A current view of hematopoiesis is that of a hierarchically organized system, with a rare population of hematopoietic stem cells (HSCs) residing at the top of the hierarchy, giving rise to all blood cell lineages. See MoreHSCs possess the ability of multipotency (i.e. one HSC can differentiate into all functional blood cells) and self–renewal (i.e. HSCs can divide and give rise to an identical daughter cell, without differentiation).1 Through a series of lineage commitment steps, HSCs give rise to progeny that progressively lose self-renewal potential and successively become more and more restricted in their differentiation capacity, generating multi-potential and lineage-committed progenitor cells, and ultimately mature functional circulating blood cells.
The ability of hematopoietic stem and progenitor cells (HSPCs) to self-renew and differentiate is fundamental for the formation and maintenance of life-long hematopoiesis and deregulation of these processes may lead to severe clinical consequences. HSPCs are also highly valuable for their ability to reconstitute the hematopoietic system when transplanted and this has enabled their use in the clinic to treat a variety of disorders including bone marrow failure, myeloproliferative disorders and other acquired or genetic disorders that affect blood cells.2,3 Given these pivotal roles of HSPCs, much research effort has been directed at developing tools for their detection, enumeration, identification and isolation, and understanding the mechanisms underlying their behavior and fate decisions.4 Exploiting key findings of such research is highly relevant for developing novel methods to obtain clinically relevant numbers of normal HSPCs and to eliminate or inhibit cancer stem cell growth in hematopoietic malignancies.
- Eaves CJ (2015) Blood 125(17): 2605-13
- Kekre N et al. (2014) Blood 124(3): 334-43
- Ballen KK et al. (2013) Blood 122(4):491-8
- Göttgens B (2015) Blood 125(17): 2614-20
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Ezh2 and Runx1 Mutations Collaborate to Initiate Lympho-Myeloid Leukemia in Early Thymic Progenitors
In a mouse model, researchers demonstrated that Ezh2 and Runx1 inactivation targeted to early lymphoid progenitors causes a marked expansion of pre-leukemic early thymic progenitors (ETPs), showing transcriptional signatures characteristic of ETP leukemia.Hematopoiesis News Volume 9.06, February 13, 2018. Read full issue at