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JNCI Journal of the National Cancer Institute 2000 92(6):438-440; doi:10.1093/jnci/92.6.438
© 2000 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 92, No. 6, 438-440, March 15, 2000
© 2000 Oxford University Press

EDITORIALS

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

Michael J. Spinella, Ethan Dmitrovsky

Affiliations of authors: M. J. Spinella, Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH, and Norris Cotton Cancer Center, Dartmouth Hitchcock Medical Center, Lebanon, NH; E. Dmitrovsky, Department of Pharmacology and Toxicology, Dartmouth Medical School, and Department of Medicine and Norris Cotton Cancer Center, Dartmouth Hitchcock Medical Center.

Correspondence to: Ethan Dmitrovsky, M.D., Department of Pharmacology and Toxicology, 7650 Remsen, Dartmouth Medical School, Hanover, NH 03755 (e-mail: ethan.dmitrovsky@dartmouth.edu).

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.

The discovery of the nuclear retinoid receptors in the 1980s revolutionized the retinoid field by providing a firm mechanistic basis for the cellular actions of retinoids (4,5). It . . . [Full Text of this Article]

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