PMID- 9150186
OWN - NLM
STAT- MEDLINE
DCOM- 19970529
LR  - 20190512
IS  - 0027-8874 (Print)
IS  - 0027-8874 (Linking)
VI  - 89
IP  - 9
DP  - 1997 May 7
TI  - Suppression of retinoic acid receptor beta in non-small-cell lung cancer in vivo: 
      implications for lung cancer development.
PG  - 624-9
AB  - BACKGROUND: Retinoids, analogues of vitamin A, are required for the normal growth 
      and differentiation of human bronchial epithelium. They are also able to reverse 
      premalignant lesions and prevent second primary tumors in some patients with 
      non-small-cell lung cancer (NSCLC). These effects are thought to result from 
      modulation of cell growth, differentiation, or apoptosis (programmed cell death). 
      When certain retinoid receptors in the cell nucleus (i.e., retinoic acid 
      receptors [RARs] and retinoid X receptors [RXRs]), which mediate most retinoid 
      actions, are suppressed, abnormal activity may result that could enhance cancer 
      development. PURPOSE: This study was designed to determine whether there are 
      abnormalities in the expression of retinoid receptors in surgical specimens from 
      patients with NSCLC. METHODS: Transcripts of nuclear retinoid receptors were 
      detected in formalin-fixed, paraffin-embedded specimens by use of 
      digoxigenin-labeled riboprobes specific for RAR alpha, RAR beta, RAR gamma, RXR 
      alpha, RXR beta, and RXR gamma for in situ hybridization to histologic specimens 
      from 79 patients with NSCLC and as control from 17 patients with non-lung cancer. 
      The quality and specificity of the digoxigenin-labeled probes were determined by 
      northern blotting, and the specificity of the binding of antisense riboprobes was 
      verified by use of sense probes as controls. RESULTS: All receptors were 
      expressed in at least 89% of control normal bronchial tissue specimens from 17 
      patients without a primary lung cancer and in distant normal bronchus specimens 
      from patients with NSCLC. RAR alpha, RXR alpha, and RXR gamma were expressed in 
      more than 95% of the NSCLC specimens. In contrast, RAR beta, RAR gamma, and RXR 
      beta expression was detected in only 42%, 72%, and 76% of NSCLC, respectively. 
      CONCLUSIONS: These data suggest that the expression of RAR alpha, RXR alpha, and 
      RXR gamma is not altered in NSCLC; however, expression of RAR beta and possibly 
      also of RAR gamma and RXR beta is suppressed in a large percentage of patients 
      with lung cancer. IMPLICATIONS: The loss of expression of one or more of these 
      nuclear retinoid receptors may be associated with lung carcinogenesis.
FAU - Xu, X C
AU  - Xu XC
AD  - Department of Tumor Biology, The University of Texas M. D. Anderson Cancer 
      Center, Houston 77030, USA.
FAU - Sozzi, G
AU  - Sozzi G
FAU - Lee, J S
AU  - Lee JS
FAU - Lee, J J
AU  - Lee JJ
FAU - Pastorino, U
AU  - Pastorino U
FAU - Pilotti, S
AU  - Pilotti S
FAU - Kurie, J M
AU  - Kurie JM
FAU - Hong, W K
AU  - Hong WK
FAU - Lotan, R
AU  - Lotan R
LA  - eng
GR  - CA68437/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Natl Cancer Inst
JT  - Journal of the National Cancer Institute
JID - 7503089
RN  - 0 (DNA Probes)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Neoplasm)
RN  - 0 (Receptors, Retinoic Acid)
SB  - IM
CIN - J Natl Cancer Inst. 1997 May 7;89(9):602-4. PMID: 9150178
MH  - Adenocarcinoma/chemistry
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Bronchi/chemistry
MH  - Carcinoma, Non-Small-Cell Lung/*chemistry/etiology/pathology
MH  - DNA Probes
MH  - Down-Regulation
MH  - Female
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - In Situ Hybridization
MH  - Lung Neoplasms/*chemistry/etiology/pathology
MH  - Male
MH  - Middle Aged
MH  - RNA, Messenger/analysis
MH  - RNA, Neoplasm/analysis
MH  - Receptors, Retinoic Acid/*analysis
EDAT- 1997/05/07 00:00
MHDA- 1997/05/07 00:01
CRDT- 1997/05/07 00:00
PHST- 1997/05/07 00:00 [pubmed]
PHST- 1997/05/07 00:01 [medline]
PHST- 1997/05/07 00:00 [entrez]
AID - 10.1093/jnci/89.9.624 [doi]
PST - ppublish
SO  - J Natl Cancer Inst. 1997 May 7;89(9):624-9. doi: 10.1093/jnci/89.9.624.