Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML.

@article{Jamieson2004GranulocytemacrophagePA,
  title={Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML.},
  author={Catriona H. M. Jamieson and Laurie E. Ailles and Scott J. Dylla and Manja Muijtjens and Carol D. Jones and James L. Zehnder and Jason Gotlib and Kevin Li and Markus G. Manz and Armand Keating and Charles L. Sawyers and Irving L. Weissman},
  journal={The New England journal of medicine},
  year={2004},
  volume={351 7},
  pages={
          657-67
        }
}
BACKGROUND The progression of chronic myelogenous leukemia (CML) to blast crisis is supported by self-renewing leukemic stem cells. In normal mouse hematopoietic stem cells, the process of self-renewal involves the beta-catenin-signaling pathway. We investigated whether leukemic stem cells in CML also use the beta-catenin pathway for self-renewal. METHODS We used fluorescence-activated cell sorting to isolate hematopoietic stem cells, common myeloid progenitors, granulocyte-macrophage… 
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The chronic myeloid leukemia stem cell.

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BCR-ABL-transformed GMP as myeloid leukemic stem cells

Results provide further evidence that BCR-ABL-transformed GMP with abnormal β-catenin activity can function as leukemic stem cells.

WNT/β-Catenin Signaling in Leukemia

Interestingly, individual components of the WNT/β-catenin signaling pathway have a lineage-specific role and regulate stem cell self-renewal, proliferation, or differentiation specifically in one leukemia ­subset.

Hes1 immortalizes committed progenitors and plays a role in blast crisis transition in chronic myelogenous leukemia.

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Bmi 1 reprograms CML B-lymphoid progenitors to become BALL – initiating cells

It is reported that Bmi1 transforms and reprograms CML B-lymphoid progenitors into stem cell leukemia (Scl) promoter-driven, self-renewing, leukemiainitiating cells to result in B-allymphoid leukemia (B-ALL) in vivo.

Bmi1 reprograms CML B-lymphoid progenitors to become B-ALL-initiating cells.

It is reported that Bmi1 transforms and reprograms CML B-lymphoid progenitors into stem cell leukemia (Scl) promoter-driven, self-renewing, leukemia-initiating cells to result in B-allymphoid leukemia (B-ALL) in vivo.

C/EBPβ promotes BCR–ABL-mediated myeloid expansion and leukemic stem cell exhaustion

Results suggest that C/EBPβ is involved in BCR–ABL-mediated myeloid expansion and further elucidation of the molecular mechanisms underlying the C/ EBPβ-mediated stem cell loss might reveal a novel therapeutic strategy for eradication of CML stem cells.

CD27 signaling on chronic myelogenous leukemia stem cells activates Wnt target genes and promotes disease progression.

The results reveal a mechanism by which adaptive immunity contributes to leukemia progression, and targeting CD27 on LSCs may represent an attractive therapeutic approach to blocking the Wnt/β-catenin pathway in CML.

Instability of BCR-ABL gene in primary and cultured chronic myeloid leukemia stem cells.

Primary CML stem cells display instability of the BCR-ABL fusion gene both in vivo and in vitro, suggesting that patients may possess leukemic stem cells with BCR -ABL kinase mutations before initiation of BCR,ABL-targeted therapies and would likely be predisposed to develop resistance to these agents.

to Maintain Cell Survival Granulocyte/Macrophage Progenitor Stages Hematopoietic Stem Cell and the Human Flt3 Is Expressed at the

It is found that human Flt3 signaling prevents stem and progenitors from spontaneous apoptotic cell death at least through up-regulating Mcl-1, an indispensable survival factor for hematopoiesis.
...

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