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Reviews |
1 University of Texas Health Science Center, Institute of Molecular Medicine, Houston, Texas and 2 Center for Human Nutrition, Johns Hopkins School of Public Health, Baltimore, Maryland
Requests for reprints: Takemi Tanaka, University of Texas Health Science Center, Institute of Molecular Medicine, 1825 Herman Pressler, Rm 537C, Houston, TX 77030. Phone: 713-500-2497; E-mail: Takemi.Tanaka{at}uth.tmc.edu.
Retinoid X receptor (RXR) is a combinatorial partner for one third of the 48 human nuclear receptor superfamily members and acts as a master coordinator of nuclear receptor signaling pathways involved in the control of cell growth and differentiation. Thus, ligand-dependent simultaneous activation of multiple pathways is an attractive strategy for molecular-targeted therapy of neoplastic disease. However, clinical trials in RXR-targeted molecular therapy with the RXR ligand (rexinoid) have yielded disappointing outcomes. In this review, we discuss a possible mechanism underlying the loss of sensitivity to rexinoid therapy. [Cancer Res 2009;69(12):4945–-47]
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