5' CpG island methylation of p16 is associated with absence of p16 expression in glioblastomas
Journal of Korean Medical Science
;
: 555-559, 2000.
Artigo
em Inglês
| WPRIM
| ID: wpr-150734
ABSTRACT
Recent evidence shows that transcriptional silencing as a consequence of hypermethylation of CpG islands is an important mechanism in the inactivation of p16INK4 tumor suppressor gene. This study is designed to clarify the significance of p16INK4 hypermethylation in 23 cases of glioblastomas (GBMs) by methylation-specific polymerase chain reaction (PCR) and p16 immunostaining. Fourteen cases (60.9%) out of 23 GBMs revealed hypermethylation on p16. p16 immunostaining revealed that 13 (93%) of these 14 hypermethylation cases showed complete loss of immunoreactivity and only one (7%) case retained immunoreactivity. Among 9 methylation-negative cases, 4 were immunonegative, which might be related to mutations or deletions other than hypermethylation. The most significant finding was that of 17 cases with immunonegativity, 13 cases (76.5%) showed hypermethylation. We reconfirmed that p16 hypermethylation may be one of the major mechanisms of tumorigenesis of GBMs and the results between the methylation specific-PCR study and p16 immunostaining had a good correlation.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Neoplasias Encefálicas
/
Reação em Cadeia da Polimerase
/
Elementos Antissenso (Genética)
/
Glioblastoma
/
Ilhas de CpG
/
Metilação de DNA
/
Inibidor p16 de Quinase Dependente de Ciclina
/
Regiões 5' não Traduzidas
/
Inativação Gênica
/
Pessoa de Meia-Idade
Limite:
Adulto
/
Feminino
/
Humanos
/
Masculino
Idioma:
Inglês
Revista:
Journal of Korean Medical Science
Ano de publicação:
2000
Tipo de documento:
Artigo
Similares
MEDLINE
...
LILACS
LIS