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c-Ha-ras1 is not deleted in aniridia–Wilms' tumour association

Nature volume 305, pages 638–641 (1983)Cite this article

Abstract

Non-random tumour-specific chromosomal abnormalities have been observed in cells of many different human tumours. In Wilms' tumour (WT) and retinoblastoma, a chromosomal deletion occurs germinally or somatically1–4 and has been considered an important step in tumour development. One class of potential cellular transforming genes comprises the cellular homologues of the transforming genes of highly oncogenic retroviruses. A remarkable concordance between the chromosomal location of human cellular oncogenes and the breakpoints involved in acquired chromosomal translocations is becoming apparent in various cancers: the oncogenes c-mos, c-myc and c-abl are located at the breakpoints that occur in acute myeloblastic leukaemia, Burkitt's lymphoma and chronic myelocytic leukaemia respectively5. Thus when the oncogene c-Ha-ras1 was localized to the short arm of human chromosome 11 (refs 6–8; region 11p11 → p15 and not 11p13 as stated in ref. 5), it was proposed as a possible aetiological agent in the aniridia–WT association (AWTA) that results from a deletion of 11p13 (although a transforming gene recently isolated from a WT cell line (G401) was shown not to be homologous to either c-Ha-ras or c-Ki-ras9). We have now looked for deletion or rearrangement of c-Ha-ras1 in the DNA from four subjects with del(11p13)-associated predisposition to Wilms' tumour, aniridia, genitourinary abnormalities and mental retardation. We report here that in no case is c-Ha-ras1 deleted, and we have further refined its location to 11p15.1 → 11p15.5. On the basis of enzyme studies and direct gene dosage determination for c-Ha-ras1 and β-globin in neoplastic and non-neoplastic tissues from one patient, we conclude that deletion of the normal counterpart of 11p cannot account for the development of the tumour.

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Authors and Affiliations

  1. Institut de Pathologie et Biologie Cellulaires et Moléculaires, INSERM U 129, 24 rue du Faubourg Sant Jacques, 75674, Paris, Cedex 14, France

    Cécile Huerre, Suzy Despoisse & Claudine Junien

  2. Centre de Transfusion Sanguine de Nancy–Brabois, Laboratoire de Cytogénétique, Avenue de Bourgogne, 54500, Vandoeuvre, France

    Simone Gilgenkrantz

  3. International Agency for Research on Cancer, 150 Cours Albert Thomas, 69372, Lyon, France

    Gilbert M. Lenoir

Authors
  1. Cécile Huerre
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  4. Gilbert M. Lenoir
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  5. Claudine Junien
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Huerre, C., Despoisse, S., Gilgenkrantz, S. et al. c-Ha-ras1 is not deleted in aniridia–Wilms' tumour association. Nature 305, 638–641 (1983). https://doi.org/10.1038/305638a0

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