일차성 아교모세포종에서 염색체 9p21-22 부위 유전자의 이상
Alterations of 9p21-22 Region Encoding Genes in Primary Glioblastomas
도홍직, 서성일, 김동원, 김일만, 임만빈, 손은익, 권건영, 이상숙, 김상표,
소속 상세정보
도홍직 ( Doh Hong-Jik )
계명대학교 의과대학 신경외과학교실
서성일 ( Suh Seong-Il )
계명대학교 의과대학 미생물학교실
김동원 ( Kim Dong-Won )
계명대학교 의과대학 신경외과학교실
김일만 ( Kim Eal-Maan )
계명대학교 의과대학 신경외과학교실
임만빈 ( Yim Man-Bin )
계명대학교 의과대학 신경외과학교실
손은익 ( Son Eun-Ik )
계명대학교 의과대학 신경외과학교실
권건영 ( Kwon Kun-Young )
계명대학교 의과대학 병리학교실
이상숙 ( Lee Sang-Sook )
계명대학교 의과대학 병리학교실
김상표 ( Kim Sang-Pyo )
계명대학교 의과대학 병리학교실
KMID : 0357920020360060394
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.
Conclusion: 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.
키워드
Brain Neoplasms;Glioblastoma;Chromosomes;Human;Pair 9-Genes;p16
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