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A new recurrent translocation t(11;14)(q24;q32) involving IGH@ and miR-125b-1 in B-cell progenitor acute lymphoblastic leukemia

Leukemia volume 24, pages 1362–1364 (2010)Cite this article

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Micro RNA (miRNA) is a recently discovered class of transcription regulators. Its role in normal and malignant transformation has been extensively investigated. It is emerging that miRNA expression profiling may be a useful tool for diagnostic and prognostic purposes; however, only a limited number of studies have shown direct involvement of miRNA genes in malignant transformation. There are examples of the role of miRNA in the pathogenesis of B-cell lymphoid malignancies: expression of miR-155, miR-221 and miR-21 can distinguish between the activated B-cell phenotype and germinal center phenotype of diffuse large B-cell lymphoma; the miR-15a/miR-16-1 cluster, located on 13q14, is deleted in chronic lymphocytic leukemia (CLL).1, 2 In myeloid disorders, a recurrent translocation, t(2;11)(p21;q24), has been shown to activate the miR-125b-1 on chromosome 11, which potentially defines a specific disease subtype.3 A second locus containing miR-125b-2 is located on 21q21; chromosome 21 is frequently duplicated or rearranged in human hematological malignancies.

In B-cell lymphoid malignancies, chromosomal translocations affecting the immunoglobulin heavy chain locus (IGH@) are known to result in the transcriptional activation of a partner gene and to represent an important step in cellular transformation. Recently, a number of novel chromosomal breakpoints have uncovered previously unknown B-cell oncogenes. We now report the transcriptional activation of miR-125b-1 in the recurrent translocation, t(11;14)(q24;q32), involving IGH@ in B-cell precursor acute lymphoblastic leukemia (BCP-ALL), thereby extending the involvement of miR-125b-1 to lymphoid precursor transformation.

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Acknowledgements

We thank F Davi, C Gervais and C Henry for their valuable help, Fiona Ross, Wessex Regional Genetics Laboratory, Salisbury, UK for providing material, and Leukaemia and Lymphoma Research for financial support.

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Author notes

  1. E Chapiro and L J Russell: These authors contributed equally to this work.

Authors and Affiliations

  1. Service d’Hématologie Biologique, Hôpital Pitié-salpêtrière, UPMC Paris 6, Paris, France

    E Chapiro & F Nguyen-Khac

  2. INSERM U985, Institut G Roussy, Villejuif, France

    E Chapiro, V D Valle & O A Bernard

  3. Univ Paris Sud 11, Orsay, France

    E Chapiro, V D Valle & O A Bernard

  4. INSERM U872, UPMC Paris 6, Paris, France

    E Chapiro & F Nguyen-Khac

  5. Leukaemia and Lymphoma Research Cytogenetics Group, Northern Institute for Cancer Research, Newcastle University, Newcastle, UK

    L J Russell & C J Harrison

  6. Laboratoire de Cytogénétique, CHU Purpan, Toulouse, France

    S Struski

  7. Département de Génétique, APHP, Hôpital Robert Debré, Université Paris 7-Denis Diderot, Paris, France

    H Cavé

  8. Laboratoire de Cytogénétique, Hôpital Necker-Enfants Malades, Paris, France

    I Radford-Weiss

  9. Service d’Hématologie, Hôpital R Debré, Paris, France

    J Lachenaud

  10. Institut National de la Santé et de la Recherche Médicale, U563, Centre de Physiopathologie de Toulouse-Purpan, Toulouse, France

    P Brousset

  11. Université Paul Sabatier, Toulouse, France

    P Brousset

  12. Département de Pathologie, Centre Hospitalier Universitaire Purpan, Toulouse, France

    P Brousset

Authors
  1. E Chapiro
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  2. L J Russell
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  3. S Struski
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  6. V D Valle
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  9. O A Bernard
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  10. C J Harrison
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  11. F Nguyen-Khac
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Corresponding author

Correspondence to F Nguyen-Khac.

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The authors declare no conflict of interest.

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Chapiro, E., Russell, L., Struski, S. et al. A new recurrent translocation t(11;14)(q24;q32) involving IGH@ and miR-125b-1 in B-cell progenitor acute lymphoblastic leukemia. Leukemia 24, 1362–1364 (2010). https://doi.org/10.1038/leu.2010.93

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