In conclusion, it is obvious that many of the abnormalities in pattern formation and organ formation that result from the exogenous addition of RA during embryogenesis are related at least in part to the ability of RA to change the pattern of expression of the clusters of homeobox genes in the mammalian embryo. The majority of experimental protocols to study RA-induced changes in embryonic development have utilized treatments with excess, exogenous RA, but it has not yet been proven that endogenous RA acts as a key signaling molecule in developing embryo. Thus, we need to develop an understanding of the metabolic enzymes that control the levels of the important endogenous retinoids, including RA, in the developing embryo. The continuing study of retinoids and their receptors will provide us with significant new information about the regulatory programs that control differentiation and development. Moreover, these studies will lead to discoveries relevant to the clinical use of retinoids in the areas of cancer prevention and treatment, and dermatology.
