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Eisenwort, Gregor; Sadovnik, Irina; Keller, Alexandra; Ivanov, Daniel; Peter, Barbara; Berger, Daniela; Stefanzl, Gabriele; Bauer, Karin; Slavnitsch, Katharina; Greiner, Georg; Gleixner, Karoline V; Sperr, Wolfgang R; Willmann, Michael; Sill, Heinz; Bettelheim, Peter; Geissler, Klaus; Deininger, Michael; Rülicke, Thomas; Valent, Peter
Leukemia, 11/2021, Letnik: 35, Številka: 11Journal Article
Chronic myelomonocytic leukemia (CMML) is a stem cell-derived neoplasm characterized by dysplasia, uncontrolled expansion of monocytes, and substantial risk to transform to secondary acute myeloid leukemia (sAML). So far, little is known about CMML-initiating cells. We found that leukemic stem cells (LSC) in CMML reside in a CD34 /CD38 fraction of the malignant clone. Whereas CD34 /CD38 cells engrafted NSGS mice with overt CMML, no CMML was produced by CD34 /CD38 progenitors or the bulk of CD34 monocytes. CMML LSC invariably expressed CD33, CD117, CD123 and CD133. In a subset of patients, CMML LSC also displayed CD52, IL-1RAP and/or CLL-1. CMML LSC did not express CD25 or CD26. However, in sAML following CMML, the LSC also expressed CD25 and high levels of CD114, CD123 and IL-1RAP. No correlations between LSC phenotypes, CMML-variant, mutation-profiles, or clinical course were identified. Pre-incubation of CMML LSC with gemtuzumab-ozogamicin or venetoclax resulted in decreased growth and impaired engraftment in NSGS mice. Together, CMML LSC are CD34 /CD38 cells that express a distinct profile of surface markers and target-antigens. During progression to sAML, LSC acquire or upregulate certain cytokine receptors, including CD25, CD114 and CD123. Characterization of CMML LSC should facilitate their enrichment and the development of LSC-eradicating therapies.
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in: SICRIS
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