Retinoids in biological control and cancer
Article first published online: 27 SEP 2007
Copyright © 2007 Wiley-Liss, Inc.
Journal of Cellular Biochemistry
Volume 102, Issue 4, pages 886–898, 1 November 2007
How to Cite
Fields, A. L., Soprano, D. R. and Soprano, K. J. (2007), Retinoids in biological control and cancer. J. Cell. Biochem., 102: 886–898. doi: 10.1002/jcb.21530
- Issue published online: 17 OCT 2007
- Article first published online: 27 SEP 2007
- Manuscript Accepted: 10 JUL 2007
- Manuscript Received: 6 JUL 2007
- NIH. Grant Number: CA64945
- retinoic acid;
- ovarian cancer;
- growth arrest;
More than 80 years ago, Wolbach and Howe provided the first evidence suggesting a link between alterations within human cells that lead to malignancies and vitamin A deficiencies (Wolbach and Howe 1925 Nutr. Rev. 36: 16–19). Since that time, epidemiological, preclinical and clinical studies have established a causative relationship between vitamin A deficiency and cancer. Laboratory research has provided insight into the intracellular targets, various signaling cascades and physiological effects of the biologically-active natural and synthetic derivatives of vitamin A, known as retinoids. Collectively, this body of research supports the concept of retinoids as chemopreventive and chemotherapeutic agents that can prevent epithelial cell tumorigenesis by directing the cells to either differentiate, growth arrest, or undergo apoptosis, thus preventing or reversing neoplasia. Continued refinement of the retinoid signaling pathway is essential to establishing their use as effective therapeutics for tumor subtypes whose oncogenic intracellular signaling pathways can be blocked or reversed by treatment with retinoids. J. Cell. Biochem. 102: 886–898, 2007. © 2007 Wiley-Liss, Inc.