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Journal of Oncology
Volume 2010, Article ID 921682, 6 pages
Review Article

New Targeted Molecular Therapies for Dedifferentiated Thyroid Cancer

1Department of Internal Medicine, Metabolism Unit, University of Pisa School of Medicine, Via Roma, 67, 56100 Pisa, Italy
2Rheumatology Unit, Department of Internal Medicine, School of Medicine, University of Modena and Reggio Emilia, Via del Pozzo, 71, 41100 Modena, Italy

Received 3 August 2009; Revised 16 January 2010; Accepted 22 March 2010

Academic Editor: Thomas J. Fahey

Copyright © 2010 Alessandro Antonelli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Dedifferentiated thyroid cancer (DeTC) derived from follicular epithelium is often incurable because it does not respond to radioiodine, radiotherapy, or chemotherapy. In cases, RET/PTC rearrangements are found in 30%–40%, RAS mutations in about 10%, and BRAF mutations in around 40%–50%, with no overlap between these mutations results in papillary thyroid cancer, while a higher prevalence of BRAF mutations (up to 70%) has been observed in DeTC. The identification of these activating mutations in DeTC makes this malignancy an excellent model to examine the effect of tyrosine kinase inhibitors (TKIs). Clinical trials with several TKIs targeting RET, and to a lesser extent BRAF, and other TKRs have shown positive results, with about one-third of DeTC showing a reduction in tumor size up to 50%, with the longest treatment duration of approximately three-four years. Angiogenesis inhibitors have also shown promising activity in DeTC. Progress is being made toward effective targeted DeTC therapy. The possibility of testing the sensitivity of primary DeTC cells from each subject to different TKIs could increase the effectiveness of the treatment.