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Increasing Expression of the Retinoic X Receptor‐B During Malignant Melanoma Progression
Author(s) -
McAlhany S.J.,
Reed J.A.
Publication year - 2005
Publication title -
journal of cutaneous pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 75
eISSN - 1600-0560
pISSN - 0303-6987
DOI - 10.1111/j.0303-6987.2005.320gj.x
Subject(s) - calcitriol receptor , melanoma , retinoid x receptor , cancer research , immunohistochemistry , retinoic acid , biology , receptor , medicine , cell culture , endocrinology , nuclear receptor , transcription factor , biochemistry , genetics , gene
Retinoic X receptor‐b (RXR‐b) is a heterodimerization partner for vitamin D receptor (VDR). 1,25‐dihydroxyvitamin D3 activation of VDR leads to growth inhibition in numerous cell lines, including some melanoma lines. Evaluation of VDR and RXR‐b expression in vivo in melanocytic neoplasms will increase our understanding of this pathways potential role in growth control. Previous studies in our laboratory showed decreased VDR expression in superficially invasive melanoma, and progressive loss of expression in deeply invasive melanomas and metastatic melanomas (MET). We next sought to evaluate RXR‐b expression. Twenty‐eight melanocytic neoplasms including 8 melanomas in situ (MIS), 9 primary invasive melanomas (PIM), and 11 MET were evaluated for RXR‐b expression by immunohistochemistry. Nuclear labeling was assessed as 0 (0%), 1+(<5%), 2+(>5% but <50%), or 3+(>=50%). A significant increase in RXR‐b expression from low (0–1+) to high (>1+) was found when comparing MIS to PIM and MET (chi2 p < 0.05). These data suggest: 1) potential loss of 1,25‐dihydroxyvitamin D3 induced growth inhibition during melanoma progression may be due to decreased VDR expression without concomitant loss of RXR‐b; and 2) increased RXR‐b expression during melanoma progression may offer selective advantage through alternative signaling pathways.