Promoter methylation of RASSF1A associates to adult secondary glioblastomas and pediatric glioblastomas
Fecha
2012Autor
Versión
Acceso abierto / Sarbide irekia
Tipo
Artículo / Artikulua
Versión
Versión publicada / Argitaratu den bertsioa
Impacto
|
10.5402/2012/576578
Resumen
While allelic losses and mutations of tumor suppressor genes implicated in the etiology of astrocytoma have been widely assessed,
the role of epigenetics is still a matter of study. We analyzed the frequency of promoter hypermethylation by methylation-specific
PCR (MSP) in five tumor suppressor genes (PTEN, MGMT, RASSF1A, p14ARF, and p16INK4A), in astrocytoma samples and cell
lines. RASSF1A wa ...
[++]
While allelic losses and mutations of tumor suppressor genes implicated in the etiology of astrocytoma have been widely assessed,
the role of epigenetics is still a matter of study. We analyzed the frequency of promoter hypermethylation by methylation-specific
PCR (MSP) in five tumor suppressor genes (PTEN, MGMT, RASSF1A, p14ARF, and p16INK4A), in astrocytoma samples and cell
lines. RASSF1A was the most frequently hypermethylated gene in all grades of astrocytoma samples, in cell lines, and in adult
secondary GBM. It was followed by MGMT. PTEN showed a slight methylation signal in only one GBM and one pilocytic astrocytoma,
and in two cell lines; while p14ARF and p16INK4A did not show any evidence of methylation in primary tumors or cell
lines. In pediatric GBM, RASSF1A was again the most frequently altered gene, followed by MGMT; PTEN, p14 and p16 showed
no alterations. Lack or reduced expression of RASSF1A in cell lines was correlated with the presence of methylation. RASSF1A
promoter hypermethylation might be used as a diagnostic marker for secondary GBM and pediatric GBM. Promoter hypermethylation
might not be an important inactivation mechanism in other genes like PTEN, p14ARF and p16INK4A, in which other
alterations (mutations, homozygous deletions) are prevalent. [--]
Materias
Glioblastomas,
RASSF1A
Editor
Hindawi / Wiley
Publicado en
ISRN Neurology, Volume 2012, Article ID 576578
Departamento
Universidad Pública de Navarra. Departamento de Ciencias de la Salud /
Nafarroako Unibertsitate Publikoa. Osasun Zientziak Saila
Versión del editor
Entidades Financiadoras
P. Lazcoz received a predoctoral fellowship from the Universidad Pública de Navarra, Pamplona, Spain. This research was supported in part by grants from the Departamentos de Salud y de Educación del Gobierno de Navarra, Pamplona; Departamento de Sanidad del Gobierno Vasco, Vitoria; Fondo de Investigación Sanitaria; Fundación Científica de la Asociación Española contra el Cáncer, Madrid, Spain.