Letter | Published:

Translocation 8;14 in an ataxia telangiectasia-derived cell line

Naturevolume 277pages5658 (1979) | Download Citation

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Abstract

THE incidence of lymphomas is 10,000 times greater than normal in patients with immunodeficiency syndromes1 and also in ataxia telangiectasia (AT), which very often involves IgA deficiency2. In addition to its other characteristic features, AT is usually associated with a defect in DNA repair3 and a translocation involving chromosome 14 in the peripheral leukocytes4. Another feature is a high prevalence of Epstein–Barr virus early antigen (EBV-EA) antibodies5 in the sera of AT patients. This is significantly higher than in normal human sera (<10%) and resembles that found in cases of Burkitt's lymphoma (BL). It is thus interesting that translocations involving chromosome 14 have been described in BL cells as well as in other lymphomatous cells6–8. This chromosome marker is also found in BL cell lines containing EB V9. It is not induced by EBV alone, however, because it is not found in EBV-positive, but non-lymphomatous cell lines, established spontaneously or by transformation of normal peripheral blood leukocytes10. We have therefore investigated whether in BL and AT some target cells of EBV infection might be genetically ‘defective’ lymphoid cells that could more easily be transformed into malignant cells (with characteristic chromosome markers) when exposed to EBV or other carcinogens. To do this we infected lymphoid cells from AT patients in vitro with EBV, and we report here a translocation t(8q; 14q+) established in one of the resulting cell lines.

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Affiliations

  1. Laboratoire de cytogénétique, Département d'anatomie, Université de Montréal

    • PIERRE JEAN
    • , CLAUDE-LISE RICHER
    •  & MANUELA MURER-ORLANDO
  2. Centre de recherche pédiatrique, Hôpital Ste-Justine, Département microbiologie et de pédiatrie, Université de Montréal, Montréal, Canada, H3C 3J7

    • DAO HUY LUU
    •  & JEAN H. JONCAS

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https://doi.org/10.1038/277056a0

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