ABSTRACT
A number of toxicogenomic studies are concerned with compounds that act via peroxisome proliferator activated receptors. A similar study of 12 substances from five functional classes included two peroxisome proliferators, ciprofibrate and Wy-14,643, to identify gene sets predictive for their respective classes. Another group reported on the effects of Wy-14,643 and three differently acting compounds and performed a careful mechanistic interpretation of array data to characterize compound-specific profiles. In addition to DNA arrays, open transcription profiling technologies have also been used to resolve mechanistic questions on the mode of toxicity of peroxisome proliferators. Two papers by John C. Rockett et al. describe the use of differential display and suppression subtractive hybridization to discover genes involved in peroxisome-proliferator-induced nongenotoxic carcinogenesis in rats. One of the few serial analysis of gene expression studies in the field of toxicogenomics was presented by M. Kurachi et al. Approximately 56,000 tags were analyzed from normal and tetrachlorodibenzo-dioxin-treated mouse liver libraries.
