Relaxation of insulin-like growth factor II gene imprinting implicated in Wilms' tumour (original) (raw)

Nature volume 362, pages 749–751 (1993)Cite this article

Abstract

GENOMIC imprinting has been implicated in the onset of several embryonal tumours but the mechanism is not well understood1–3. Maternal chromosome 11p15 loss of heterozygosity4 and paternal chromosome 11 isodisomy5,6 suggest that imprinted genes are involved in the onset of Wilms' tumour and the Beckwith–Wiedemann syndrome. The insulin-like growth factor II (IGF2) gene located at 11pl5.5 has been put forward as a candidate gene as it is maternally imprinted (paternally expressed) in the mouse7, and is expressed at high levels in Wilms' tumours8,9. We report here that the IGF2 gene is expressed from the paternal allele in human fetal tissue, but that in Wilms' tumour expression can occur biallelically. These results provide, to our knowledge, the first evidence that relaxation of imprinting may play a role in the onset of disease and suggest a new genetic mechanism involved in the development of cancer.

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Author notes

  1. Kankatsu Yun: Department of Pathology, University of Otago, Dunedin, New Zealand
  2. Peter J. Smith: Department of Pathology, University of Queensland, Herston, Queensland 4006, Australia
  3. Anthony E. Reeve: To whom correspondence should be addressed.

Authors and Affiliations

  1. Cancer Genetics Laboratory, Department of Biochemistry, University of Otago, Dunedin, New Zealand
    Osamu Ogawa, Michael R. Eccles, Jenny Szeto, Leslie A. McNoe, Kankatsu Yun, Marion A. Maw, Peter J. Smith & Anthony E. Reeve

Authors

  1. Osamu Ogawa
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  2. Michael R. Eccles
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  3. Jenny Szeto
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  4. Leslie A. McNoe
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  5. Kankatsu Yun
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  6. Marion A. Maw
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  7. Peter J. Smith
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  8. Anthony E. Reeve
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Ogawa, O., Eccles, M., Szeto, J. et al. Relaxation of insulin-like growth factor II gene imprinting implicated in Wilms' tumour.Nature 362, 749–751 (1993). https://doi.org/10.1038/362749a0

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