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Originally published online as doi:10.1189/jlb.1102581 on June 16, 2003

Published online before print June 16, 2003
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(Journal of Leukocyte Biology. 2003;74:302-305.)
© 2003 by Society for Leukocyte Biology

DLX genes as targets of ALL-1: DLX 2,3,4 down-regulation in t(4;11) acute lymphoblastic leukemias

Nicoletta Ferrari*, Giulio L. Palmisano*, Laura Paleari*, Giuseppe Basso{dagger}, Manuela Mangioni{ddagger}, Vincenzo Fidanza§, Adriana Albini*, Carlo M. Croce§, Giovanni Levi and Claudio Brigati*

* Molecular Biology Laboratory, Istituto Nazionale per la Ricerca sul Cancro IST, Genova, Italy;
{dagger} Department of Pediatrics, University of Padova, Italy;
{ddagger} CBA, Genova, Italy;
§ Department of Microbiology and Immunology, Kimmel Cancer Center, Philadelphia, Pennsylvania; and
Evolution des Regulations Endocriennes, Paris, France

Correspondence: Claudio Brigati, Istituto Nazionale per la Ricerca sul Cancro IST, Largo Rosanna Benzi, 10, 16132, Genova, Italy. E-mail: claudio.brigati{at}istge.it

Dlx genes constitute a gene family thought to be essential in morphogenesis and development. We show here that in vertebrate cells, Dlx genes appear to be part of a regulatory cascade initiated by acute lymphoblastic leukemia (ALL)-1, a master regulator gene whose disruption is implicated in several human acute leukemias. The expression of Dlx2, Dlx3, Dlx5, Dlx6, and Dlx7 was absent in All-1 -/- mouse embryonic stem cells and reduced in All-1 +/- cells. In leukemic patients affected by the t(4;11)(q21;q23) chromosomal abnormality, the expression of DLX2, DLX3, and DLX4 was virtually abrogated. Our data indicate that Dlx genes are downstream targets of ALL-1 and could be considered as important tools for the study of the early leukemic cell phenotype.

Key Words: trithorax • RT-PCR • HOM-C • ES cells




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