与ATRT-CNS肿瘤发生。肿瘤细胞表达的组织蛋白酶D也可能参与肿瘤细胞的侵袭和生长。ATRT-CNS的确切发病机制仍有待阐明。
Insulin-like growth factor (IGF)-II is a potent growth factor, normally controlled by a number of other factors, including IGF binding proteins and IGF binding protein proteases. In general, the latter increase the bioavailability of IGF by cleaving IGF binding proteins. Cathepsin D (an IGF binding protein protease) was also implicated in tumor invasion. Although IGF-II was implicated in the pathogeneses of various childhood neoplasms, its significance in the pathogenesis of atypical teratoid/rhabdoid tumor of the central nervous system (ATRT-CNS) was not studied to date. We present clinicopathologic features of two cases of ATRT-CNS. In addition, formalin-fixed, paraffin-embedded tissue sections were stained immunohistochemically for IGF-II, IGF receptor type 1, cathepsin D, and Ki-67. Both tumors demonstrated diffuse strong cytoplasmic positivity for IGF-II, diffuse cytoplasmic and focal membranous positivity for IGF receptor type I, and diffuse cytoplasmic positivity for cathepsin D. The Ki-67 labeling indices were 10.0% and 1.4%. We conclude that ATRT-CNS cells express both IGF-II and IGF receptor type 1, supporting the hypothesis that autocrine/paracrine stimulation of cell growth by IGF-II might be one mechanism involved in ATRT-CNS tumorigenesis. Cathepsin D expressed by the tumor cells might also be involved in both tumor cell invasion and growth. The exact pathogenesis of ATRT-CNS remains to be elucidated.