Bello M, Leone P, Nebreda P, Kusak M, Decampos J, Vaquero J, Sarasa J, Pestana A, Rey J
CSIC,INST INVEST BIOMED,E-28029 MADRID,SPAIN. HOSP PRINCESA,DEPT NEUROSURG,MADRID,SPAIN. FDN JIMENEZ DIAZ,DEPT NEUROSURG,E-28040 MADRID,SPAIN. CLIN PUERTA HIERRO,DEPT NEUROSURG,MADRID,SPAIN. FDN JIMENEZ DIAZ,DEPT ANAT PATHOL,E-28040 MADRID,SPAIN.
Int J Oncol. 1995 Mar;6(3):655-8. doi: 10.3892/ijo.6.3.655.
A deletion mapping analysis of chromosome 19 was performed on a series of 101 samples derived from malignant gliomas. A total of 35 tumors displayed different deletions for the loci studied (D19S21, D19S11, D19S74, D19S7, D19S8, CKM, and D19S22). In most instances, losses involving the long arm markers of chromosome 19 were observed, and only four samples were characterized by losses on the short arm. No tumor was found displaying loss of both short and long arm markers. The higher frequency of deletions was detected in tumors with a major oligodendroglial component: 76% of samples included in this group displayed losses at 19q. Among the astrocytic tumors, the frequency of 19q alterations varied as follows: 11% in pilocytic astrocytomas, 17% in astrocytomas grade II, 10% in anaplastic astrocytomas and 21% in glioblastoma multiforme. No ependymoma was found displaying allele loss on chromosome 19. The common region of overlap for the 19q deletions observed involves primarily the distal portion of the long arm, 19q13.2-q13.4. In agreement with previous reports, these data suggest the non-random involvement of a tumor suppressor gene located at 19q13 in the genesis or progression of malignant gliomas.
对一系列来自恶性胶质瘤的101个样本进行了19号染色体的缺失图谱分析。在所研究的位点(D19S21、D19S11、D19S74、D19S7、D19S8、肌酸激酶M亚基(CKM)和D19S22)中,共有35个肿瘤显示出不同的缺失。在大多数情况下,观察到涉及19号染色体长臂标记的缺失,只有4个样本表现为短臂缺失。未发现同时存在短臂和长臂标记缺失的肿瘤。在具有主要少突胶质细胞成分的肿瘤中检测到更高的缺失频率:该组中的76%的样本在19q处显示缺失。在星形细胞瘤中,19q改变的频率变化如下:毛细胞型星形细胞瘤中为11%,二级星形细胞瘤中为17%,间变性星形细胞瘤中为10%,多形性胶质母细胞瘤中为21%。未发现室管膜瘤在19号染色体上显示等位基因缺失。观察到的19q缺失的共同重叠区域主要涉及长臂的远端部分,即19q13.2 - q13.4。与先前的报道一致,这些数据表明位于19q13的一个肿瘤抑制基因在恶性胶质瘤的发生或进展中存在非随机参与。