Abstract

Oncocytes are cells that have abundant eosinophilic cytoplasm due to the accumulation of mitochondria; they are also known as oxyphils. In the thyroid they have been called Hürthle cells but this is a misnomer, since Hürthle described C cells; for this reason, we propose the use of “oncocyte” as a scientific term rather than an incorrect eponym. Oncocytic change occurs in nontumorous thyroid disorders, in benign and malignant tumors of thyroid follicular cells, in tumors composed of thyroid C cells, and intrathyroidal parathyroid proliferations as well as in metastatic lesions. The morphology of primary oncocytic thyroid tumors is similar to that of their non-oncocytic counterparts but also is complicated by the cytologic features of these cells that include both abundant eosinophilic cytoplasm and large cherry red nucleoli. The molecular alterations in oncocytic thyroid tumors echo those of their non-oncocytic counterparts but in addition feature mitochondrial DNA mutations as well as chromosomal gains and losses. In this review we emphasize the importance of recognition of the spectrum of oncocytic thyroid pathology. The cell of origin, morphologic features including architecture, nuclear atypia and invasive growth, as well as high grade features such as mitoses and necrosis, enable accurate classification of these lesions. The molecular alterations underlying the pathological entity are associated with genetic alterations associated with oncocytic change. The arbitrary cut-off of 75% oncocytic change to classify a lesion as an oncocytic variant brings another complexity to the classification scheme of tumors that frequently have mixed oncocytic and non-oncocytic components. This controversial and often confusing area of thyroid pathology requires thoughtful and cautious investigation to clarify accurate diagnosis, prognosis and prediction for patients with oncocytic thyroid lesions.

Highlights

  • The term “oncocyte” was applied to describe cells that have abundant eosinophilic cytoplasm due to the accumulation of mitochondria

  • (ubiquinone- cytochrome-c-oxidoreductase) and complex IV of the respiratory chain and somatic mitochondrial DNA mutations in NADH dehydrogenase genes and cytochrome c oxidase activity-impairing genes have been found in non-neoplastic oncocytes in parathyroid glands [14, 15], suggesting that these mechanisms are responsible for nonneoplastic, non-clonal oncocytic change

  • This review has identified the unique features of oncocytic cells and tumors in the thyroid but has emphasized the importance of recognizing the similarities of oncocytic pathologies in this gland with those of their nononcocytic counterparts

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Summary

Oncocytic Change in Thyroid Pathology

Reviewed by: Zubair Wahid Baloch, University of Pennsylvania, United States Liborio Torregrossa, University of Pisa, Italy. The morphology of primary oncocytic thyroid tumors is similar to that of their non-oncocytic counterparts and is complicated by the cytologic features of these cells that include both abundant eosinophilic cytoplasm and large cherry red nucleoli. The arbitrary cut-off of 75% oncocytic change to classify a lesion as an oncocytic variant brings another complexity to the classification scheme of tumors that frequently have mixed oncocytic and non-oncocytic components. This controversial and often confusing area of thyroid pathology requires thoughtful and cautious investigation to clarify accurate diagnosis, prognosis and prediction for patients with oncocytic thyroid lesions

INTRODUCTION
THYROID FOLLICULAR NODULAR DISEASE AND ADENOMAS
PAPILLARY THYROID CARCINOMA
POORLY DIFFERENTIATED CARCINOMA
MEDULLARY THYROID CARCINOMA
CONCLUSIONS
Findings
AUTHOR CONTRIBUTIONS
Full Text
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