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Hypermethylation of the retinoic acid receptor-beta(2) gene in head and neck carcinogenesis.
Emile M Youssef; Dafna Lotan; Jean-Pierre Issa; Kenichi Wakasa; You-Hong Fan; Li Mao; Khaled Hassan; Lei Feng; J Jack Lee; Scott M Lippman; et al. (Profiled Author: Li Mao)
Departments of Thoracic/Head and Neck Medical Oncology,The University of Texas, MD Anderson Cancer Center, Houston, Texas 77345, USA.
Clinical cancer research : an official journal of the American Association for Cancer Research 2004;10(5):1733-42.
PURPOSE: Retinoic acid receptor-beta(2) (RAR-beta(2)) expression is suppressed in oral premalignant lesions and head and neck squamous cell carcinomas (HNSCCs). This study was conducted to determine whether RAR-beta(2) gene expression in such lesions can be silenced by promoter methylation. EXPERIMENTAL DESIGN: RAR-beta(2) methylation was analyzed in DNA samples from 22 pairs of primary HNSCC and adjacent normal epithelium, 124 samples of oral leukoplakia, and 18 HNSCC cell lines using methylation-specific PCR. RAR-beta(2) promoter was methylated in 67, 56, and 53% of HNSCC tumors, HNSCC cell lines, and microdissected oral leukoplakia specimens, respectively. RAR-beta(2) hypermethylation was confirmed by sodium bisulfite-PCR combined with restriction enzyme digestion analysis and by random cloning and sequencing of bisulfite-treated DNA isolates. RESULTS: Significantly higher RAR-beta(2) hypermethylation levels were found in tumor tissue compared with adjacent normal tissue (P = 0.002). RAR-beta(2) methylation in the cell lines was correlated with loss of RAR-beta(2) expression (P = 0.013) and inversely related to the presence of mutated p53 (P = 0.025). The demethylating agent 5-aza-2'-deoxycytidine (5-aza-CdR) restored RAR-beta(2) inducibility by all-trans-retinoic acid (ATRA) in some of the cell lines, which posses a methylated RAR-beta(2) promoter. In some cell lines, this effect was associated with increased growth inhibition after combined treatment with 5-aza-CdR and ATRA. CONCLUSIONS: RAR-beta(2) silencing by methylation is an early event in head and neck carcinogenesis; 5-Aza-CdR can restore RAR-beta(2) inducibility by ATRA in most cell lines, and the combination of 5-aza-CdR and ATRA is more effective in growth inhibition than single agents.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
L MaoClinical cancer research : an official journal of the American Association for Cancer Research 2000;6(2):321-2.
S Y Sun; P Yue; L Mao; M I Dawson; B Shroot; W W Lamph; R A Heyman; R A Chandraratna; K Shudo; W K Hong; et al.Clinical cancer research : an official journal of the American Association for Cancer Research 2000;6(4):1563-73.
V Papadimitrakopoulou; J Izzo; S M Lippman; J S Lee; Y H Fan; G Clayman; J Y Ro; W N Hittelman; R Lotan; W K Hong; et al.Oncogene 1997;14(15):1799-803.
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