Korshunov Andrey, Cherekaev Vasiliy, Bekyashev Ali, Sycheva Regina
Department of Neuropathology, N.N. Burdenko Neurosurgical Institute, 4-th Tverskaya-Yamskaya str. 16, Fadeeva str. 5, Moscow, 125047, Russia.
J Neurooncol. 2007 Jan;81(2):131-7. doi: 10.1007/s11060-006-9214-1. Epub 2006 Jul 19.
Meningiomas that arise in the sphenoid region (MSR) often display growth patterns leading to widespread invasion and destruction of the surrounding structures. Consequently, there is still estimated recurrence rate up to 30% with MSR. Conventional cytogenetic studies have failed to reveal aberrations characteristic of invasive meningiomas. Here we investigated 10 invasive and 5 non-invasive MSR using the array-based comparative genomic hybridization (array-CGH) with the GenoSensor Array 300. Mean number of aberrations detected per tumor was significantly greater for invasive meningiomas-67.4 compared with 40.5 for non-invasive MSR. Additionally, invasive MSR disclosed frequent losses on 1p, 6q, 14q and gains on 15q and 20, which were identified previously as molecular hallmarks of stepwise meningioma progression. Thus, the presence of a complex cytogenetic profile and progression-associated chromosomal aberrations in benign MSR is associated with their increased invasive potential. Inasmuch as no reliable adjuvant therapy for recurrent meningiomas is available thus far, revealed genomic aberrations can provide a potential targets for drug discovery and therapeutic intervention in a future.
起源于蝶骨区域（MSR）的脑膜瘤通常呈现出导致周围结构广泛侵袭和破坏的生长模式。因此，MSR的估计复发率仍高达30%。传统的细胞遗传学研究未能揭示侵袭性脑膜瘤的特征性畸变。在此，我们使用GenoSensor Array 300基于阵列的比较基因组杂交（array-CGH）技术，对10例侵袭性和5例非侵袭性MSR进行了研究。侵袭性脑膜瘤每个肿瘤检测到的平均畸变数量显著多于非侵袭性MSR，分别为67.4个和40.5个。此外，侵袭性MSR显示出1p、6q、14q的频繁缺失以及15q和20号染色体的增加，这些先前已被确定为脑膜瘤逐步进展的分子标志。因此，良性MSR中复杂的细胞遗传学特征和与进展相关的染色体畸变与它们增加的侵袭潜能相关。鉴于目前尚无针对复发性脑膜瘤的可靠辅助治疗方法，所揭示的基因组畸变可为未来的药物发现和治疗干预提供潜在靶点。
