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Human Molecular Genetics, 1999, Vol. 8, No. 9 1741-1749
© 1999 Oxford University Press

The signal transducer and activator of transcription STAT5b gene is a new partner of retinoic acid receptor {alpha} in acute promyelocytic-like leukaemia

Cécile Arnould+, Christophe Philippe+, Violaine Bourdon, Marie José Grégoire, Roland Berger1 and Philippe Jonveaux§

Laboratoire de Génétique, UPRES-INRA 952, CHRU, Rue du Morvan, 54511 Vandoeuvre les Nancy, France and 1INSERM U434, SD 401 No. 434 CNRS, CEPH, 27 Rue Juliette Dodu, 75010 Paris, France

Acute promyelocytic leukaemia (APL) exhibits a characteristic t(15;17) translocation that fuses the promyelocytic leukaemia (PML) gene on 15q22 to the retinoic acid receptor {alpha} (RARA) gene on 17q12–q21.1. In a small subset of acute promyelocytic-like leukaemias (APL-L), RARA is fused to a different partner: the pro­myelocytic leukaemia zinc finger (PLZF) gene on 11q23, the nucleophosmin (NPM) gene on 5q35 or the nuclear mitotic apparatus (NuMA) gene on 11q13. We report on the molecular characterization of a RARA gene re­arrangement in a patient with APL-L and demonstrate that the signal transducer and activator of transcription STAT5b gene is fused with RARA. STAT5b belongs to the janus kinase (JAK)–STAT signalling pathway. Remarkably, the STAT5b component of the chimeric protein is delocalized from the cytoplasm to the nucleus, where it displays a microspeckled pattern. Therefore, unusual features of this APL-L might result from dysregulation of the JAK/STAT5 signal transducing pathways in the patient leukaemic cells. In this study, we identified STAT5b as a new gene fused to RARA in leukaemia; this is the first human tumour bearing a structurally abnormal STAT gene.

+ These authors contributed equally to this work

§ To whom correspondence should be addressed. Tel: +33 3 83 15 37 69; Fax: +33 3 83 15 37 72; Email: p.jonveaux{at}chu-nancy.fr


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