@article {cite-key,
	title = {Localization of the oncogene c-Ha-ras1 outside the aniridia-Wilms{\textquoteright} tumor-associated deletion of chromosome 11(del 11p13) using somatic cell hybrids.},
	journal = {Cancer Genet Cytogenet},
	volume = {15},
	number = {1-2},
	year = {1985},
	month = {Feb},
	pages = {79{\textendash}84},
	abstract = {Hybrid cell lines, obtained after fusion of rodent cells with leukocytes from a patient with the aniridia-Wilms{\textquoteright} tumor syndrome and carrying a specific constitutional deletion in chromosome $\#$11 (del.11p13), were assayed for the presence of the c-Ha-ras1 oncogene. This sequence has recently been assigned to the p-arm of chromosome $\#$11 and, hence, has been suggested to be involved in the development of renal tumors in patients with this syndrome. Positive hybridization of a cellular Ha-ras1 probe to hybrid cell DNA was observed, irrespective of whether the normal chromosome $\#$11 or its deleted homologue was present. The results presented here suggest that c-Ha-ras1 is located outside the region 11p12-11p14, bounded by the chromosomal breakpoints observed in the patient used. Therefore, we conclude that predisposition of aniridia patients to develop Wilms{\textquoteright} tumors is not due to a constitutional deletion of one of the c-Ha-ras1 alleles.},
	issn = {0165-4608 (Print); 0165-4608 (Linking)},
	author = {van Kessel, A G and Nusse, R and Slater, R and Tetteroo, P and Hagemeijer, A}
}
