Clinical Cancer Research The Science of Cancer Health Disparities Infection and Cancer: Biology, Therapeutics, and Prevention
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takahashi, N.
Right arrow Articles by Breitman, T. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takahashi, N.
Right arrow Articles by Breitman, T. R.

Clinical Cancer Research, Vol 1, Issue 6 637-642, Copyright © 1995 by American Association for Cancer Research

ARTICLES

N-(4-hydroxyphenyl)retinamide (Fenretinide) in combination with retinoic acid enhances differentiation and retinoylation of proteins

N Takahashi, EA Sausville and TR Breitman
Laboratory of Biological Chemistry, Developmental Therapeutics Program, Division of Cancer Treatment, National Cancer Institute, NIH, Bethesda, Maryland 20892-4255, USA.

The synthetic retinoid, N-(4-hydroxyphenyl)retinamide (4-HPR; Fenretinide), is a cancer chemopreventive and antiproliferative agent whose mechanism of action is unknown. 4-HPR alone is a poor inducer of differentiation of HL-60 cells compared to all-trans-retinoic acid (RA). Here, we found that combinations of 4-HPR and RA synergistically induced differentiation of HL-60 cells. In addition, 4-HPR increased the level of retinoylation, the covalent binding of RA to proteins. Retinoylation occurs in many eukaryotic cell lines and may be involved in RA-induced differentiation. These results suggest that 4-HPR may be a member of a class of retinoids that are active because they displace RA from extracellular and intracellular sites or because they inhibit RA catabolism. On the basis of these proposed mechanisms, retinoids that do not cause differentiation as sole agents may have utility in the clinic in combination with RA.


This article has been cited by other articles:


Home page
 Cancer Res.Home page
M. G. Villani, V. Appierto, E. Cavadini, A. Bettiga, A. Prinetti, M. Clagett-Dame, R. W. Curley, and F. Formelli
4-Oxo-Fenretinide, a Recently Identified Fenretinide Metabolite, Induces Marked G2-M Cell Cycle Arrest and Apoptosis in Fenretinide-Sensitive and Fenretinide-Resistant Cell Lines.
Cancer Res., March 15, 2006; 66(6): 3238 - 3247.
[Abstract] [Full Text] [PDF]

Home page
 Reproductive SciencesHome page
C. Zou, A.-T. Vlastos, L. Yang, J. Wang, M. Brewer, and M. Follen
Effect of 4-Hydroxyphenylretinamide on Human Cervical Epithelial and Cancer Cell Lines
Reproductive Sciences, January 1, 2003; 10(1): 41 - 48.
[Abstract] [PDF]

Home page
 Clin. Cancer Res.Home page
K. Tamagawa, K. Shimizu, T. Ebine, Y. Maitani, T. Fukui, K.-i. Kawai, and N. Takahashi
Antitumor Efficacy in Vitro and in Vivo of Falconensones, a New Type of Polyene
Clin. Cancer Res., November 1, 2001; 7(11): 3551 - 3558.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1995 by the American Association for Cancer Research.