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Loss of heterozygosity at chromosome regions 22q11–12 and 11p15.5 in renal rhabdoid tumors

✍ Scribed by Deborah E. Schofield; J. Bruce Beckwith; Jeffrey Sklar

Publisher
John Wiley and Sons
Year
1996
Tongue
English
Weight
663 KB
Volume
15
Category
Article
ISSN
1045-2257

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✦ Synopsis

Rhabdoid tumors of the kidney are highly malignant neoplasms that occur primarily within the first 3 years of life. Although they are regarded as distinct from Wilms' tumors, their pathogenesis remains unclear. Whereas most cytogenetic studies of these tumors have revealed normal karyotypes, a few reports have indicated abnormalities at chromosome regions 22q and I I p 15.5. We analyzed 30 primary renal rhabdoid tumors for loss of heterozygosity (LOH) at both regions and found that 24 of 30 tumors (80%) had LOH at chromosome arm 22q and that 5 of 30 ( I 7%) had LOH at chromosome band I I p I 5.5. All of the five tumors with LOH at chromosome arm I I p also had LOH at chromosome arm 22q. The data suggest that there is a gene in chromosome 22, probably a tumor suppressor, inactivation of which may be involved in the genesis of renal rhabdoid tumors. A second gene in chromosome segment I I p 15.5, in the region of the putative W 2 gene, may also be involved, in at least a subset of rhabdoid tumors. In addition, five tumors were characterized by microsatellite instability at three or more of 21 loci examined, suggesting a possible role for a replicative error in tumorigenesis or progression in some cases of renal rhabdoid tumors.

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