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A Third Wilms' Tumor Locus on Chromosome 16q¹

Molecular Carcinogenesis Laboratory, Department of Biochemistry, University of Otago, P. O. Box 56, Dunedin, New Zealand [M. A. M., L. J. M., M. R. E., A. E. R.]; Departments of Pediatrics and Medicine, Cross Cancer Institute and Faculty of Medicine, University of Alberta, Edmonton, Alberta, T6G 1Z2 Canada [P. E. G., M. C. P., P. E. T.]; Department of Pathology, University of Queensland, Herston, Queensland, Australia 4006 [R. S. D., P. J. S.]; Howard Hughes Medical Institute and Departments of Internal Medicine and Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan 48109-0650 [A. P. F., D. J. L.]; and Department of Cytogenetics and Molecular Genetics, Adelaide Children's Hospital, North Adelaide, South Australia, 5006 [D. F. C., A. D. T., R. I. R.]

Loss of heterozygosity studies have been used to identify chromosomal regions which are frequently deleted and thus indicate areas which may harbor tumor suppressor genes. As a result, both the WT1 gene located in chromosome 11p13 and an unidentified gene(s) within chromosome 11p15 have been implicated in Wilms' tumorigenesis. Cytogenetic and linkage studies suggest that additional non-chromosome 11 sites are involved in Wilms' tumor. Because these sites may also involve loss of heterozygosity, loci on 33 autosomal arms were screened for allele loss in a series of Wilms' tumors. We found that in addition to loss on chromosome 11p (11 of 25 informative tumors) there was significant loss on chromosome 16q (9 of 45 informative tumors), while the total frequency of allele loss excluding these loci was low (9 of 426 total informative loci). These data indicate that losses of both chromosome 11p and 16q alleles are nonrandom events and suggest that 16q is the location of a third tumor suppressor gene underlying Wilms' tumorigenesis. The parental origin of the lost chromosome 16q allele was determined in eight sporadic tumors. Alleles of paternal and of maternal origin were each lost in four sporadic tumors indicating that, unlike chromosome 11p, alleles of either parental origin are lost on 16q.

¹ This work was supported by the Cancer Society of New Zealand, Alberta Heritage Foundation for Medical Research, Medical Research Council of Canada, Howard Hughes Medical Institute, and the Queensland Cancer Fund.

² To whom requests for reprints should be addressed.

Received 10/16/91. Accepted 3/25/92.

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