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Tuberc Respir Dis. 2008 Dec;65(6):495-503. English. Original Article. https://doi.org/10.4046/trd.2008.65.6.495
Kwon MH , Lee GE , Kwon SJ , Choi E , Na MJ , Cho HM , Kim YJ , Sul HJ , Cho YJ , Son JW .
Department of Internal Medicine, Konyang University School of Medicine, Daejeon, Korea. sk1609@hanmail.net
Department of Chest Surgery, Konyang University School of Medicine, Daejeon, Korea.
Department of Pathology, Konyang University School of Medicine, Daejeon, Korea.
Department of Radiology, Konyang University School of Medicine, Daejeon, Korea.
Abstract

BACKGROUND: Epigenetic alterations in certain genes are now known as at least important as genetic mutation in pathogenesis of cancer. Especially abnormal hypermethylation in or near promoter region of tumor suppressor genes (TSGs) are known to result in gene silencing and loss of gene function eventually. The authors tried to search for new lung cancer-specific TSGs which have CpG islands and HpaII sites, and are thought to be involved in carcinogenesis by epigenetic mechanism. METHODS: Tumor tissue and corresponding adjacent normal tissue were obtained from 10 patients who diagnosed with non small cell lung cancer (NSCLC) and underwent surgery in Konyang university hospital in 2005. Methylation profiles of promoter region of 21 genes in tumor tissue & non-tumor tissue were examined with HpaII-MspI methylation microarray (Methyl-Scan DNA chip(R), Genomic tree, Inc, South Korea). The rates of hypermethylation were compared in tumor and non-tumor group, and as a normal control, we obtained lung tissue from two young patients with pneumothorax during bullectomies, methylation profiles were examined in the same way. RESULTS: Among the 21 genes, 10 genes were commonly methylated in tumor, non-tumor, and control group. The 6 genes of APC, AR, RAR-b, HTR1B, EPHA3, and CFTR, among the rest of 11 genes were not methylated in control, and more frequently hypermethylated in tumor tissue than non-tumor tissue. CONCLUSION: In the present study, HTR1B, EPHA3, and CFTR are suggested as possible novel TSGs of NSCLC by epigenetic mechanism.

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