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JNCI Journal of the National Cancer Institute 1999 91(13):1099-1100; doi:10.1093/jnci/91.13.1099
© 1999 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 91, No. 13, 1099-1100, July 7, 1999
© 1999 Oxford University Press

EDITORIALS

Fenretinide: the Death of a Tumor Cell

John C. Reed

Correspondence to: John C. Reed, M.D., Ph.D., The Burnham Institute, La Jolla, CA 92037 (e-mail: jreed@burnham-inst.org).

Synthetic retinoids hold great promise as new agents for the prevention and treatment of cancer. Attempts by chemists to generate novel retinoid-like structures have resulted in several compounds with potent antitumor activity [reviewed in (1)]. However, not all of these synthetic retinoid-like compounds bind known members of the retinoic acid receptor (RAR; RXR [i.e., retinoid X receptor]) or nuclear receptor families of transcriptional regulators. The compound N-(4-hydroxylphenyl)retinamide (4-HPR; fenretinide) represents a synthetic "retinoid" for which the primary cellular target is unidentified. Although 4-HPR can induce expression of RARß, it remains controversial whether the antitumor effects of this compound can be explained by binding to retinoid receptors (2,3). 4-HPR has been demonstrated to induce apoptosis at concentrations typically in the range of 1-5 . . . [Full Text of this Article]

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