TY - JOUR
T1 - Concordant methylation of the ER and N33 genes in glioblastoma multiforme
AU - Li, Qing
AU - Jedlicka, Ann
AU - Ahuja, Nita
AU - Gibbons, M. Christopher
AU - Baylin, Stephen B.
AU - Burger, Peter C.
AU - Issa, Jean Pierre J.
N1 - Funding Information:
The N33 probe was kindly provided by Dr Bookstein (Canji Corporation). This work was supported by NIH grants P30CA06973, 5RO1CA43318 and 5UO1CA64928 and a grant from the Brain Tumor Society (Boston, USA). NA is supported by NIH training grant 1-T32-DK07713. J-PJ is a Kimmel Foundation Scholar.
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
U2 - 10.1038/sj.onc.1201831
DO - 10.1038/sj.onc.1201831
M3 - Article
C2 - 9671399
AN - SCOPUS:0032543784
SN - 0950-9232
VL - 16
SP - 3197
EP - 3202
JO - Oncogene
JF - Oncogene
IS - 24
ER -