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 Blood, 19 February 2009, Vol. 113, No. 8, pp. 1730-1740.
Prepublished online as a Blood First Edition Paper on November 4, 2008; DOI 10.1182/blood-2008-02-138172.

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LYMPHOID NEOPLASIA

NOTCH is a key regulator of human T-cell acute leukemia initiating cell activity

Florence Armstrong1,2, Philippe Brunet de la Grange1,2, Bastien Gerby1,2, Marie-Christine Rouyez1,2, Julien Calvo1,2, Michaéla Fontenay1,2, Nicolas Boissel3, Hervé Dombret3, André Baruchel3, Judith Landman-Parker4, Paul-Henri Roméo1,2, Paola Ballerini4, and Françoise Pflumio1,2

1 Institut Cochin, Université Paris Descartes, Centre National de la Recherche Scientifique (CNRS), Unite Mixte de Recherche (UMR) 8104, Paris; 2 Inserm, U567, Paris; 3 Services d'Hématologie et d'Oncologie Pédiatrique et Adulte, Hôpital Saint-Louis, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris; and 4 Laboratoire d'Hématologie, Service d'Hématologie et d'Oncologie Pédiatrique, Hôpital Trousseau, Paris, France

Understanding the pathways that regulate the human T-cell acute lymphoblastic leukemia (T-ALL) initiating cells (T-LiC) activity has been hampered by the lack of biologic assays in which this human disease can be studied. Here we show that coculture of primary human T-ALL with a mouse stromal cell line expressing the NOTCH ligand delta-like-1 (DL1) reproducibly allowed maintenance of T-LiC and long-term growth of blast cells. Human T-ALL mutated or not on the NOTCH receptor required sustained activation of the NOTCH pathway via receptor/ligand interaction for growth and T-LiC activity. On the reverse, inhibition of the NOTCH pathway during primary cultures abolished in vitro cell growth and in vivo T-LiC activity. Altogether, these results demonstrate the major role of the NOTCH pathway activation in human T-ALL development and in the maintenance of leukemia-initiating cells.


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