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PMID: 2542777 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Loss of allelic heterozygosity at a second locus on chromosome 11 in sporadic Wilms' tumor cells.

Molecular and cellular biology ·Vol. 9 ·No. 4 ·1989-04-00 ·Pages 1799-803

Reeve AE, Sih SA, Raizis AM, Feinberg AP

Abstract

Children with associated Wilms' tumor, aniridia, genitourinary malformations, and mental retardation (WAGR syndrome) frequently have a cytogenetically visible germ line deletion of chromosomal band 11p13. In accordance with the Knudson hypothesis of two-hit carcinogenesis, the absence of this chromosomal band suggests that loss of both alleles of a gene at 11p13 causes Wilms' tumor. Consistent with this model, chromosomes from sporadically occurring Wilms' tumor cells frequently show loss of allelic heterozygosity at polymorphic 11p15 loci, and therefore it has been assumed that allelic loss extends proximally to include 11p13. We report here that in samples from five sporadic Wilms' tumors, allelic loss occurred distal to the WAGR locus on 11p13. In cells from one tumor, mitotic recombination occurred distal to the gamma-globin gene on 11p15.5. Thus, allelic loss in sporadic Wilms' tumor cells may involve a second locus on 11p.

MeSH Terms
Alleles Child Child, Preschool Chromosome Aberrations Chromosome Mapping Chromosomes, Human, Pair 11 Female Heterozygote Humans Infant Kidney Neoplasms/genetics Male Models, Genetic Wilms Tumor/genetics
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Reeve A E
Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor 48109-0650.
Sih S A
Raizis A M
Feinberg A P
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Article Info
Journal
Molecular and cellular biology
Abbr.
Mol Cell Biol
ISSN
0270-7306
Published
1989-04-00
Pages
1799-803
Language
English
Region
United States
NLM ID
8109087
PMCID
PMC362601
Subset
IM
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