Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
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Honey V. Reddi Alicia Algeciras-Schimnich Bryan McIver Norman L. Eberhardt Stefan K.G. Grebe
Received: 1 June 2007 Accepted in revised form: 20 June 2007
S.K.G. Grebe (쾷), Department of Laboratory Medicine/Pathology, 200 First Street SW, Mayo Clinic, Rochester, MN 55905, USA. Tel.: +1-507-284-3345 Fax: +1-507-284-9758 e-mail: [email protected]
H.V. Reddi • B. McIver N.L. Eberhardt Department of Medicine, Division of Endocrinology Mayo Clinic, Rochester, MN 55905, USA A. Algeciras-Schimnich S.K.G. Grebe Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA N.L. Eberhardt Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA
REVIEW
Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer
Abstract 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, fus-
Differentiated thyroid cancer Endocrine glands are uniquely susceptible to neoplastic transformation. Based on autopsy and radiographic surveys, incidental adrenal, pituitary, and thyroid adenomas and car-
ing 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.
Key words Follicular thyroid carcinoma • Papillary thyroid carcinoma • RET protooncogene • Peroxisome proliferators activated receptorgamma • PAX8 • Chromosomal translocations
cinomas affect 5%–20% of the population [1–6]. While most tumours in endocrine glands remain undetected and are benign, there are significant numbers of clinically evident malignant tumours of the thyroid. Indeed, thyroid carcinoma represents the most common endocrine malignancy, with an estimated 33,500 new cases, predicted to cause 1,500 deaths
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