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- W2565147622 abstract "Aberrant proliferation, symmetric self-renewal, increased survival, and defective differentiation of malignant blasts are key oncogenic drivers in acute myeloid leukemia (AML). Stem cell gene signatures predict poor prognosis in AML patients; however, with few exceptions, these deregulated molecular pathways cannot be targeted therapeutically. In this study, we demonstrate that the TNF superfamily ligand–receptor pair CD70/CD27 is expressed on AML blasts and AML stem/progenitor cells. CD70/CD27 signaling in AML cells activates stem cell gene expression programs, including the Wnt pathway, and promotes symmetric cell divisions and proliferation. Soluble CD27, reflecting the extent of CD70/CD27 interactions in vivo, was significantly elevated in the sera of newly diagnosed AML patients and is a strong independent negative prognostic biomarker for overall survival. Blocking the CD70/CD27 interaction by mAb induced asymmetric cell divisions and differentiation in AML blasts and AML stem/progenitor cells, inhibited cell growth and colony formation, and significantly prolonged survival in murine AML xenografts. Importantly, hematopoietic stem/progenitor cells from healthy BM donors express neither CD70 nor CD27 and were unaffected by blocking mAb treatment. Therefore, targeting CD70/CD27 signaling represents a promising therapeutic strategy for AML." @default.
- W2565147622 created "2017-01-06" @default.
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- W2565147622 date "2016-12-28" @default.
- W2565147622 modified "2023-10-17" @default.
- W2565147622 title "CD70/CD27 signaling promotes blast stemness and is a viable therapeutic target in acute myeloid leukemia" @default.
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- W2565147622 doi "https://doi.org/10.1084/jem.20152008" @default.
- W2565147622 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5294846" @default.
- W2565147622 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28031480" @default.
- W2565147622 hasPublicationYear "2016" @default.
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