Abstract
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.
Original language | English (US) |
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Pages (from-to) | 4945-4947 |
Number of pages | 3 |
Journal | Cancer Research |
Volume | 69 |
Issue number | 12 |
DOIs | |
State | Published - Jun 15 2009 |
ASJC Scopus subject areas
- Oncology
- Cancer Research