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Fusion of ZMIZ1 to ABL1 in a B-cell acute lymphoblastic leukaemia with a t(9;10)(q34;q22.3) translocation

Leukemia volume 22, pages 1278–1280 (2008)Cite this article

The ABL1 gene has been found to be fused to four identified partner genes in haematological malignancies. It is rearranged with BCR by the t(9;22)(q34;q11.2) translocation in more than 95% of chronic myeloid leukaemia and in over 25% of adult B-cell acute lymphoblastic leukaemia.1, 2 It is rearranged with TEL (also known as ETV6) in rare cases of chronic myeloid leukaemia and acute leukaemia.3 In T-cell acute lymphoblastic leukaemia, ABL1 can be fused with NUP214 (a gene located in 9q34) on episomes4 or with EML1 by a t(9;14)(q34;q32) translocation.5 Moreover, a recent publication described a t(1;9)(q24;q34) translocation in a B-cell acute lymphoblastic leukaemia case with a putative RCSD1-ABL1 fusion without molecular confirmation.6 Here we report the cytogenetic and molecular analysis of a t(9;10)(q34;q23) translocation, from a case of B-lineage ALL, with recombination of ABL1 to a new partner gene, ZMIZ1 (zinc-finger MIZ-type containing 1).

The patient is an 18-month-old Japanese girl, with no personal or familial medical history other than bronchiolitis and an episode of atopic dermatitis treated with dermocorticosteroids in November 2006. In December 2006, at the age of 14 months, she presented with pallor, asthenia and fever. Physical examination was found normal. Laboratory investigation showed an abnormal white blood cell count (2.2 G l−1 with neutropenia 0 G l−1) and non-regenerative anaemia (Hb 3.5 g per 100 ml). Bone marrow analysis showed heterogeneous density with 3–10% of immature cells. Immunophenotyping analysis of the bone marrow sample did not reveal aberrant surface marker expression. No karyotypic or molecular abnormality was detected at the time. Blood culture was positive for alpha-haemolytic streptococcus. The girl was treated for her septicaemia and transfused. The neutropenia (1.4 G l−1) persisted for 3 months. In April 2007, she presented with fever. Clinical examination was normal. Blood cell count showed bicytopaenia (neutrophils 0 G l−1, Hb 6.6 g per 100 ml). Bone marrow examination showed 90% of CD19+, CD10+, CD34+ CD13−, CD33− lymphoblasts, corresponding to a diagnosis of B-cell acute lymphoblastic leukaemia II, according to the immunological EGIL (European Group for the Immunological Characterization of Acute Leukemias) classification. The patient was then treated abroad, according to the standard risk protocol without kinase inhibitors. She is in first complete remission.

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Acknowledgements

We thank S Nusbaum, F Poulain and MC Waill for valuable help. This work was supported by INSERM, L'Association pour la Recherche sur le Cancer (ARC) and INCa Grants PL038 and PL054.

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Authors and Affiliations

  1. Service de Cytogénétique, Assistance Publique–Hôpitaux de Paris (APHP), Centre Hospitalier Universitaire (CHU) Necker-Enfants Malades, Paris, France

    G Soler, I Radford-Weiss, J F Ponceau, M Vekemans & S P Romana

  2. Institut National de la Santé et de la Recherche Scientifique (INSERM), EMI0210, Paris, France,

    G Soler, O A Bernard & S P Romana

  3. Université Paris V René Descartes, Paris, France

    G Soler, E A Macintyre, M Vekemans, O A Bernard & S P Romana

  4. Laboratoire d'Hématologie Biologique, APHP, CHU Necker-Enfants Malades, Paris, France

    R Ben-abdelali & E A Macintyre

  5. Service d'Immuno-Hématologie Pédiatrique, APHP, CHU Necker-Enfants Malades, Paris, France

    N Mahlaoui

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  1. G Soler
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Soler, G., Radford-Weiss, I., Ben-abdelali, R. et al. Fusion of ZMIZ1 to ABL1 in a B-cell acute lymphoblastic leukaemia with a t(9;10)(q34;q22.3) translocation. Leukemia 22, 1278–1280 (2008). https://doi.org/10.1038/sj.leu.2405033

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