PRESERVATION OF CELL TYPE
Differentiated thyroid cancer represents most (90%-95%) types of thyroid cancer and includes papillary, follicular, and Hürthle cell carcinomas (HCCs) (6). Cellular differentiation is a central aspect in the histopathologic classification for thyroid follicular epithelial cell-derived cancers and refers to the process by which a cell becomes specialized to perform a specific function. Differentiated thyroid cancers maintain the characteristics and behavior of normal follicular epithelial cells in thyroid tissue. These cells retain many of the physiologic functions of thyroid cells, including thyroid-stimulating hormone (TSH, also called thyrotropin) stimulation of growth, iodine uptake (expression of sodium iodine symporter), and thyroid hormone production (9). Differentiated thyroid cancers maintain radioactive iodine (RAI) avidity, which permits the use of RAI scintigraphy and treatment as part of the disease management strategy. As a general rule, differentiated cancers tend to be less aggressive than undifferentiated cancers (9).
Poorly differentiated thyroid cancer (PDTC) was at one time considered a variant of differentiated thyroid cancer; however, the World Health Organization began recognizing it as a distinct pathologic entity in 2004 because the clinical and histologic features occupy an intermediate position between differentiated thyroid cancer and undifferentiated thyroid cancer (10-13). PDTC occurs de novo; however, there is a theory that PDTC may also transform from differentiated thyroid cancers through the accumulation of genetic abnormalities (11,14). This theory is supported by the frequent cooccurrence of PDTC and differentiated thyroid cancer in the same tumor specimen and the overlap of genetic mutations (11). When PDTC and well-differentiated thyroid cancer are present in the same tissue sample, it is important to note the presence of PDTC, as prognosis and treatment strategies may be guided by the PDTC component (10). Given that PDTCs are often resistant to RAI therapy, these cancers present a therapeutic challenge (11,12). Outcome statistics for PDTCs are worse than for differentiated thyroid cancers. In PDTCs, approximately 50% of patients survive after 10 y, whereas in differentiated thyroid cancers, particularly papillary thyroid carcinoma (PTC), 95% of patients survive after 10 y (13).
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Undifferentiated thyroid cancer includes anaplastic thyroid carcinoma (ATC), a very rare form of thyroid carcinoma accounting for less than 1% of all thyroid carcinomas (15). Undifferentiated thyroid cancer may occur de novo or may transform from a previously differentiated thyroid cancer (more commonly PTC, but also follicular thyroid carcinoma [FTC] and PDTC) (12,14). A signature attribute of many advanced tumors is cellular dedifferentiation, whereby cancerous cells maintain little to no resemblance to the normal cells from which the cancer originated. In the context of thyroid cancer, loss of RAI avidity most commonly develops from cellular dedifferentiation, resulting in the impairment of the sodium iodine symporter function (14,15). Loss of iodine avidity excludes the use of RAI scintigraphy and treatment. As thyroid cancer cells dedifferentiate, their glucose metabolism increases, allowing for evaluation with 18F-FDG PET/CT (16). Overall outcomes and survival statistics are poor for undifferentiated thyroid cancer, with a mean survival of 0.5 y after diagnosis (15).
Figure 1 illustrates the cellular differentiation stage for follicular epithelial cell-derived thyroid carcinomas and how it relates to radioiodine scintigraphy/treatment and overall prognosis.
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