Retinoids have been described to be potent modulators of cell proliferation, differentiation and apoptosis in various types of squamous-cell carcinoma (SCC) and myeloid cancer cells in vitro (Bollag and Holdener, 1992;Lotan et al., 1995). It has also been demonstrated that treatment of cells with retinoic acid (RA) in combination with ionizing radiation resulted in significantly enhanced radiation cytotoxicity. In these studies, the reduction of cell survival could be attributed to a supra-additive inhibition of clonogenic activity and concomitantly to a stimulation of differentiation processes induced either by retinoids and or interferon-a in combination with irradiation (Hoffmann et al., 1994). The underlying molecular mechanism of these effects is not understood. It is thought that the cell biological activities of retinoids, and especially the radiosensitizing effect of RA, result from changes in gene expression mediated via the binding of RA to CRABP I/II and the transport of RA into the nucleus. It then can bind to the nuclear receptors RAR or RXR or to the dimer forms of these subunits (Mangelsdorf et al., 1995). Subsequently, the nuclear receptor is able to bind to specific RA-response elements of specific genes which are involved in the regulation of cell proliferation and differentiation. To study the underlying mechanism of the growthinhibitory and radiosensitizing effects of RA, we analyzed in various SCC lines the basal level as well as the RA-and/or irradiation-modulated gene expression of RAR, RXR and CRABP I/II. To increase the level of sensitivity, we therefore established the method of semi-quantitative RT-PCR.