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      Anaplastic thyroid carcinoma: from clinicopathology to genetics and advanced therapies

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          Abstract

          Although anaplastic thyroid carcinoma (ATC) is a rare form of thyroid cancer, the limited efficacy of conventional treatment options and challenges in histological diagnosis make this an almost invariably lethal disease. In this Review, the authors describe the clinical and pathological features of ATC, highlight recent advances in uncovering the genetics and molecular biology of this disease, and discuss both conventional and future treatment modalities.

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          BRAF mutation in thyroid cancer.

          M Xing (2005)
          Genetic alteration is the driving force for thyroid tumorigenesis and progression, based upon which novel approaches to the management of thyroid cancer can be developed. A recent important genetic finding in thyroid cancer is the oncogenic T1799A transversion mutation of BRAF (the gene for the B-type Raf kinase, BRAF). Since the initial report of this mutation in thyroid cancer 2 years ago, rapid advancements have been made. BRAF mutation is the most common genetic alteration in thyroid cancer, occurring in about 45% of sporadic papillary thyroid cancers (PTCs), particularly in the relatively aggressive subtypes, such as the tall-cell PTC. This mutation is mutually exclusive with other common genetic alterations, supporting its independent oncogenic role, as demonstrated by transgenic mouse studies that showed BRAF mutation-initiated development of PTC and its transition to anaplastic thyroid cancer. BRAF mutation is mutually exclusive with RET/PTC rearrangement, and also displays a reciprocal age association with this common genetic alteration in thyroid cancer. The T1799A BRAF mutation occurs exclusively in PTC and PTC-derived anaplastic thyroid cancer and is a specific diagnostic marker for this cancer when identified in cytological and histological specimens. This mutation is associated with a poorer clinicopathological outcome and is a novel independent molecular prognostic marker in the risk evaluation of thyroid cancer. Moreover, preclinical and clinical evaluations of the therapeutic value of novel specific mitogen-activated protein kinase pathway inhibitors in thyroid cancer are anticipated. This newly discovered BRAF mutation may prove to have an important impact on thyroid cancer in the clinic.
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            International patterns and trends in thyroid cancer incidence, 1973-2002.

            Briseis A Kilfoy, Tongzhang Zheng, Theodore R. Holford … (2009)
            During the past several decades, an increasing incidence of thyroid cancer has been reported in many parts of the world. To date, no study has compared the trends in thyroid cancer incidence across continents. We examined incidence data from cancer incidence in five continents (CI5) over the 30-year period 1973-2002 from 19 populations in the Americas, Asia, Europe, and Oceania. Thyroid cancer rates have increased from 1973-1977 to 1998-2002 for most of the populations except Sweden, in which the incidence rates decreased about 18% for both males and females. The average increase was 48.0% among males and 66.7% among females. More recently, the age-adjusted international thyroid cancer incidence rates from 1998 to 2002 varied 5-fold for males and nearly 10-fold for females by geographic region. Considerable variation in thyroid cancer incidence was present for every continent but Africa, in which the incidence rates were generally low. Our analysis of published CI5 data suggests that thyroid cancer rates increased between 1973 and 2002 in most populations worldwide, and that the increase does not appear to be restricted to a particular region of the world or by the underlying rates of thyroid cancer.
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              Dysregulation of the TSC-mTOR pathway in human disease.

              Ken Inoki, Michael Corradetti, Kun-Liang Guan … (2005)
              The mammalian target of rapamycin (mTOR) has a central role in the regulation of cell growth. mTOR receives input from multiple signaling pathways, including growth factors and nutrients, to stimulate protein synthesis by phosphorylating key translation regulators such as ribosomal S6 kinase and eukaryote initiation factor 4E binding protein 1. High levels of dysregulated mTOR activity are associated with several hamartoma syndromes, including tuberous sclerosis complex, the PTEN-related hamartoma syndromes and Peutz-Jeghers syndrome. These disorders are all caused by mutations in tumor-suppressor genes that negatively regulate mTOR. Here we discuss the emerging evidence for a functional relationship between the mTOR signaling pathway and several genetic diseases, and we present evidence supporting a model in which dysregulation of mTOR may be a common molecular basis, not only for hamartoma syndromes, but also for other cellular hypertrophic disorders.
              Article 0 comments Cited 212 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Nature Reviews Endocrinology
                Abbreviated Title: Nat Rev Endocrinol
                Publisher: Springer Nature
                ISSN (Print): 1759-5029
                ISSN (Electronic): 1759-5037
                Publication date Created: July 14 2017
                Publication date (Print): July 14 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/nrendo.2017.76
                PubMed ID: 28707679
                SO-VID: 18d5f0c5-3c35-4a25-b630-76c160b4decf
                Copyright © © 2017
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