Abstract
Recent advances in high-throughput molecular and multi-omics technologies have improved our understanding of the molecular changes associated with thyroid cancer initiation and progression. The translation into clinical use based on molecular profiling of thyroid tumors has allowed a significant improvement in patient risk stratification and in the identification of targeted therapies, and thereby better personalized disease management and outcome. This review compiles the following: (1) the major molecular alterations of the genome, epigenome, transcriptome, proteome, and metabolome found in all subtypes of thyroid cancer, thus demonstrating the complexity of these tumors and (2) the great translational potential of multi-omics studies to improve patient outcome.
Highlights
The incidence of thyroid cancer has been increasing by almost 300% in the past four decades with an estimated 54,000 patients diagnosed each year in the United States [1]
Earlier data has suggested that the rising incidence of thyroid cancer has been due to the increased detection of small, commonly incidental, and subclinical papillary thyroid cancer (PTC) with indolent behavior [1,2,3,4], the more recent analysis of the Surveillance, Epidemiology, and End Results (SEER) cancer registry data has shown an increase in advanced-stage PTC and PTC larger than 5 cm which were believed to be clinically detectable or were symptomatic [5]
Other common mutations in fatal non-anaplastic thyroid cancer include mutations in genes involved in phosphoinositide 3-kinase (PI3K)/AKT/PTEN/mTOR pathway, TP53, ATM, RB1, and POLE as well as genes involved in the chromatin remodeling complex and histone methyltransferases [97] (Figure 1) and 11% of Poorly Differentiated Thyroid Cancer (PDTC) harbored EIF1AX mutations which were strongly associated with RAS
Summary
The incidence of thyroid cancer has been increasing by almost 300% in the past four decades with an estimated 54,000 patients diagnosed each year in the United States [1]. From 1994 to 2013, incidence-based mortality from PTC increased 1.1% per year overall and 2.9% per year in those with metastatic PTC, consistent with a true increase in the incidence of thyroid cancer in the United States [6]. It is critically important to understand the molecular events associated with thyroid cancer initiation and progression to improve diagnostic accuracy, risk stratification, and to personalize treatment and surveillance plans. Medullary thyroid cancer (MTC) derives from C-cells and has its unique clinical characteristics and more uniform molecular features that have been discussed elsewhere
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