Concordant methylation of the ER and N33 genes in glioblastoma multiforme

Qing Li, Anne Elizabeth Jedlicka, Nita Ahuja, M Christopher Gibbons, Stephen B Baylin, Peter C. Burger, Jean Pierre J Issa

Research output: Contribution to journalArticle

Abstract

Methylation of promoter-associated CpG islands appears to be a potential way by which tumor suppressor genes are inactivated in cancer. Using Southern blot analysis, me have studied the methylation of several genes in glioblastoma multiforme (GBM), trying to determine their contribution to tumorigenesis. Genes studied included the estrogen receptor (ER), N33, the candidate tumor-suppressors P15, P16 and HIC1 and a control gene, c-abl. Hypermethylation of N33, ER, HIC1, P16, P15 and c-abl were found in 61%, 59%, 60%, 5%, 2% and 0% of GBM respectively. HIC1 methylation was detected in normal brain as well, but appeared to be more extensive in tumors. ER and N33 methylation were significantly more frequent in tumors from individuals over the age of 40 (70% and 88% vs 36% and 14%). In addition, there was a strong association between ER and N33 methylation, which were concordant in 81% of the cases (P <0.01). ER and N33 methylation in GBM may therefore appear as a result of shared etiologic factors, which may relate in part to aging cell populations in the brain.

Original languageEnglish (US)
Pages (from-to)3197-3202
Number of pages6
JournalOncogene
Volume16
Issue number24
StatePublished - Jun 18 1998

Fingerprint

Glioblastoma
Estrogen Receptors
Methylation
Genes
Neoplasms
abl Genes
CpG Islands
Cell Aging
Brain
Southern Blotting
Tumor Suppressor Genes
Carcinogenesis
Population

Keywords

  • Aging
  • DNA methylation
  • Estrogen receptor
  • Glioblastoma multiforme
  • N33

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

Cite this

Li, Q., Jedlicka, A. E., Ahuja, N., Gibbons, M. C., Baylin, S. B., Burger, P. C., & Issa, J. P. J. (1998). Concordant methylation of the ER and N33 genes in glioblastoma multiforme. Oncogene, 16(24), 3197-3202.

Concordant methylation of the ER and N33 genes in glioblastoma multiforme. / Li, Qing; Jedlicka, Anne Elizabeth; Ahuja, Nita; Gibbons, M Christopher; Baylin, Stephen B; Burger, Peter C.; Issa, Jean Pierre J.

In: Oncogene, Vol. 16, No. 24, 18.06.1998, p. 3197-3202.

Research output: Contribution to journalArticle

Li, Q, Jedlicka, AE, Ahuja, N, Gibbons, MC, Baylin, SB, Burger, PC & Issa, JPJ 1998, 'Concordant methylation of the ER and N33 genes in glioblastoma multiforme', Oncogene, vol. 16, no. 24, pp. 3197-3202.
Li, Qing ; Jedlicka, Anne Elizabeth ; Ahuja, Nita ; Gibbons, M Christopher ; Baylin, Stephen B ; Burger, Peter C. ; Issa, Jean Pierre J. / Concordant methylation of the ER and N33 genes in glioblastoma multiforme. In: Oncogene. 1998 ; Vol. 16, No. 24. pp. 3197-3202.
@article{ba317353947646b6a56e067db99274c2,
title = "Concordant methylation of the ER and N33 genes in glioblastoma multiforme",
abstract = "Methylation of promoter-associated CpG islands appears to be a potential way by which tumor suppressor genes are inactivated in cancer. Using Southern blot analysis, me have studied the methylation of several genes in glioblastoma multiforme (GBM), trying to determine their contribution to tumorigenesis. Genes studied included the estrogen receptor (ER), N33, the candidate tumor-suppressors P15, P16 and HIC1 and a control gene, c-abl. Hypermethylation of N33, ER, HIC1, P16, P15 and c-abl were found in 61{\%}, 59{\%}, 60{\%}, 5{\%}, 2{\%} and 0{\%} of GBM respectively. HIC1 methylation was detected in normal brain as well, but appeared to be more extensive in tumors. ER and N33 methylation were significantly more frequent in tumors from individuals over the age of 40 (70{\%} and 88{\%} vs 36{\%} and 14{\%}). In addition, there was a strong association between ER and N33 methylation, which were concordant in 81{\%} of the cases (P <0.01). ER and N33 methylation in GBM may therefore appear as a result of shared etiologic factors, which may relate in part to aging cell populations in the brain.",
keywords = "Aging, DNA methylation, Estrogen receptor, Glioblastoma multiforme, N33",
author = "Qing Li and Jedlicka, {Anne Elizabeth} and Nita Ahuja and Gibbons, {M Christopher} and Baylin, {Stephen B} and Burger, {Peter C.} and Issa, {Jean Pierre J}",
year = "1998",
month = "6",
day = "18",
language = "English (US)",
volume = "16",
pages = "3197--3202",
journal = "Oncogene",
issn = "0950-9232",
publisher = "Nature Publishing Group",
number = "24",

