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

被引：126

作者：

Armstrong, Florence ^{[1
,2
]}

de la Grange, Philippe Brunet ^{[1
,2
]}

Gerby, Bastien ^{[1
,2
]}

Rouyez, Marie-Christine ^{[1
,2
]}

Calvo, Julien ^{[1
,2
]}

Fontenay, Michaela ^{[1
,2
]}

Boissel, Nicolas ^{[3
,4
]}

Dombret, Herve ^{[3
,4
]}

Baruchel, Andre ^{[3
,4
]}

Landman-Parker, Judith ^{[5
]}

Romeo, Paul-Henri ^{[1
,2
]}

Ballerini, Paola ^{[5
]}

Pflumio, Francoise ^{[1
,2
]}

机构：

[1] Univ Paris 05, Inst Cochin, CNRS, UMR 8104, Paris, France

[2] Inserm, U567, Paris, France

[3] Hop St Louis, AP HP, Serv Hematol, Paris, France

[4] Hop St Louis, AP HP, Serv Oncol Pediat & Adulte, Paris, France

[5] Hop Trousseau, Hematol Lab, Serv Hematol & Oncol Pediat, F-75571 Paris, France

来源：

BLOOD | 2009年 / 113卷 / 08期

关键词：

ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; PROGENITOR CELLS; STEM-CELLS; DIFFERENTIATION; MUTATIONS; GENE; PATHOGENESIS; ACTIVATION; SCL/TAL1;

D O I：

10.1182/blood-2008-02-138172

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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. (Blood. 2009; 113: 1730-1740)

引用

页码：1730 / 1740

页数：11

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