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Targeting self-renewal pathways in myeloid malignancies

William A Sands, Mhairi Copland and Helen Wheadon*

Author Affiliations

Paul O’Gorman Leukaemia Research Centre, College of Medical, Veterinary and Life Sciences, University of Glasgow, Gartnavel General Hospital, 1053 Great Western Road, Glasgow G12 0ZD, UK

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Cell Communication and Signaling 2013, 11:33  doi:10.1186/1478-811X-11-33

Published: 15 May 2013


A fundamental property of hematopoietic stem cells (HSCs) is the ability to self-renew. This is a complex process involving multiple signal transduction cascades which control the fine balance between self-renewal and differentiation through transcriptional networks. Key activators/regulators of self-renewal include chemokines, cytokines and morphogens which are expressed in the bone marrow niche, either in a paracrine or autocrine fashion, and modulate stem cell behaviour. Increasing evidence suggests that the downstream signaling pathways induced by these ligands converge at multiple levels providing a degree of redundancy in steady state hematopoiesis. Here we will focus on how these pathways cross-talk to regulate HSC self-renewal highlighting potential therapeutic windows which could be targeted to prevent leukemic stem cell self-renewal in myeloid malignancies.

Myeloid; Leukemia; Self-renewal; Cross-talk; Therapy; Hematopoietic stem cell