Targeting self-renewal pathways in myeloid malignancies (original) (raw)

Sands, W.A., Copland, M. ORCID: https://orcid.org/0000-0002-7655-016X and Wheadon, H. ORCID: https://orcid.org/0000-0001-9902-3170(2013) Targeting self-renewal pathways in myeloid malignancies.Cell Communication and Signaling, 11(33), (doi: 10.1186/1478-811X-11-33)

Abstract

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.

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