Aberrant Retinoid Signaling and Breast Cancer: the View From Outside the Nucleus

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Abstract
Retinoids are synthetic and natural analogues of vitamin A (retinol). In 1925, Wolbach and Howe (1) reported that the epithelium of vitamin A-deficient rats develops squamous metaplasia resembling lesions that occur early during carcinogenesis. Notably, this squamous metaplasia reversed with vitamin A treatment. This notion that retinoids inhibit carcinogenesis was supported by extensive animal studies conducted in the 1970s that demonstrated retinoid chemopreventive effects on the epithelium of various tissues after exposure to chemical mutagens (2). However, the mechanisms involved were unknown. Several cytosolic or cellular proteins that bind retinoids with high affinity were identified (3), yet it was unclear what direct role, if any, these proteins had in mediating retinoid actions.

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