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

Nature volume 316, pages 330–334 (1985)Cite this article

Abstract

Children with the Beckwith-Wiedemann 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 mechanism that entails the somatic development of homozygosity for a mutant allele at a locus on human chromosome 11.

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Author notes

  1. Neal G. Copeland & Nancy A. Jenkins

    Present address: Mammalian Genetics Laboratory, LBI Basic Research Program, NCI-Frederick, Maryland, 21701, USA

Authors and Affiliations

  1. Department of Microbiology and Molecular Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio, 45267-0524, USA

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

  2. Division of Hematology/Oncology, Children's Hospital Medical Center, Cincinnati, Ohio, 45267, USA

    Alex Koufos & Beatrice C. Lampkin

Authors
  1. Alex Koufos
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  2. Marc F. Hansen
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  3. Neal G. Copeland
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  4. Nancy A. Jenkins
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  5. Beatrice C. Lampkin
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  6. Webster K. Cavenee
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Koufos, A., Hansen, M., Copeland, N. et al. Loss of heterozygosity in three embryonal tumours suggests a common pathogenetic mechanism. Nature 316, 330–334 (1985). https://doi.org/10.1038/316330a0

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