Alterations of 9p21-22 Region Encoding Genes in Primary Glioblastomas.
- Author:
Hong Jik DOH
1
;
Seong Il SUH
;
Dong Won KIM
;
Il Man KIM
;
Man Bin YIM
;
Eun Ik SON
;
Kun Young KWON
;
Sang Sook LEE
;
Sang Pyo KIM
Author Information
1. Department of Neurosurgery, Keimyung University School of Medicine, Daegu, Korea.
- Publication Type:Original Article
- Keywords:
Brain Neoplasms;
Glioblastoma;
Chromosomes;
Human;
Pair 9;
Genes;
p16
- MeSH:
Brain Neoplasms;
Carcinogenesis;
Central Nervous System;
Genes, p16;
Glioblastoma*;
Humans;
Polymerase Chain Reaction;
Tumor Suppressor Protein p14ARF
- From:Korean Journal of Pathology
2002;36(6):394-399
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Glioblastomas are one of the most common and aggressive malignant glial tumors occuring in the central nervous system. This study analyzed the status of p15INK4b, p14ARF, p16INK4a, MTAP, IFNA, and IFNB genes in 36 primary glioblastomas to investigate whether the inactivation of these genes participate in primary glioblastoma tumorigenesis. METHODS: We used polymerase chain reaction, polymerase chain reaction/single strand conformational polymorphism (PCR/SSCP) analysis, and methylation-specific PCR. RESULTS: Homozygous deletions at the p16INK4a gene were detected in 11 cases (30.5%) of 36 primary glioblastomas, and the promoter hypermethylation was found in 3 cases (8.3%) of 36 primary glioblastomas. In mutational analysis for the p16INK4a gene by PCR/SSCP, there was no abnormal mobility-shifted band in 36 cases of primary glioblastomas. The overall frequency of p16INK4a alterations including homozygous deletion and promoter hypermethylation in 36 primary glioblastomas was 38.8% (14 of 36). Deletions of p15INK4b were noted in 4 cases (11.1%), whereas deletions of the p14ARF and MTAP genes were detected in 1 case of 36 cases of primary glioblastomas. But deletions of the INFA and B genes were not found. CONCLUSIONS: These results suggest that alterations of the p16INK4a gene can be important mechanisms of the tumorigenesis of primary glioblastomas, and the p16INK4a gene is inactivated by mechanisms including homozygous deletion and promoter hypermethylation.
