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PPAR Research
Volume 2008, Article ID 672829, 10 pages
Review Article

The Role of the PAX8/PPAR Fusion Oncogene in Thyroid Cancer

1Division of Endocrinology, Department of Medicine, Mayo Clinic & Foundation, Rochester, MN 55905, USA
2Department of Laboratory Medicine and Pathology, Mayo Clinic & Foundation, Rochester, MN 55905, USA
3Department of Biochemistry and Molecular Biology, Mayo Clinic & Foundation, Rochester, MN 55905, USA

Received 30 July 2008; Accepted 9 September 2008

Academic Editor: Dipak Panigrahy

Copyright © 2008 Kimberly A. Placzkowski 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.


Thyroid cancer is uncommon and exhibits relatively low mortality rates. However, a subset of patients experience inexorable growth, metastatic spread, and mortality. Unfortunately, for these patients, there have been few significant advances in treatment during the last 50 years. While substantial advances have been made in recent years about the molecular genetic events underlying papillary thyroid cancer, the more aggressive follicular thyroid cancer remains poorly understood. The recent discovery of the PAX8/PPAR translocation in follicular thyroid carcinoma has promoted progress in the role of PPAR as a tumor suppressor and potential therapeutic target. The PAX8/PPAR fusion gene appears to be an oncogene. It is most often expressed in follicular carcinomas and exerts a dominant-negative effect on wild-type PPAR , and stimulates transcription of PAX8-responsive promoters. PPAR agonists have shown promising results in vitro, although very few studies have been conducted to assess the clinical impact of these agents.