Loss of heterozygosity in three embryonal tumours suggests a common pathogenetic mechanism

Alex Koufos, Marc F. Hansen, Neal G. Copeland, Nancy A. Jenkins, Beatrice C. Lampkin, Webster K. Cavenee

Research output: Contribution to journalArticle

401 Scopus citations

Abstract

Children with the Beckwith-Wiedeman syndrome have a greatly increased potential for the specific development of the embryonal tumours hepatoblastoma, rhabdomyosarcoma and Wilms' tumour. Data obtained with molecular probes suggest that the association between these disparate, rare tumour types reflects a common pathogenetic mechanisms that entails the somatic development of homozygosity for a mutant allele at a locus on human chromosome 11.

Original languageEnglish (US)
Pages (from-to)330-334
Number of pages5
JournalNature
Volume316
Issue number6026
DOIs
StatePublished - Dec 1 1985

ASJC Scopus subject areas

  • General

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