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CLINICAL REVIEW 158 |
Washington Hospital Center, MedStar Research Institute (M.B.-B., M.D.R.), Washington, D.C. 20010; and SEMPR, Serviço de Endocrinologia e Metabologia do Hospital das Clínicas da Universidade Federal do Paraná (M.B.-B.), Curitiba 80.060-240, Brazil
Address all correspondence and requests for reprints to: Matthew D. Ringel, M.D., 110 Irving Street NW, Room 2A-46B, Washington, D.C. 20010. E-mail: matthew.ringel{at}medstar.net.
Abstract
One of the greatest challenges in the management of patients with follicular cell-derived thyroid cancer is the treatment of tumors that progress despite surgery, radioiodine, and T4 suppression of TSH. As knowledge of thyroid cancer biology improves, the potential exists to develop compounds targeted to treat thyroid cancers that do not respond to traditional therapy. Recently, the development of therapies targeted against specific molecular pathways involved in cancer progression has resulted in dramatic responses in patients with chronic myelogenous leukemia, gastrointestinal stromal tumors, and other cancers. A number of compounds are currently being evaluated in clinical trials that alter pathways involved thyroid cancer, and several of these agents have been tested in thyroid cancer in vitro and in vivo. In this review we will discuss the mechanisms of action and preclinical/clinical data for several of these compounds that have the potential to play an important role in the management of thyroid cancer in the future.
Footnotes
This work was supported by grants from the American Cancer Society (RSG CNE-103291) and the NIH (CAN8339479), to M.D.R.
Abbreviations: 17-AAG, 17-N-allylamino-17-demethoxy-geldanamycin; COX-2, cyclooxygenase-2; EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; HDAC, histone deacetylase; Hsp90, 90-kDa heat shock protein; MEK, MAPK kinase; mTOR, mammalian target of rapamycin; NIS, sodium-iodide symporter; TK, thymidine kinase; TRAIL, TNF-related apoptosis-inducing ligand; VEGF, vascular endothelial growth factor.
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