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FLT3-ITD Knockin Impairs Hematopoietic Stem Cell Quiescence/Homeostasis, Leading to Myeloproliferative Neoplasm

Chu, S. Haihua, Heiser, Diane, Li, Li, Kaplan, Ian, Collector, Michael, Huso, David, Sharkis, Saul J., Civin, Curt, Small, Don·2012·Cell Stem Cell

DOI 10.1016/j.stem.2012.05.027PMC PMC3725984

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Abstract

SUMMARY Internal tandem duplication (ITD) mutations within the FMS-Like Tyrosine Kinase gene (FLT3) render the receptor constitutively active, driving proliferation and survival in leukemic blasts. Expression of Flt3-ITD from the endogenous promoter in a murine knock-in model results in progenitor expansion and a myeloproliferative neoplasm. In this study, we show that this expansion begins with over-proliferation within a compartment of normally quiescent long-term hematopoietic stem cells (LT-HSCs), which become rapidly depleted. This depletion is reversible upon treatment with the small molecule inhibitor Sorafenib, which also ablates the disease. Although the normal LT-HSC has been defined as Flt3-negative by flow cytometric detection, we demonstrate that Flt3 is capable of playing a role within this compartment by examining the effects of constitutively activated Flt3-ITD. This indicates an important link between stem cell quiescence/homeostasis and myeloproliferative disease while also giving novel insight into the emergence of FLT3-ITD mutations in the evolution of leukemic transformation.

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Shih, A. H., Jiang, Y., Meydan, C., Shank, K., Pandey, S., Barreyro, L., Antony-Debre, I., Viale, A., Socci, N., Sun, Y., et al. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.03.009 · Cited by 236
“This is in contrast to reported FLT3 inhibition in Flt3ITD mice where aberrant differentiation is effectively reversed (Chu et al., 2012).”
Result
IDH2 and NPM1 Mutations Cooperate to Activate Hoxa9/Meis1 and Hypoxia Pathways in Acute Myeloid Leukemia
Ogawara, Y., Katsumoto, T., Aikawa, Y., Shima, Y., Kagiyama, Y., Soga, T., Matsunaga, H., Seki, T., Araki, K., & Kitabayashi, I. (2015) · Cancer Research · doi:10.1158/0008-5472.can-14-2200 · Cited by 58
Leukemia mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness
Pawar, A. S., Somers, P., Alex, A., Grana, J., Feist, V. K., George, S. S., Jalnapurkar, S. S., Antony, C., Verner, R., White-Brown, S. K., et al. (2025) · Genes & Development · doi:10.1101/gad.352602.125 · Cited by 3

See all 79

Authors: Chu, S. H., Heiser, D., Li, L., Kaplan, I., Collector, M., Huso, D., Sharkis, S. J., Civin, C., & Small, D.
Venue: Cell Stem Cell
Publisher: Elsevier BV
Published: 2012-09
Volume: 11
Issue: 3
Pages: 346-358
ISSN: 1934-5909
DOI: 10.1016/j.stem.2012.05.027
PMC: PMC3725984
Cited by: 79
References: 73
Language: en
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 374 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)

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FLT3-ITD Knockin Impairs Hematopoietic Stem Cell Quiescence/Homeostasis, Leading to Myeloproliferative Neoplasm

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