Abstract
Thyroid cancer is rare in the pediatric population, but thyroid carcinomas occurring in children carry a unique set of clinical, pathologic, and molecular characteristics. In comparison to adults, children more often present with aggressive, advanced stage disease. This is at least in part due to the underlying biologic and molecular differences between pediatric and adult thyroid cancer. Specifically, papillary thyroid carcinoma (which accounts for approximately 90% of pediatric thyroid cancer) has a high rate of gene fusions which influence the histologic subtypes encountered in pediatric thyroid tumors, are associated with more extensive extrathyroidal disease, and offer unique options for targeted medical therapies. Differences are also seen in pediatric follicular thyroid cancer, although there are few studies of non-papillary pediatric thyroid tumors published in the literature due to their rarity, and in medullary carcinoma, which is most frequently diagnosed in the pediatric population in the setting of prophylactic thyroidectomies for known multiple endocrine neoplasia syndromes. The overall shift in the spectrum of histotypes and underlying molecular alterations common in pediatric thyroid cancer is important to recognize as it may directly influence diagnostic test selection and therapeutic recommendations.
Highlights
Thyroid cancer is the leading cause of pediatric endocrine cancer, accounting for over 6% of all pediatric cancers from 2012 to 2016 [1]
Increases are reported for follicular thyroid carcinoma (FTC) [2]
The contribution of medullary (MTC), anaplastic (ATC), and poorly differentiated (PDTC) thyroid carcinomas is minor given their rarity in the pediatric population [1,3,4,5]
Summary
Thyroid cancer is the leading cause of pediatric endocrine cancer, accounting for over 6% of all pediatric cancers from 2012 to 2016 [1]. This figure reflects the rising incidence of pediatric thyroid carcinoma over the last four decades [1]. Between 1975 and 1995, the annual percent change (APC) of pediatric thyroid carcinoma was +0.8%/year; with an accelerated +4.6%/year APC from 1996 to 2016 [1]. Recommendations for the evaluation and management of thyroid cancer in the pediatric population have been extrapolated from adult guidelines. Genes 2019, 10, 723 adults, thyroid cancers in the pediatric population differ in clinical presentation, pathophysiology, and long-term outcomes [8]. We review the clinicopathologic presentation and treatment of pediatric thyroid carcinoma, highlighting key morphomolecular findings and their impact on clinical management
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