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Exp Hematol. 2010 Feb;38(2):132-40. doi: 10.1016/j.exphem.2009.11.002. Epub 2009 Nov 14.

GAS6/Mer axis regulates the homing and survival of the E2A/PBX1-positive B-cell precursor acute lymphoblastic leukemia in the bone marrow niche.

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  • 1Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI 48109-1078, USA.

Abstract

OBJECTIVE:

Despite improvements in current combinational chemotherapy regimens, the prognosis of the (1;19)(q23;p13) translocation (E2A/PBX1)-positive B-cell precursor acute lymphoblastic leukemia (ALL) is poor in pediatric leukemia patients.

MATERIALS AND METHODS:

In this study, we examined the roles of growth arrest-specific-6 (GAS6)/Mer axis in the interactions between E2A/PBX1-positive B-cell precursor ALL cells and the osteoblastic niche in the bone marrow.

RESULTS:

Data show that primary human osteoblasts secrete GAS6 in response to the Mer-overexpressed E2A/PBX1-positive ALL cells through mitogen-activated protein kinase signaling pathway and that leukemia cells migrate toward GAS6 using pathways activated by Mer. Importantly, GAS6 supports survival and prevents apoptosis from chemotherapy of E2A/PBX1-positive ALL cells by inducing dormancy.

CONCLUSIONS:

These data suggest that GAS6/Mer axis regulates homing and survival of the E2A/PBX1-positive B-cell precursor ALL in the bone marrow niche.

Copyright 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.

PMID:
19922767
[PubMed - indexed for MEDLINE]
PMCID:
PMC2815170
Free PMC Article

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