Abstract
Among the most promising new antineoplastic therapies for poorly differentiated or undifferentiated thyroid cancer are the histone deacetylase inhibitors and the peroxisome proliferator-activated receptor (PPAR)-γ agonists. These two classes of drugs have been shown to inhibit growth and induce apoptosis and redifferentiation in a variety of hematologic and solid cancer cell lines and animal models. In this article we review the molecular mechanisms,
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