Loss of genes on the short arm of chromosome 11 in bladder cancer

Eric R. Fearon, Andrew P. Feinberg, Stanley H. Hamilton, Bert Vogelstein

Research output: Contribution to journalArticle

Abstract

Recent studies have shown that normal cellular sequences on chromosome 13 are lost during the development of retinoblastomas1 and that sequences on chromosome 11 are similarly lost during the development of Wilms' kidney tumours2-5 and embryonal tumours6. Cells from these tumours have been found to contain either the paternal or maternal copies of loci on the affected chromosome, but not both. Thus, the somatic loss of heterozygosity for sequences on chromosome 13 or 11 is hypothesized to result in homozygosity for a recessive mutant allele on these chromosomes1, and in this way the chromosomal loss may contribute to the development of these tumours. We sought to investigate whether similar losses of heterozygosity for chromosome 11 sequences occurred in a common adult tumour. We chose to analyse bladder cancers, since such cancers are common in the adult population and are derived from urogenital tissue, as are Wilms' tumours. We examined constitutional and tumour genotypes at loci on the short arm of chromosome 11 (11p) in 12 patients with transitional cell carcinomas. In five tumours, we observed the somatic loss of genes on 11p resulting in homozygosity or hemizygosity of the non-deleted alleles in the tumour cells. Our results show that the frequency of loss of 11p sequences in bladder cancer approaches that seen in Wilms' tumour (42% compared with 55%)7, and suggest that recessive genetic changes involving sequences on 11p may contribute to the development of bladder neoplasms.

Original languageEnglish (US)
Pages (from-to)377-380
Number of pages4
JournalNature
Volume318
Issue number6044
DOIs
StatePublished - Dec 1 1985

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