Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer

  • Honey V. Reddi | grebe.stefan@mayo.edu Department of Medicine, Division of Endocrinology Mayo Clinic, Rochester, United States.
  • Alicia Algeciras-Schimnich Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, United States.
  • Bryan McIver Department of Medicine, Division of Endocrinology Mayo Clinic, Rochester, United States.
  • Norman L. Eberhardt Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester; Department of Medicine, Division of Endocrinology Mayo Clinic, Rochester, United States.
  • Stefan K.G. Grebe Department of Laboratory Medicine/Pathology, Mayo Clinic, Rochester; Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, United States.

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, 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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Published
2011-12-18
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Issue
Section
Reviews
Keywords:
Follicular thyroid carcinoma - Papillary thyroid carcinoma - RET protooncogene - Peroxisome proliferators activated receptorgamma - PAX8 - Chromosomal translocations
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How to Cite
Reddi, H. V., Algeciras-Schimnich, A., McIver, B., Eberhardt, N. L., & Grebe, S. K. (2011). Chromosomal rearrangements and the pathogenesis of differentiated thyroid cancer. Oncology Reviews, 1(2), 81-90. https://doi.org/10.4081/oncol.2007.143