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Review
. 2021 Dec 11;10(24):5805.
doi: 10.3390/jcm10245805.

Shedding Light on Targeting Chronic Myeloid Leukemia Stem Cells

Affiliations
Review

Shedding Light on Targeting Chronic Myeloid Leukemia Stem Cells

Mohammad Houshmand et al. J Clin Med. .

Abstract

Chronic myeloid leukemia stem cells (CML LSCs) are a rare and quiescent population that are resistant to tyrosine kinase inhibitors (TKI). When TKI therapy is discontinued in CML patients in deep, sustained and apparently stable molecular remission, these cells in approximately half of the cases restart to grow, resuming the leukemic process. The elimination of these TKI resistant leukemic stem cells is therefore an essential step in increasing the percentage of those patients who can reach a successful long-term treatment free remission (TFR). The understanding of the biology of the LSCs and the identification of the differences, phenotypic and/or metabolic, that could eventually allow them to be distinguished from the normal hematopoietic stem cells (HSCs) are therefore important steps in designing strategies to target LSCs in a rather selective way, sparing the normal counterparts.

Keywords: bone marrow microenvironment; chronic myeloid leukemia; leukemia stem cells; treatment free remission.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Possible signaling pathways in CML LSCs.

References

    1. Saglio G., Gale R.P. Prospects for achieving treatment-free remission in chronic myeloid leukaemia. Br. J. Haematol. 2020;190:318–327. doi: 10.1111/bjh.16506. - DOI - PMC - PubMed
    1. Houshmand M., Simonetti G., Circosta P., Gaidano V., Cignetti A., Martinelli G., Saglio G., Gale R.P. Chronic myeloid leukemia stem cells. Leukemia. 2019;33:1543–1556. doi: 10.1038/s41375-019-0490-0. - DOI - PMC - PubMed
    1. MacDonald B.T., Tamai K., He X. Wnt/beta-catenin signaling: Components, mechanisms, and diseases. Dev. Cell. 2009;17:9–26. doi: 10.1016/j.devcel.2009.06.016. - DOI - PMC - PubMed
    1. Zhao C., Blum J., Chen A., Kwon H.Y., Jung S.H., Cook J.M., Lagoo A., Reya T. Loss of beta-catenin impairs the renewal of normal and CML stem cells in vivo. Cancer Cell. 2007;12:528–541. doi: 10.1016/j.ccr.2007.11.003. - DOI - PMC - PubMed
    1. Jamieson C.H., Ailles L.E., Dylla S.J., Muijtjens M., Jones C., Zehnder J.L., Gotlib J., Li K., Manz M.G., Keating A., et al. Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML. N. Engl. J. Med. 2004;351:657–667. doi: 10.1056/NEJMoa040258. - DOI - PubMed

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