Related Experiment Video
Updated: Jun 30, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
Gene-specific promoter hypermethylation without global hypomethylation in follicular thyroid cancer
Jia-Jing Lee1, Janos Geli, Catharina Larsson
1Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, CMM L8:01, SE-171 76 Stockholm, Sweden. jia.jing.lee@ki.se
Abstract:
Genome-wide hypomethylation and hypermethylation at CpG promoters are common in cancer. To date, little is known about global methylation changes in follicular thyroid cancer (FTC). Two independent quantitative methods, bisulphite Pyrosequencing of Long Interspersed Nucleotide Elements-1 (LINE-1) and LUminometric Methylation Assay (LUMA) were used to quantify genome-wide methylation in 21 FTC and corresponding normal thyroid tissues. Unexpectedly global methylation was not found significantly altered in tumors compared to normal thyroid by either LINE-1 (p=0.57) or LUMA (p=0.42), whilst the promoter of a tumor suppressor that is often epigenetically dysregulated, RASSF1A was found to be significantly hypermethylated by Pyrosequencing (p=0.0001). Moreover, allelic imbalance at the RASSF1A locus was observed in 15/21 of the tumors. mRNA expression of RASSF1A was significantly lower in tumors compared to corresponding normal tissues (p=0.0002). In summary, the epigenetic inactivation of RASSF1A is a frequent event in FTC, but is not coupled to changes in global methylation.
Related Concept Videos
Epigenetic Regulation
X-chromosome...
Epigenetic Regulation
Hyperthyroidism II: Pathophysiology
Hyperthyroidism I: Introduction
Synthesis and Regulation of Thyroid Hormones
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
