PMID- 19302287
OWN - NLM
STAT- MEDLINE
DCOM- 20090708
LR  - 20210816
IS  - 1349-7006 (Electronic)
IS  - 1347-9032 (Linking)
VI  - 100
IP  - 6
DP  - 2009 Jun
TI  - Methylation of estrogen receptor 1 in colorectal adenomas is not age-dependent, 
      but is correlated with K-ras mutation.
PG  - 1005-11
LID - 10.1111/j.1349-7006.2009.01140.x [doi]
AB  - The promoter region of estrogen receptor 1 (ESR1) has been shown to be methylated 
      in normal colorectal mucosa in an age-dependent manner. However, the methylation 
      of this region in colorectal tumors has not sufficiently been investigated. The 
      methylation status of ESR1 in 105 colorectal adenoma tissues was examined by 
      MethyLight and presented as the percentage of methylated references (PMR). 
      Factors that affect the PMR of ESR1 in adenomas were determined using parameters 
      including patient age, sex, past history of malignancy, family history of 
      colorectal cancer, smoking and drinking habits, clinical characteristics of 
      adenomas (location, size, macroscopic appearance, and histology), and K-ras 
      mutation. Multiple linear regression revealed that the PMR was not correlated 
      with patient age. K-ras mutation was significantly correlated with the higher 
      methylation status of ESR1 in adenoma (t-value = 3.21, P = 0.0018), whereas 
      alcohol exposure was significantly correlated with lower methylation status 
      (t-value = -2.37, P = 0.02). Because methylation of O6-methylguanine DNA 
      methyltransferase (MGMT) has been reported to be correlated with K-ras G-to-A 
      transition, methylation of ESR1 was compared with that of MGMT with regard to 
      K-ras mutation. Contrary to expectations, methylation of MGMT was not 
      significantly correlated with K-ras G-to-A transition, but that of ESR1 was 
      strongly correlated with K-ras G-to-A transition. Thus, the methylation status of 
      ESR1 in adenomas was not correlated with patient age, but was associated with 
      K-ras mutation, suggesting that methylation of ESR1 in tumors functions 
      differently from that in normal colon mucosa.
FAU - Horii, Joichiro
AU  - Horii J
AD  - Department of Gastroenterology and Hepatology, Okayama University Graduate School 
      of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
FAU - Hiraoka, Sakiko
AU  - Hiraoka S
FAU - Kato, Jun
AU  - Kato J
FAU - Saito, Shunsuke
AU  - Saito S
FAU - Harada, Keita
AU  - Harada K
FAU - Fujita, Hideyuki
AU  - Fujita H
FAU - Kaji, Eisuke
AU  - Kaji E
FAU - Yamamoto, Kazuhide
AU  - Yamamoto K
LA  - eng
PT  - Journal Article
DEP - 20090316
PL  - England
TA  - Cancer Sci
JT  - Cancer science
JID - 101168776
RN  - 0 (Codon)
RN  - 0 (DNA Primers)
RN  - 0 (ESR1 protein, human)
RN  - 0 (Estrogen Receptor alpha)
SB  - IM
MH  - Adenoma/*genetics/*metabolism/pathology
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Aging
MH  - Codon/genetics
MH  - Colorectal Neoplasms/*genetics/*metabolism/pathology
MH  - DNA Primers
MH  - Estrogen Receptor alpha/*genetics/*metabolism
MH  - Female
MH  - *Genes, ras
MH  - Humans
MH  - Male
MH  - Methylation
MH  - Middle Aged
MH  - *Mutation
MH  - Smoking
EDAT- 2009/03/24 09:00
MHDA- 2009/07/09 09:00
CRDT- 2009/03/24 09:00
PHST- 2009/03/24 09:00 [entrez]
PHST- 2009/03/24 09:00 [pubmed]
PHST- 2009/07/09 09:00 [medline]
AID - CAS1140 [pii]
AID - 10.1111/j.1349-7006.2009.01140.x [doi]
PST - ppublish
SO  - Cancer Sci. 2009 Jun;100(6):1005-11. doi: 10.1111/j.1349-7006.2009.01140.x. Epub 
      2009 Mar 16.