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Loss of a Harvey ras allele in sporadic Wilms' tumour

Loss of a Harvey ras allele in sporadic Wilms' tumour Genomic changes within chromosome band 11p13 appear to have a role in the initiation of Wilms' tumour1–7. The human Harvey ras oncogene, c-Ha-ras1, has been located by Jhanwar et al. 8 immediately adjacent to this region at band 11p14.1, although several groups have assigned the gene more distally at band 11p15 (refs 9–11). We have examined tumour DNA from two cases of sporadic Wilms' tumour, and report here that in both cases one of the two constitutional c-Ha-ras1 alleles was absent. One tumour had a reciprocal translocation between the short arm of chromosome 11 (at band 11p13), and the long arm of chromosome 12, with no visible loss of chromosomal material. The loss of a c-Ha-ras1 allele in association with this translocation indicates that a submicroscopic deletion had occurred. The resulting hemizygosity may have had a role in tumour initiation. Our results indicate that the c-Ha-ras1 gene and the ‘Wilms' tumour locus’ may be in close proximity. It would, therefore, be premature to exclude the possibility that these two sites are functionally related. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Springer Journals

Loss of a Harvey ras allele in sporadic Wilms' tumour

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References (16)

Publisher
Springer Journals
Copyright
Copyright © 1984 by Nature Publishing Group
Subject
Science, Humanities and Social Sciences, multidisciplinary; Science, Humanities and Social Sciences, multidisciplinary; Science, multidisciplinary
ISSN
0028-0836
eISSN
1476-4687
DOI
10.1038/309174a0
Publisher site
See Article on Publisher Site

Abstract

Genomic changes within chromosome band 11p13 appear to have a role in the initiation of Wilms' tumour1–7. The human Harvey ras oncogene, c-Ha-ras1, has been located by Jhanwar et al. 8 immediately adjacent to this region at band 11p14.1, although several groups have assigned the gene more distally at band 11p15 (refs 9–11). We have examined tumour DNA from two cases of sporadic Wilms' tumour, and report here that in both cases one of the two constitutional c-Ha-ras1 alleles was absent. One tumour had a reciprocal translocation between the short arm of chromosome 11 (at band 11p13), and the long arm of chromosome 12, with no visible loss of chromosomal material. The loss of a c-Ha-ras1 allele in association with this translocation indicates that a submicroscopic deletion had occurred. The resulting hemizygosity may have had a role in tumour initiation. Our results indicate that the c-Ha-ras1 gene and the ‘Wilms' tumour locus’ may be in close proximity. It would, therefore, be premature to exclude the possibility that these two sites are functionally related.

Journal

Nature – Springer Journals

Published: May 10, 1984

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