E-submission
Search
- Page Path
- HOME > Search
Original Articles
- Adequate Microsatellite Markers for 1p/19q Loss of Heterozygosity of Oligodendroglial Tumors in Korean Patients.
- Se Hoon Kim, Hoguen Kim, Tai Seung Kim
- Korean J Pathol. 2005;39(1):23-33.
- 2,187 View
- 40 Download
-
Abstract
PDF - BACKGROUND
It is well known that oligodendrogliomas can be divided into two groups according to the 1p/19q or 1p loss of heterozygosity (LOH) status because oligodendrogliomas with the 1p/19q LOH or the 1p LOH have a better prognosis and chemosensitivity. In this study, we investigated the adequate microsatellite markers for 1p/19q LOH of oligodendroglial tumors in Korean patients.
METHODS
We performed PCR that was based on the LOH test with the 1p (D1S508, D1S199, D1S2734, D1S186 & D1S312) and 19q (D19S219, D19S112, D19S412 & D19S596) microsatellite markers; these were the markers that were recommended by other researchers. We performed this PCR on microdissected paraffin embedded tissue blocks of 67 tumors from 56 cases.
RESULTS
The PCR based LOH analysis revealed that 3 microsatellite markers (D1S508, D1S2734 & D1S186) of 1p and 2 markers (D19S219 & D19S412) of 19q had higher heterozygosity scores than other markers. In addition, chromosomal LOH status using these selective markers showed a statistically significant difference of prognosis for oligodendroglial tumors.
CONCLUSIONS
We can suggest that the microsatellite markers with high heterozygosity scores (D1S508, D1S2734, D1S186, D19S219 and D19S412) would be adequate microsatellite markers for a PCR based LOH test of oligodendroglial tumors in Korean patients.
- Alterations of 9p21-22 Region Encoding Genes in Primary Glioblastomas.
- Hong Jik Doh, Seong Il Suh, Dong Won Kim, Il Man Kim, Man Bin Yim, Eun Ik Son, Kun Young Kwon, Sang Sook Lee, Sang Pyo Kim
- Korean J Pathol. 2002;36(6):394-399.
- 1,987 View
- 16 Download
-
Abstract
PDF
- 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.
First
Prev
