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64 - Oncogenic events and therapeutic targets in thyroid cancer

from Part 3.4 - Molecular pathology: endocrine cancers

Published online by Cambridge University Press:  05 February 2015

By
James A. Fagin  and
Julio C. Ricarte Filho
Edited by
Edward P. Gelmann ,
Charles L. Sawyers  and
Frank J. Rauscher, III
James A. Fagin
Affiliation:
Department of Medicine and Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA
Julio C. Ricarte Filho
Affiliation:
Department of Medicine and Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY,USA
Edward P. Gelmann
Affiliation:
Columbia University, New York
Charles L. Sawyers
Affiliation:
Memorial Sloan-Kettering Cancer Center, New York
Frank J. Rauscher, III
Affiliation:
The Wistar Institute Cancer Centre, Philadelphia
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Summary

The thyroid contains two endocrine cell types: follicular cells, which secrete thyroid hormones, and parafollicular or C cells, the primary source of calcitonin. Most of this chapter is dedicated to reviewing the molecular and phenotypic characteristics of cancers derived from follicular cells, as they represent about 95% of all cancers arising from this gland, focusing in particular on oncoproteins that represent potential therapeutic targets for the disease.

The oncogenic repertoire of thyroid cancers of follicular cells

There are two major histological types of differentiated thyroid cancer: papillary (PTC) and follicular (FTC; Figure 64.1). PTCs arise as sporadic tumors, with a female preponderance, and are the most common form of the disease. Several key genetic events involved in PTC pathogenesis have been identified. Mutations of the receptor tyrosine kinases (RTK) RET or TRK, of the three RAS genes (NRAS>HRAS>KRAS), or of BRAF account for about 70% of these tumors. With very rare exceptions mutations in these genes is mutually exclusive in thyroid carcinomas of all stages of differentiation, suggesting that just one activating event in the RTK-Ras-Raf-MEK-ERK pathway is sufficient to drive tumorigenesis (1).

Type
Chapter
Information
Molecular Oncology
Causes of Cancer and Targets for Treatment
 , pp. 704 - 711
Publisher: Cambridge University Press
Print publication year: 2013

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