Wiley Interdiscip Rev Syst Biol Med - Mechanisms controlling hematopoietic stem cell functions during normal hematopoiesis and hematological malignancies.

Tópicos

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Resumo

Hematopoiesis, the process by which all mature blood cells are generated from multipotent hematopoietic stem cells (HSCs), is a finely tuned balancing act in which HSCs must constantly decide between different cell fates: to proliferate, to self-renew or differentiate, to stay quiescent in the bone marrow niche or migrate to the periphery, to live or die. These fates are regulated by a complex interplay between cell-extrinsic cues and cell-intrinsic regulatory pathways whose function is to maintain a homeostatic balance between HSC self-renewal and life-long replenishment of lost blood cells. Improper regulation of these competing cellular programs can transform HSCs and progenitor cells into disease-initiating leukemic stem cells (LSCs). Strikingly, many of the mechanisms required for maintenance of normal HSC fate decisions are equally critical for the aberrant functions of LSCs. Because of the inherent complexities of these molecular mechanisms, a systematic approach to understanding the regulatory networks underlying HSC self-renewal is critical for uncovering the similarities and differences between HSCs and LSCs. In this review, we focus on recent developments in elucidating the regulatory networks governing normal HSC self-renewal programs and their implications for leukemic transformation. We describe the current technical and methodological limitations in isolating and characterizing HSCs and LSCs, and the emerging approaches that may afford a better understanding of the regulation of normal and leukemic hematopoiesis. Finally, we discuss how such basic mechanistic information may be of use for the design of novel therapies that will selectively reprogram and/or eliminate LSCs.

Resumo Limpo

hematopoiesi process matur blood cell generat multipot hematopoiet stem cell hscs fine tune balanc act hscs must constant decid differ cell fate prolifer selfrenew differenti stay quiescent bone marrow nich migrat peripheri live die fate regul complex interplay cellextrins cue cellintrins regulatori pathway whose function maintain homeostat balanc hsc selfrenew lifelong replenish lost blood cell improp regul compet cellular program can transform hscs progenitor cell diseaseiniti leukem stem cell lscs strike mani mechan requir mainten normal hsc fate decis equal critic aberr function lscs inher complex molecular mechan systemat approach understand regulatori network under hsc selfrenew critic uncov similar differ hscs lscs review focus recent develop elucid regulatori network govern normal hsc selfrenew program implic leukem transform describ current technic methodolog limit isol character hscs lscs emerg approach may afford better understand regul normal leukem hematopoiesi final discuss basic mechanist inform may use design novel therapi will select reprogram andor elimin lscs

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