Abstract
Metabolic dysregulation within the tumor microenvironment (TME) is critical to the process of tumorigenesis in various cancer types. Thyrocyte metabolism in papillary and anaplastic thyroid cancer, however, remains poorly characterized, and studies analyzing the role of multicompartment metabolism in thyrocyte oncogenesis are sparse. We present a review of the current knowledge on cellular metabolism in non-cancerous and cancerous thyroid tissues, focusing on the monocarboxylate transporters MCT1 and MCT4, and on a transporter of the outer mitochondrial membrane TOMM20. Understanding the metabolic phenotype of tumor cells and associated stromal cells in thyroid cancer can have profound implications on the use of biomarker staining in detecting subclinical cancer, imaging as it relates to expression of various transport proteins, and therapeutic interventions that manipulate this dysregulated tumor metabolism to halt tumorigenesis and eradicate the cancer. Future studies are required to confirm the prognostic significance of these biomarkers and their correlation with existing staging schemas such as the AGES, AMES, ATA and MACIS scoring systems.
Highlights
Thyroid cancer is the most common endocrine malignancy in the United States, with the fifth highest incidence of all cancers affecting females [1] and the highest prevalence of any malignancy affecting women under 35 years old
This prognostic disparity emphasizes the importance of classifying the type of thyroid cancer as the primary step in assessment, which is usually diagnosed via fine needle aspiration (FNA)
The BRAF gene mutation, which has been detected in 30-80% of papillary thyroid cancer (PTC) [61], has been an area of interest to improve the diagnostic yield in cases of indeterminate cytology
Summary
Thyroid cancer is the most common endocrine malignancy in the United States, with the fifth highest incidence of all cancers affecting females [1] and the highest prevalence of any malignancy affecting women under 35 years old. A two-compartment model of tumor metabolism has been set forth wherein carcinoma cells secrete hydrogen peroxide to induce oxidative stress in tumor fibroblasts or stromal cells [22] These fibroblasts in turn increase their production of ROS, which induces aerobic glycolysis and autophagy, resulting in increased levels of intermediate catabolites such as lactate, glutamine and ketone bodies [18]. Mast cells were significantly more abundant in the intratumoral and peritumoral regions of follicular variant of PTC compared to adenoma, suggesting its usefulness in distinguishing between benign and malignant forms of follicular thyroid lesions [42] This paradigm of shuttling high-yield metabolites from stromal fibroblasts to fuel cancer cell growth and metastasis has resulted in increased research of various transport proteins. There was significantly more TOMM20 staining in ATC compared to NCT (p
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
