Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, China National Clinical Research Center for Neurological Diseases, Center of Brain Tumor, Beijing Institute for Brain Disorders and Beijing Key Laboratory of Brian Tumor; and.
Department of Pathology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China.
J Neurosurg. 2016 Oct;125(4):995-1001. doi: 10.3171/2015.8.JNS15879. Epub 2016 Jan 15.
OBJECTIVE 1p/19q co-deletion is a well-established tumor cell-specific chromosomal abnormality in oligodendroglial tumors. The endothelial cells (ECs) of oligodendroglial tumor vessels are considered to be normal cells that do not acquire mutations. METHODS A total of 30 samples from 16 male and 14 female patients (median age of 46.5 years) with a histological diagnosis of primary anaplastic oligodendroglioma (AO) were collected in the study. The immunofluorescence technique was used to identify vascular ECs, and the 1p/19q status was detected with fluorescence in situ hybridization. Kaplan-Meier plots were compared using the log-rank method. RESULTS The ECs in AO had a higher 1p36 (detected signal) deletion rate than 1q25 (reference signal) (p < 0.01) and a higher 19q13 (detected signal) deletion rate than 19p13 (reference signal) (p < 0.01). The survival analysis results showed that both the progression-free survival (PFS) and overall survival (OS) of the patients with 1p/19q-co-deleted ECs were significantly longer than those with 1p/19q-intact ECs (PFS, p < 0.001; OS, p < 0.001). This correlation was validated by an independent cohort. In addition, the Cox regression model revealed that 1p/19q co-deletion in ECs was an independent prognostic factor (HR 0.056 [95% CI 0.012-0.261], p < 0.001 for PFS; HR 0.061 [95% CI 0.013-0.280], p < 0.01 for OS). CONCLUSIONS 1p/19q co-deletion and polysomy can be also found in the ECs of AO, which suggests that the ECs are, in part, tumor related and reflect a novel aspect of tumor angiogenesis.
目的 1p/19q 共缺失是少突胶质细胞瘤中一种明确的肿瘤细胞特异性染色体异常。少突胶质细胞瘤血管的内皮细胞(ECs)被认为是正常细胞,不会发生突变。方法 本研究共收集了 30 例组织学诊断为原发性间变性少突胶质细胞瘤(AO)的患者的样本,其中男性 16 例,女性 14 例,中位年龄为 46.5 岁。采用免疫荧光技术鉴定血管内皮细胞,荧光原位杂交检测 1p/19q 状态。采用对数秩检验比较 Kaplan-Meier 图。结果 AO 的 EC 中 1p36(检测信号)缺失率高于 1q25(参考信号)(p<0.01),19q13(检测信号)缺失率高于 19p13(参考信号)(p<0.01)。生存分析结果显示,1p/19q 共缺失 EC 的患者无进展生存期(PFS)和总生存期(OS)均显著长于 1p/19q 完整 EC 的患者(PFS,p<0.001;OS,p<0.001)。这一相关性在独立队列中得到了验证。此外,Cox 回归模型显示,EC 中 1p/19q 共缺失是独立的预后因素(HR 0.056[95%CI 0.012-0.261],PFS;HR 0.061[95%CI 0.013-0.280],OS)。结论 AO 的 EC 中也可以发现 1p/19q 共缺失和三倍体,这表明 EC 部分与肿瘤有关,反映了肿瘤血管生成的一个新方面。