Loss of heterozygosity of chromosome 16q occurs in 17-25% of Wilms' tumors. Two cadherin genes mapping to 16q22 were chosen as candidate gens: E-CAD, encoding epithelial cadherin, because it is involved in kidney development and it was recently reported to be a WT1 target; and KSP-CAD because it encodes a kidney-specific cadherin. By RT-PCR analysis in a series of 39 Wilms' tumors, we identified a very low expression of E-CAD and KSP-CAD in 72% and 95% of the tumors, respectively. To ascertain whether down-expression of these genes could be related to WT1 alterations in tumors, we looked for a relationship between WT1 and CAD expression. Our data suggest (i) the existence of alternative mechanisms for regulating E-CAD expression, and (ii) that E-CAD does not belong to the WT1 pathway that is altered in Wilms' tumorigenesis.