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Expression of insulin-like growth factor-II transcripts in Wilms' tumour

Nature volume 317, pages 258–260 (1985)Cite this article

Abstract

Wilms' tumour probably arises from embryonal kidney cells and occurs in both hereditary and sporadic forms1. Knudson and Strong have suggested that both forms of the disease are initiated by two mutational events2. In the case of the inherited form, cytogenetic evidence indicates that a germline deletion of chromosome band 11p13 may correspond to one of the two mutations3–5. DNA mapping evidence is consistent with the notion that the tumour susceptibility gene (Wg) on chromosome 11 is actually recessive6–9. Comings has proposed that the dominantly inherited tumours may arise by the inactivation or loss of a diploid pair of regulatory genes which normally suppress the expression of a structural transforming gene (Tg)10. It has recently been suggested that the N-myc oncogene may serve as a transforming gene in retinoblas-toma11, although no such gene has yet been identified in Wilms' tumour. We now report that in four cases of Wilms' tumour, insulin-like growth factor-II (IGF-II) transcripts are highly elevated compared with the adjacent normal kidney. In addition, we have mapped the gene for IGF-II to chromosome band 11p14.1, which is in the immediate vicinity of Wg. These findings suggest that IGF-II may be involved in the aetiology of Wilms' tumour.

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Authors and Affiliations

  1. Molecular Carcinogenesis Laboratory, Department of Biochemistry, University of Otago, PO Box 56, Dunedin, New Zealand

    Anthony E. Reeve, Michael R. Eccles, Richard J. Wilkins & Lynn J. Millow

  2. Chiron Corporation, 4560 Horton Street, Emeryville, California, 94608, USA

    Graeme I. Bell

Authors
  1. Anthony E. Reeve
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  2. Michael R. Eccles
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  3. Richard J. Wilkins
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  4. Graeme I. Bell
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  5. Lynn J. Millow
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Reeve, A., Eccles, M., Wilkins, R. et al. Expression of insulin-like growth factor-II transcripts in Wilms' tumour. Nature 317, 258–260 (1985). https://doi.org/10.1038/317258a0

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