This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kaneko, Y. Articles by Hata, J.-i. Search for Related Content PubMed PubMed Citation Articles by Kaneko, Y. Articles by Hata, J.-i.

Correlation of Chromosome Abnormalities with Histological and Clinical Features in Wilms' and Other Childhood Renal Tumors¹

Department of Laboratory Medicine [Y. K., C. H.] and Hematology Clinic [N. M., M. S.], Saitama Cancer Center Hospital, Ina, Saitama 362, Japan, and Department of Pathology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160, Japan [J. H.]

Chromosomes and histology were successfully studied in 33 childhood renal tumors. Thirty-one tumors were classified as one of four subtypes of Wilms' tumor. Of 24 typical Wilms' tumors, 12 had hyperdiploidy with nonrandom trisomies, mostly including +6 and/or +12. Three typical Wilms' tumors with an 11p13 deletion or a pericentric inversion with a break in 11p13 were not associated with aniridia. Two other typical Wilms' tumors with the 11p13 deletion and one fetal rhabdomyomatous nephroblastoma with an 11p13 translocation were associated with aniridia. Two cystic partially differentiated nephroblastomas showed hyperdiploidy with +12. Of four clear cell sarcomas of the kidney, three had normal diploidy and the other had a 2;22 translocation. Two congenital mesoblastic nephromas had hyperdiploid karyotype with trisomy 11, which was never seen in the 31 Wilms' tumors. Our findings and a review of data on 102 reported Wilms' tumors revealed 11p13 abnormalities in 24 tumors, 11p15 abnormalities in five tumors, and partial deletions of 1p, 7p, 11q, 12q, 16q, or 17p or monosomy of No. 21 or No. 22 each in four or more tumors.

These findings suggest that increased copy number of genes on the nonrandom trisomic chromosomes might contribute to the genesis of many Wilm's tumors and that deletion of various tumor suppressor genes other than a Wilms' tumor gene, WT1 in 11p13, might also play a critical role in the development of some tumors.

¹ This work was supported in part by Grants-in-Aid from the Ministry of Health and Welfare and the Ministry of Education, Science, and Culture of Japan.

² To whom requests for reprints should be addressed, at Department of Laboratory Medicine, Saitama Cancer Center, Ina, Saitama, 362, Japan.

Received 5/20/91. Accepted 8/19/91.

This article has been cited by other articles:

				E. Yuan, C.-M. Li, D. J. Yamashiro, J. Kandel, H. Thaker, V. V. Murty, and B. Tycko Genomic Profiling Maps Loss of Heterozygosity and Defines the Timing and Stage Dependence of Epigenetic and Genetic Events in Wilms' Tumors Mol. Cancer Res., September 1, 2005; 3(9): 493 - 502. [Abstract] [Full Text] [PDF]

				G J Hannon, D Demetrick, and D Beach Isolation of the Rb-related p130 through its interaction with CDK2 and cyclins. Genes & Dev., December 1, 1993; 7(12a): 2378 - 2391. [Abstract] [PDF]