Gene Methylation Associated with Differentiated Thyroid Cancer.
10.11106/cet.2014.7.2.118
- Author:
Soon Young TAE
1
;
Hyun Keun CHI
;
Su Jin KIM
;
Kyu Eun LEE
;
Yeo Kyu YOUN
Author Information
1. Department of Surgery, Seoul National University Hospital and College of Medicine, Division of Surgery, Thyroid Center, Seoul National University Cancer Center and Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea. kyulee@medimail.co.kr
- Publication Type:Review
- Keywords:
Epigenetics;
Methylation;
Thyroid cancer;
Genes;
Tumor suppressor
- MeSH:
Base Sequence;
Carcinogenesis;
Epigenomics;
Genes, Tumor Suppressor;
Ion Transport;
Methylation*;
Prognosis;
Promoter Regions, Genetic;
Thyroid Neoplasms*;
Thyrotropin
- From:Journal of Korean Thyroid Association
2014;7(2):118-128
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Epigenetic alteration changes expression of many genes, such as tumor suppressor gene and molecular specific gene, without change in DNA sequence. Cancers, including thyroid cancer, often exhibit an aberrant methylation of gene promoter regions, which is associated with loss of gene function. Aberrant methylation plays a fundamental role in tumorigenesis. Methylation of some genes tends to occur in certain types of thyroid cancer. Methylation of TIMP3, SLC5A8, p16, RARbeta2, DAPK genes is associated with papillary thyroid cancer. Some studies show that aberrant methylation is related to the BRAF V600E mutation. Methylation of PTEN and RASSF1A genes occurs commonly in follicular thyroid cancer. Methylation of thyroid-specific genes, such as sodium/iodide symporter, thyroid-stimulating hormone receptor, and SLC26A4 which encodes pendrine, also has a relation to thyroid cancer. Methylation of these genes could be utilized as markers to detect early disease, to define prognosis and to predict therapeutic targets of thyroid cancer.
