BACKGROUND AND OBJECTIVE: The epigenetic silencing of tumor suppressor genes plays an important role in gliomagenesis. Recently, tissue factor pathway inhibitor 2 (TFPI-2) has been suggested as a tumor suppressor gene involved in tumorigenesis and metastasis in some cancers. However, to date, little is known about the methylation status of TFPI-2 gene in glioblastoma tissues. In this study, we aimed to investigate the methylation status of TFPI-2 promoter and its associations with patient prognosis in glioblastoma. MATERIAL AND METHODS: The methylation status of TFPI-2 was investigated by methylation-specific polymerase chain reaction in 99 glioblastoma patients. The associations between patients' clinical variables and overall survival time were assessed. RESULTS. TFPI-2 was aberrantly methylated in 22.2% (22/99) of glioblastoma tumors, but was not methylated in normal brain samples. The survival of patients with glioblastoma differed significantly between the methylated and unmethylated TFPI-2 groups (P=0.047). The 2-year survival among patients carrying methylated TFPI-2 tumors was significantly lower compared with that of patients with unmethylated TFPI-2 (27% versus 4.7%, P=0.037). CONCLUSIONS: The present work demonstrated that the epigenetic inactivation of TFPI-2 by promoter hypermethylation was a frequent and tumor-specific event in glioblastoma, and TFPI-2 promoter methylation might be considered as a prognostic marker in glioblastoma.
BACKGROUND AND OBJECTIVE: The epigenetic silencing of tumor suppressor genes plays an important role in gliomagenesis. Recently, tissue factor pathway inhibitor 2 (TFPI-2) has been suggested as a tumor suppressor gene involved in tumorigenesis and metastasis in some cancers. However, to date, little is known about the methylation status of TFPI-2 gene in glioblastoma tissues. In this study, we aimed to investigate the methylation status of TFPI-2 promoter and its associations with patient prognosis in glioblastoma. MATERIAL AND METHODS: The methylation status of TFPI-2 was investigated by methylation-specific polymerase chain reaction in 99 glioblastomapatients. The associations between patients' clinical variables and overall survival time were assessed. RESULTS. TFPI-2 was aberrantly methylated in 22.2% (22/99) of glioblastoma tumors, but was not methylated in normal brain samples. The survival of patients with glioblastoma differed significantly between the methylated and unmethylated TFPI-2 groups (P=0.047). The 2-year survival among patients carrying methylated TFPI-2tumors was significantly lower compared with that of patients with unmethylated TFPI-2 (27% versus 4.7%, P=0.037). CONCLUSIONS: The present work demonstrated that the epigenetic inactivation of TFPI-2 by promoter hypermethylation was a frequent and tumor-specific event in glioblastoma, and TFPI-2 promoter methylation might be considered as a prognostic marker in glioblastoma.