The hematopoietic stem cell niche—home for friend and foe?

Krause, Daniela; Scadden, David T.; Preffer, Frederic I.

doi:10.1002/cyto.b.21066

Cited by 79 publications

(72 citation statements)

References 112 publications

(89 reference statements)

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“…Additional areas of interest include the newly described Abelson helper integration site 1 (AHI-1), an adapter protein which interacts with BCR-ABL1 and JAK2 to mediate the response of CML cells to imatinib, and the haematologica | 2014; 99(5) mechanisms by which CML stem cells interact with their microenvironment. 18 Several groups have recently demonstrated the successful targeting of both BCR-ABL-1 and JAK2 in the CML stem cells in in vitro models of CML stem cells procured from imatinib-resistant patients. 19 The notion of combining ABL-1 TKIs and JAK inhibitors, however, remains uncertain at this time.…”

Section: Stem Cells and Efforts To Target Themmentioning

confidence: 99%

Current pre-clinical and clinical advances in the BCR-ABL1-positive and -negative chronic myeloproliferative neoplasms

et al. 2014

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Section: Stem Cells and Efforts To Target Themmentioning

confidence: 99%

Current pre-clinical and clinical advances in the BCR-ABL1-positive and -negative chronic myeloproliferative neoplasms

et al. 2014

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“…It is well documented that surviving residual tumor cells that persist after treatment contribute to relapse of disease that is often more aggressive than that at diagnosis and is often less effectively treated [1][2][3][4][5][6][7][8] . Models that include leukemic cells in isolation, such as those limited to culture of cells in media alone, for testing of therapeutic approaches do not factor in these critical signals, or the heterogeneity of disease that occurs in response to availability of niche derived cues in which tumor cell subpopulations with very specific interactions with niche cells derive enhanced protection.…”

Section: Introductionmentioning

confidence: 99%

Modeling Chemotherapy Resistant Leukemia <em>In Vitro</em>

Slone

Moses

Evans

et al. 2016

JoVE

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It is well established that the bone marrow microenvironment provides a unique site of sanctuary for hematopoietic diseases that both initiate and progress in this site. The model presented in the current report utilizes human primary bone marrow stromal cells and osteoblasts as two representative cell types from the marrow niche that influence tumor cell phenotype. The in vitro co-culture conditions described for human leukemic cells with these primary niche components support the generation of a chemoresistant subpopulation of tumor cells that can be efficiently recovered from culture for analysis by diverse techniques. A strict feeding schedule to prevent nutrient fluxes followed by gel type 10 cross-linked dextran (G10) particles recovery of the population of tumor cells that have migrated beneath the adherent bone marrow stromal cells (BMSC) or osteoblasts (OB) generating a "phase dim" (PD) population of tumor cells, provides a consistent source of purified therapy resistant leukemic cells. This clinically relevant population of tumor cells can be evaluated by standard methods to investigate apoptotic, metabolic, and cell cycle regulatory pathways as well as providing a more rigorous target in which to test novel therapeutic strategies prior to pre-clinical investigations targeted at minimal residual disease. Video LinkThe video component of this article can be found at

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“…Fascinatingly, these properties appear to be largely intrinsically stable within the original HSC and its progeny (reviewed in [2]), although external stimuli (usually described under the blanket term of "niche") can influence HSC behaviour (reviewed in [3]). This heterogeneity of HSC has been brought to light specifically in terms of MK differentiation by the demonstration by two independent groups of a previously undescribed subpopulation of HSCs which is "primed" to preferentially differentiate to the MK lineage [4,5].…”

Section: Introductionmentioning

confidence: 99%

Transcriptional Regulation of Platelet Formation: Harnessing the Complexity for Efficient Platelet Production In Vitro

Tijssen

Moreau

Ghevaert

2016

Molecular and Cellular Biology of Platelet Formation

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It is now common knowledge that specific repertoires of transcription factors (TFs) determine a cell's protein content and thereby its phenotype. The expression of a given TF is not necessarily cell specific, and many TFs play a pivotal role in several different cell types. For example, TAL1, FLI1, RUNX1, ERG and GATA2 are important regulators of stem cells, but also play a vital role in megakaryopoiesis. Although the megakaryocyte (MK) and its closest relative, the red blood cell, share key TFs like GATA1 and NFE2, the bifurcation between the two lineages has been associated with pairs of TFs that act as a toggle switch (such as FLI1 and KLF1). This chapter will summarise the current knowledge of key transcriptional regulators of MK differentiation and how some of these TFs, despite being expressed in several cell types, can impose MK cell identity. Since the discovery of TPO in 1994, our knowledge of MK biology and differentiation has increased exponentially, but we still lack a deep understanding of what triggers the transition from MK growth and maturation to proplatelet formation. We describe how some well-known TFs control the expression of proteins that play a pivotal role in the dramatic cytoplasmic and cytoskeletal events that accompany proplatelet formation. Finally, we show how TFs can be harnessed in a powerful way to produce MKs and, potentially, platelets in vitro for future clinical applications.

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The hematopoietic stem cell niche—home for friend and foe?

Cited by 79 publications

References 112 publications

Current pre-clinical and clinical advances in the BCR-ABL1-positive and -negative chronic myeloproliferative neoplasms

Current pre-clinical and clinical advances in the BCR-ABL1-positive and -negative chronic myeloproliferative neoplasms

Modeling Chemotherapy Resistant Leukemia <em>In Vitro</em>

Transcriptional Regulation of Platelet Formation: Harnessing the Complexity for Efficient Platelet Production In Vitro

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