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Acute Myeloid Leukemia Stem Cells: The Challenges of Phenotypic Heterogeneity

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Arnone Marlon, Konantz Martina, Hanns Pauline, Paczulla Stanger Anna M., Bertels Sarah, Godavarthy Parimala Sonika, Christopeit Maximilian, Lengerke Claudia,
Project Absence of NKG2D ligands on leukemia-initiating cells links stemness to immune evasion
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Original article (peer-reviewed)

Journal Cancers
Volume (Issue) 12(12)
Page(s) 3742 - 3742
Title of proceedings Cancers
DOI 10.3390/cancers12123742

Open Access

URL http://doi.org/10.3390/cancers12123742
Type of Open Access Publisher (Gold Open Access)

Abstract

Patients suffering from acute myeloid leukemia (AML) show highly heterogeneous clinical outcomes. Next to variabilities in patient-specific parameters influencing treatment decisions and outcome, this is due to differences in AML biology. In fact, different genetic drivers may transform variable cells of origin and co-exist with additional genetic lesions (e.g., as observed in clonal hematopoiesis) in a variety of leukemic (sub)clones. Moreover, AML cells are hierarchically organized and contain subpopulations of more immature cells called leukemic stem cells (LSC), which on the cellular level constitute the driver of the disease and may evolve during therapy. This genetic and hierarchical complexity results in a pronounced phenotypic variability, which is observed among AML cells of different patients as well as among the leukemic blasts of individual patients, at diagnosis and during the course of the disease. Here, we review the current knowledge on the heterogeneous landscape of AML surface markers with particular focus on those identifying LSC, and discuss why identification and targeting of this important cellular subpopulation in AML remains challenging.
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