The c-Ha-ras1, insulin and beta-globin loci map outside the deletion associated with aniridia-Wilms' tumour.

The localization of protooncogenes on human chromosomes may coincide with chromosome breakpoints of consistent translocations in leukaemias or lymphomas, suggesting a direct involvement of oncogenes in carcinogenesis. For example, in Burkitt's lymphoma consistent translocations may be associated with rearrangements of c-myc. Our assignment of the c-Harvey-ras1 oncogene to chromosome 11, precisely to region 11p11 leads to p15 (ref. 5; not 11p13 as stated in ref. 6), has raised the possibility that this oncogene might have a role in the predisposition to nephroblastoma (Wilms' tumour, WT) seen in the aniridia-WT association (AWTA) that is frequently caused by an interstitial deletion of band 11p (ref. 8). We have now studied the organization and copy number of sequences at three loci mapped to 11p: c-Ha-ras1, insulin and gamma-globin in cells from four individuals with structural rearrangements of the short arm of chromosome 11. Our results reported here rule out a close physical linkage between c-Ha-ras1 and the genes responsible for AWTA, and suggest a more distal localization of the beta-globin cluster than currently assumed.