}

TY - JOUR

T1 - Concordant methylation of the ER and N33 genes in glioblastoma multiforme

AU - Li, Qing

AU - Jedlicka, Anne Elizabeth

AU - Ahuja, Nita

AU - Gibbons, M Christopher

AU - Baylin, Stephen B

AU - Burger, Peter C.

AU - Issa, Jean Pierre J

PY - 1998/6/18

Y1 - 1998/6/18

N2 - Methylation of promoter-associated CpG islands appears to be a potential way by which tumor suppressor genes are inactivated in cancer. Using Southern blot analysis, me have studied the methylation of several genes in glioblastoma multiforme (GBM), trying to determine their contribution to tumorigenesis. Genes studied included the estrogen receptor (ER), N33, the candidate tumor-suppressors P15, P16 and HIC1 and a control gene, c-abl. Hypermethylation of N33, ER, HIC1, P16, P15 and c-abl were found in 61%, 59%, 60%, 5%, 2% and 0% of GBM respectively. HIC1 methylation was detected in normal brain as well, but appeared to be more extensive in tumors. ER and N33 methylation were significantly more frequent in tumors from individuals over the age of 40 (70% and 88% vs 36% and 14%). In addition, there was a strong association between ER and N33 methylation, which were concordant in 81% of the cases (P <0.01). ER and N33 methylation in GBM may therefore appear as a result of shared etiologic factors, which may relate in part to aging cell populations in the brain.

AB - Methylation of promoter-associated CpG islands appears to be a potential way by which tumor suppressor genes are inactivated in cancer. Using Southern blot analysis, me have studied the methylation of several genes in glioblastoma multiforme (GBM), trying to determine their contribution to tumorigenesis. Genes studied included the estrogen receptor (ER), N33, the candidate tumor-suppressors P15, P16 and HIC1 and a control gene, c-abl. Hypermethylation of N33, ER, HIC1, P16, P15 and c-abl were found in 61%, 59%, 60%, 5%, 2% and 0% of GBM respectively. HIC1 methylation was detected in normal brain as well, but appeared to be more extensive in tumors. ER and N33 methylation were significantly more frequent in tumors from individuals over the age of 40 (70% and 88% vs 36% and 14%). In addition, there was a strong association between ER and N33 methylation, which were concordant in 81% of the cases (P <0.01). ER and N33 methylation in GBM may therefore appear as a result of shared etiologic factors, which may relate in part to aging cell populations in the brain.

KW - Aging

KW - DNA methylation

KW - Estrogen receptor

KW - Glioblastoma multiforme

KW - N33

UR - http://www.scopus.com/inward/record.url?scp=0032543784&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032543784&partnerID=8YFLogxK

M3 - Article

VL - 16

SP - 3197

EP - 3202

JO - Oncogene

JF - Oncogene

SN - 0950-9232

IS - 24

ER -