Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer

The majority of thyroid cancers arise from the follicular cells of the thyroid gland, which yield a wide variety of distinct morphotypes, ranging from relatively indolent lesions to the most malignant forms of cancer known. The remaining primary thyroid cancers arise from C cells within the gland an...

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Main Authors: Honey V. Reddi, Alicia Algeciras-Schimnich, Bryan McIver, Norman L. Eberhardt, Stefan K.G. Grebe
Format: Article
Language:English
Published: Frontiers Media S.A. 2011-12-01
Series:Oncology Reviews
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Online Access:http://oncologyreviews.org/index.php/or/article/view/143
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author Honey V. Reddi
Alicia Algeciras-Schimnich
Bryan McIver
Norman L. Eberhardt
Stefan K.G. Grebe
author_facet Honey V. Reddi
Alicia Algeciras-Schimnich
Bryan McIver
Norman L. Eberhardt
Stefan K.G. Grebe
author_sort Honey V. Reddi
collection DOAJ
description The majority of thyroid cancers arise from the follicular cells of the thyroid gland, which yield a wide variety of distinct morphotypes, ranging from relatively indolent lesions to the most malignant forms of cancer known. The remaining primary thyroid cancers arise from C cells within the gland and result primarily from mutations of the RET protooncogene, germ line mutations of which give rise to the various forms of multiple endocrine neoplasia. The most common of the follicular cell-derived cancers are papillary carcinomas, (PTC), followed by follicular carcinomas (FTC) and its Hurthle cell variant (HCC) and finally anaplastic carcinomas (ATC). The pathogenesis of many thyroid cancers, of both PTC and FTC morphotype, involves chromosomal translocations. Rearrangements of the RET protoconcogene are known to be involved in the pathogenesis of ca. 50% of PTC. A similar proportion of FTC have been associated with a t(2;3)(q13;p25) translocation, fusing the thyroid-specific transcription factor PAX8 with the peroxisome proliferator-activated receptor gamma (PPARγ) nuclear receptor, a ubiquitously expressed transcription factor. These rearrangements have analogy with translocations in erythropoetic cells, which form the only other known group of human malignancies that are largely the result of chromosomal translocation events. In this review we compare and contrast the oncogenic properties of thyroid and erythroid chromosomal transformations and speculate on mechanisms leading to their formation.
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spelling doaj.art-fb3f20c757e0448c9e18c660700fd1792023-01-03T02:38:01ZengFrontiers Media S.A.Oncology Reviews1970-55571970-55652011-12-01128190137Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancerHoney V. Reddi0Alicia Algeciras-Schimnich1Bryan McIver2Norman L. Eberhardt3Stefan K.G. Grebe4Department of Medicine, Division of Endocrinology Mayo Clinic, RochesterDepartment of Laboratory Medicine and Pathology, Mayo Clinic, RochesterDepartment of Medicine, Division of Endocrinology Mayo Clinic, RochesterDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester; Department of Medicine, Division of Endocrinology Mayo Clinic, RochesterDepartment of Laboratory Medicine/Pathology, Mayo Clinic, Rochester; Department of Laboratory Medicine and Pathology, Mayo Clinic, RochesterThe majority of thyroid cancers arise from the follicular cells of the thyroid gland, which yield a wide variety of distinct morphotypes, ranging from relatively indolent lesions to the most malignant forms of cancer known. The remaining primary thyroid cancers arise from C cells within the gland and result primarily from mutations of the RET protooncogene, germ line mutations of which give rise to the various forms of multiple endocrine neoplasia. The most common of the follicular cell-derived cancers are papillary carcinomas, (PTC), followed by follicular carcinomas (FTC) and its Hurthle cell variant (HCC) and finally anaplastic carcinomas (ATC). The pathogenesis of many thyroid cancers, of both PTC and FTC morphotype, involves chromosomal translocations. Rearrangements of the RET protoconcogene are known to be involved in the pathogenesis of ca. 50% of PTC. A similar proportion of FTC have been associated with a t(2;3)(q13;p25) translocation, fusing the thyroid-specific transcription factor PAX8 with the peroxisome proliferator-activated receptor gamma (PPARγ) nuclear receptor, a ubiquitously expressed transcription factor. These rearrangements have analogy with translocations in erythropoetic cells, which form the only other known group of human malignancies that are largely the result of chromosomal translocation events. In this review we compare and contrast the oncogenic properties of thyroid and erythroid chromosomal transformations and speculate on mechanisms leading to their formation.http://oncologyreviews.org/index.php/or/article/view/143Follicular thyroid carcinoma - Papillary thyroid carcinoma - RET protooncogene - Peroxisome proliferators activated receptorgamma - PAX8 - Chromosomal translocations
spellingShingle Honey V. Reddi
Alicia Algeciras-Schimnich
Bryan McIver
Norman L. Eberhardt
Stefan K.G. Grebe
Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
Oncology Reviews
Follicular thyroid carcinoma - Papillary thyroid carcinoma - RET protooncogene - Peroxisome proliferators activated receptorgamma - PAX8 - Chromosomal translocations
title Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
title_full Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
title_fullStr Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
title_full_unstemmed Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
title_short Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
title_sort chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
topic Follicular thyroid carcinoma - Papillary thyroid carcinoma - RET protooncogene - Peroxisome proliferators activated receptorgamma - PAX8 - Chromosomal translocations
url http://oncologyreviews.org/index.php/or/article/view/143
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