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Aberrant CpG island methylation of multiple
genes in ependymal tumors
M. Eva Alonso, M. Josefa
Bello, Pilar Gonzalez-Gomez, Dolores Arjona, Jose M. de Campos, Manuel
Gutierrez and Juan A. Rey
Laboratorio de Oncogenetica
Molecular, Dept. C. Experimental, Hospital Universitario La Paz, Madrid (M.E.A.,
M.J.B., P.G.-G., D.A., J.A.R.); Departamento de Neurocirugía, Hospital del Rio
Hortega, Valladolid (J.M.D.); Departamento de Anatomía Patologica, Hospital
Universitario La Paz, Madrid (M.G.), Spain. jarey.hulp@salud.madrid.org
Aberrant methylation of promoter CpG islands in human genes represents an
alternative mechanism for genetic inactivation, and contributes to the
development of human tumors.
Nevertheless, thus far, few reports have analyzed methylation in
ependymomas.
We determined the frequency of aberrant CpG island methylation of several
tumor-associated genes: p16(INK4a), RB1, MGMT, DAPK, TIMP3, THBS1, TP73, NF2 and
Caspase 8 in a group of 27 ependymomas, consisting of 22 WHO grade II samples
and five anaplastic WHO grade III tumors.
The respective methylation indices (number of genes methylated/total genes
analyzed) for both tumor groups was 0.195 and 0.198.
Overall methylation rates greater than 20% were detected in MGMT, TIMP3, THBS1
and TP73. NF2 and Caspase 8 each presented hypermethylation in less than 10% of
cases, and the cell-cycle regulators RB1/p16(INK4a) were hypermethylated in 4%
and 18% of the samples, respectively, mostly affecting the low-grade
forms.
Our findings suggest that methylation commonly contributes to the inactivation
of cancer-related genes in ependymomas.
PMID: 15072463 [PubMed - indexed for MEDLINE]
Source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15072463
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