Objective: To explore the clinical significance of methylation status of promoter CpG island of p16 gene in glioma tissue and plasma. Methods: Methylation specific polymerase chain reaction (MSP) was used to determine...Objective: To explore the clinical significance of methylation status of promoter CpG island of p16 gene in glioma tissue and plasma. Methods: Methylation specific polymerase chain reaction (MSP) was used to determine the methylation status of the promoter for p16 gene within glioma tissue and plasma. Immunohistochemical method (SP) was used to analyze the expressions of p16 and Ki-67 proteins. Results: Hypermethylation was found in 17/40 (42.5%) of brain gliomas, in com-parison with 11/40 (27.5%) plasma specimens (χ2 = 1.9780, P = 0.1596). Loss of p16 expression was associated (P = 0.0229) with hypermethylation of CpG island of promoter regions. Hypermethylation of p16 gene CpG island was significantly related to the increase of malignant grade of brain glioma (Tissue: χ2 = 11.4288, P = 0.0007; Plasma: χ2 = 8.9439, P = 0.0028). The Ki-67 index increased significantly (P < 0.05) in brain gliomas methylated in contrast to those unmethylated. Conclusion: P16 hypermethylation may be one of the major mechanisms of tumorigenesis of gliomas. Methylated tumor-specific DNA may be as a plasma biomarker for prognosis in patients with glioma.展开更多
基金Scientific Planing Program on Medicine and Health from Shandong Province (No: 20030151)
文摘Objective: To explore the clinical significance of methylation status of promoter CpG island of p16 gene in glioma tissue and plasma. Methods: Methylation specific polymerase chain reaction (MSP) was used to determine the methylation status of the promoter for p16 gene within glioma tissue and plasma. Immunohistochemical method (SP) was used to analyze the expressions of p16 and Ki-67 proteins. Results: Hypermethylation was found in 17/40 (42.5%) of brain gliomas, in com-parison with 11/40 (27.5%) plasma specimens (χ2 = 1.9780, P = 0.1596). Loss of p16 expression was associated (P = 0.0229) with hypermethylation of CpG island of promoter regions. Hypermethylation of p16 gene CpG island was significantly related to the increase of malignant grade of brain glioma (Tissue: χ2 = 11.4288, P = 0.0007; Plasma: χ2 = 8.9439, P = 0.0028). The Ki-67 index increased significantly (P < 0.05) in brain gliomas methylated in contrast to those unmethylated. Conclusion: P16 hypermethylation may be one of the major mechanisms of tumorigenesis of gliomas. Methylated tumor-specific DNA may be as a plasma biomarker for prognosis in patients with glioma.
