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JNCI Journal of the National Cancer Institute 2004 96(17):1264-1265; doi:10.1093/jnci/djh268
© 2004 by Oxford University Press
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© 2004 Oxford University Press

EDITORIAL

Fenretinide Activates a Distinct Apoptotic Pathway

Ethan Dmitrovsky

Affiliations of author: Department of Pharmacology and Toxicology, Department of Medicine, and Norris Cotton Cancer Center, Dartmouth Medical School, Hanover, NH, and Dartmouth-Hitchcock Medical Center, Lebanon, NH

Correspondence to: Ethan Dmitrovsky, MD, Remsen 7650, Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH 03755-3835 (e-mail ethan.dmitrovsky@dartmouth.edu)

The first 10% of the full text of this article appears below.

This is an exciting period in molecular oncology. Molecular pharmacologic pathways are being discovered that regulate tumor cell proliferation, differentiation, and apoptosis. In this regard, retinoids are worthy of study because these natural and synthetic derivatives of vitamin A can inhibit proliferation, promote differentiation, trigger apoptosis, and affect other signaling pathways. Moreover, retinoids are worthy of study because the two major types of retinoids—classical (such as all-trans-retinoic acid) and nonclassical (such as fenretinide)—exert distinct biologic effects. Understanding how fenretinide preferentially engages the apoptotic pathway is the subject of the work by Lovat et al. (1) in this issue of the Journal.

Classical retinoids activate the family of nuclear retinoic acid receptors (RARs) of which there are three members (RAR{alpha}, RAR{beta}, and . . . [Full Text of this Article]


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