Chen H J, Cho C L, Liang C L, Chen L, Chang H W, Lu K, Lee T C
Department of Neurosurgery, Chang Gung Memorial Hospital, 123, Tao-Pei Road, Niaosung, Kaohsiung, Taiwan, R.O.C.
Chang Gung Med J. 2001 Jun;24(6):352-60.
Telomerase activity and telomere length have been shown to be involved in controlling cell proliferation and regulating cell senescence. The authors examined telomerase activity and telomere length in intracranial tumors to determine the clinicopathological behavior of primary intracranial tumors with respect to telomerase expression and alteration of telomere length.
Telomerase activity was examined in 139 brain tumor samples. Telomere length was examined in 138 of the 139 samples. These tumors included 61 meningiomas, 27 schwannomas, 19 high-grade neuroepithelial tumors, and 32 low-grade neuroepithelial tumors. Telomerase activity was measured with a telomerase polymerase chain reaction, enzyme-linked immunosolvent assay kit. Telomere length was examined by Southern blot analysis for the terminal restriction fragment length.
Telomerase activity was detected in 39.2% (20/51) of the neuroepithelial tumors. Detection rates were 47.4% (9/19) for anaplastic astrocytomas and glioblastomas and 34.4% (11/32) for low-grade neuroepithelial tumors. However, detectable telomerase activity was found in 30.8% (4/13) of atypical or malignant meningiomas, but was not detected in any schwannomas. There was a highly significant difference in the telomerase detection rate in neuroepithelial or non-neuroepithelial tumors (p = 0.001). Telomere elongation was found in 11.7% (7/60) of all meningiomas, 46.1% (6/13) of atypical or malignant meningiomas, and 14.8% (4/27) of schwannomas. Elongation of telomere length was detected in 12.6% (11/87) of the cases and 23.5% (12/51) in neuroepithelial tumors. This difference was also significant (p < 0.05). Telomere length was reduced in the majority, (75%, 3/4) of malignant or atypical meningiomas with detectable telomerase activity, but only 45% (9/20) of the neuroepithelial tumors.
These results indicate that telomerase activation may be a critical step in the pathogenesis of intracranial tumors. Telomere length elongation also indicates a high potential for malignant behavior in these tumors.
端粒酶活性和端粒长度已被证明参与控制细胞增殖和调节细胞衰老。作者检测了颅内肿瘤中的端粒酶活性和端粒长度，以确定原发性颅内肿瘤在端粒酶表达和端粒长度改变方面的临床病理行为。
检测了139个脑肿瘤样本中的端粒酶活性。在139个样本中的138个样本中检测了端粒长度。这些肿瘤包括61例脑膜瘤、27例神经鞘瘤、19例高级别神经上皮肿瘤和32例低级别神经上皮肿瘤。使用端粒酶聚合酶链反应、酶联免疫吸附测定试剂盒测量端粒酶活性。通过Southern印迹分析检测端粒长度，以确定末端限制片段长度。
在39.2%（20/51）的神经上皮肿瘤中检测到端粒酶活性。间变性星形细胞瘤和胶质母细胞瘤的检测率为47.4%（9/19），低级别神经上皮肿瘤的检测率为34.4%（11/32）。然而，在30.8%（4/13）的非典型或恶性脑膜瘤中检测到可检测到的端粒酶活性，但在任何神经鞘瘤中均未检测到。神经上皮或非神经上皮肿瘤的端粒酶检测率存在高度显著差异（p = 0.001）。在所有脑膜瘤的11.7%（7/60）、非典型或恶性脑膜瘤的46.1%（6/13）和神经鞘瘤的14.8%（4/27）中发现端粒延长。在12.6%（11/87）的病例中检测到端粒长度延长，在神经上皮肿瘤中为23.5%（12/51）。这种差异也具有统计学意义（p < 0.05）。在具有可检测到的端粒酶活性的大多数恶性或非典型脑膜瘤（75%，3/4）中，端粒长度缩短，但在神经上皮肿瘤中仅为45%（9/20）。
这些结果表明，端粒酶激活可能是颅内肿瘤发病机制中的关键步骤。端粒长度延长也表明这些肿瘤具有高度的恶性行为潜能。
