Abstract
Thyroid cancer is the most common endocrine malignancy and its incidence goes on increasing worldwide. The majority of thyroid tumours comprise well-differentiated (papillary and follicular) thyroid carcinomas that usually carry an excellent prognosis, while a minority progress to poorly differentiated carcinoma (PDTC) and, ultimately, to the highly aggressive and lethal undifferentiated carcinoma (UTC). Recently, some major advances have been made on the histologic and imunohistochemical identification, as well as on the molecular characterization of PDTC and UTC. In this review we summarize the most recent immunohistochemical and molecular findings in PDTC and UTC, giving a particular emphasis to the diagnostic and prognostic meaning of the genetic alterations.
Highlights
The most important difference between the classifications of thyroid tumours in the WHO books of 1988 and 2004 concerns the individualization in the latter of the group of poorly differentiated carcinomas (PDTC) [1, 2]
It was recognized that all sorts of benign and malignant thyroid tumours may be composed by the individualization of oncocytic cells, leading to oncocytic/Hürthle cell variants of adenoma and of follicular papillary and poorly differentiated thyroid carcinoma [1]
It is usually advanced that the absence of an oncocytic/ Hürthle cell variant of undifferentiated carcinoma (UTC) reflects the high mitotic ratio of such tumours [3]
Summary
The most important difference between the classifications of thyroid tumours in the WHO books of 1988 and 2004 concerns the individualization in the latter of the group of poorly differentiated carcinomas (PDTC) [1, 2]. Received : 29.05.2015 Accepted : 03.06.2015 a widely invasive follicular carcinoma with a trabecular/ solid growth pattern – and the intrinsic heterogeneity of both groups of carcinoma Another problem regards the existence of several clinicopathological entities in thyroid oncology that may be considered as a sort of poorly differentiated carcinoma [e.g. Such entities have been recently described and discussed in the 2014 - AFIP book on Thyroid and Parathyroid Tumours [8] and will not be addressed in the present review. Molecular alterations TP53 TERT promoter mutation RAS BRAF CTNNB1 PI3KCA PTEN AKT1 ALK
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