PMID- 20113835
OWN - NLM
STAT- MEDLINE
DCOM- 20100219
LR  - 20100201
IS  - 1873-4456 (Electronic)
IS  - 0165-4608 (Linking)
VI  - 197
IP  - 1
DP  - 2010 Feb
TI  - Epigenetic inactivation of retinoid X receptor genes in non-small cell lung 
      cancer and the relationship with clinicopathologic features.
PG  - 39-45
LID - 10.1016/j.cancergencyto.2009.10.008 [doi]
AB  - Retinoid X receptors (RXRs) are nuclear receptors for retinoids that play a 
      critical role in the regulation of growth and differentiation in normal and tumor 
      cells. Deregulation of RXR expression has been reported in non-small cell lung 
      cancer (NSCLC); however, the mechanism underlying the impaired expression of RXRs 
      in lung cancer is not known. Aberrant methylation of promoter CpG islands is 
      known to be a major mechanism for inactivation of tumor suppressor genes. We 
      investigated the methylation status of the RXR genes in 139 surgically resected 
      NSCLCs and correlated the results with the clinicopathologic characteristics of 
      the patients. Methylation in the tumors was detected in all three genes: RXRA, 
      5.7%; RXRB, 4.3%; RXRG, 23.7%. Reverse transcriptase-polymerase chain reaction 
      analysis showed that RXRG methylation correlates with mRNA expression. 
      Methylation of the RXRG gene was not significantly associated with the prognosis 
      of patients. When the patients were categorized by smoking status, however, the 
      effect of RXRG methylation on prognosis was significantly different between 
      never- and ever-smokers (P=0.003, test for homogeneity). Specifically, RXRG 
      methylation was associated with a significantly worse survival in never-smokers; 
      a trend to better survival outcome was observed for ever-smokers, although not 
      statistically significant. This finding suggests that methylation-associated 
      downregulation of the RXRG gene may play a differential role in the 
      carcinogenesis of NSCLCs according to smoking status, but further studies are 
      needed to confirm this.
CI  - Copyright (c) 2010 Elsevier Inc. All rights reserved.
FAU - Lee, Su Man
AU  - Lee SM
AD  - Department of Anatomy, School of Medicine, Kyungpook National University, Dong In 
      2Ga 101, Daegu, Republic of Korea.
FAU - Lee, Ji Yun
AU  - Lee JY
FAU - Choi, Jin Eun
AU  - Choi JE
FAU - Lee, Shin Yup
AU  - Lee SY
FAU - Park, Jae Yong
AU  - Park JY
FAU - Kim, Dong Sun
AU  - Kim DS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
RN  - 0 (Retinoid X Receptors)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Carcinoma, Non-Small-Cell Lung/*genetics/mortality/pathology
MH  - DNA Methylation
MH  - *Epigenesis, Genetic
MH  - Female
MH  - Humans
MH  - Lung Neoplasms/*genetics/mortality/pathology
MH  - Male
MH  - Middle Aged
MH  - Retinoid X Receptors/*genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2010/02/02 06:00
MHDA- 2010/02/20 06:00
CRDT- 2010/02/02 06:00
PHST- 2009/04/29 00:00 [received]
PHST- 2009/09/12 00:00 [revised]
PHST- 2009/10/13 00:00 [accepted]
PHST- 2010/02/02 06:00 [entrez]
PHST- 2010/02/02 06:00 [pubmed]
PHST- 2010/02/20 06:00 [medline]
AID - S0165-4608(09)00602-5 [pii]
AID - 10.1016/j.cancergencyto.2009.10.008 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 2010 Feb;197(1):39-45. doi: 
      10.1016/j.cancergencyto.2009.10.008.