 | | Vol. 12.31 – 10 August, 2021 |
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| Investigators compared glucose metabolism in hematopoiesis and leukemia. Thymus T cell progenitors were glucose avid and oxidized more glucose in the tricarboxylic acid cycle through pyruvate dehydrogenase as compared with other hematopoietic cells.
[Cell Metabolism] |
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 | | PUBLICATIONSRanked by the impact factor of the journal |
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| Scientists found STAT5B to be specifically activated in HSCs and leukemic stem cells, where it induced many genes associated with quiescence and self-renewal, including the surface marker CD9.
[Blood] |
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| The authors examined the consequences of conditional inactivation of Lsd1 in adult red blood cells using a new Gata1creERT2 BAC transgene. The analogous phenotype was observed in human hematopoietic stem and progenitor cells, coincident with induction of myeloid transcription factors.
[Blood] |
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| Transcriptomic analysis showed that IFN-γ and IFN-α signaling was downregulated in IRF8-deficient HSCs, while their response to proinflammatory cytokines was unchanged ex vivo.
[Advanced Science] |
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| ZMYND8 was essential for acute myeloid leukemia proliferation in vitro and in vivo and associated with MYC and IRF8 enhancer elements that scientists defined in cell lines and in patient samples.
[Molecular Cell] |
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| Researchers found that the levels of the histone acetyltransferase males absent on the first and its target modification histone H4 lysine 16 acetylation were heterogeneous among HSCs and influenced their proliferation capacities.
[Science Advances] |
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| Investigators identified tetraspanin CD63 as a novel functional marker of HSCs in mice and showed that CD63 was unevenly expressed on the cell surface in HSC populations.
[Cell Death & Differentiation] |
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| Scientists reported that telomerase RNA component regulated the expression of master myeloid genes in zebrafish and humans by recruiting the transcription machinery. Induced pluripotent stem cells derived from dyskeratosis congenita patients with a telomerase RNA mutation in a specific domain, the CR4-CR5, showed impaired myelopoiesis.
[Proceedings of the National Academy of Sciences of the United States of America] |
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| Loss of both SHMT1 and SHMT2 was necessary for impaired growth and cell cycle arrest, with suppression of both SHMT1 and SHMT2 inhibiting leukemia progression in vivo.
[Leukemia] |
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| Treatment of human acute myeloid leukemia (AML) cells with a PAICS inhibitor suppressed their proliferation by inhibiting DNA synthesis and promoting apoptosis and had anti-leukemic effects in AML PDX models.
[Leukemia] |
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| | The authors investigated whether fenofibrate increased circulating hematopoietic stem/progenitor cells (HSPCs). When compared with placebo, fenofibrate significantly increased levels of HSPCs expressing CD34 and/or CD133.
[Diabetologia] |
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| Investigators evaluated the most optimal donor for young acute leukemia patients with multiple donors available for allogeneic hematopoietic stem cell transplantation, including HLA-matched sibling donors, HLA-matched unrelated donors, haploidentical parental donors, and haploidentical sibling donors.
[American Journal of Hematology] |
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| Researchers reported two cases of the serial use of anti-B-cell maturation antigen (BCMA) therapies with parallel monitoring of BCMA expression and anti-CAR antibodies and discussed recent data from clinical studies about the different mechanisms of resistance to anti-BCMA therapies.
[Blood Advances] |
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| MYC regulation and the mechanisms by which MYC adjusts cellular functions and its implication in hematologic malignancies are summarized. Scientists also discuss potential inhibitors of MYC that could be beneficial for treating hematologic malignancies.
[Journal of Hematology & Oncology] |
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| The authors describe the “self-renewal, multi-lineage differentiation, apoptosis, rest, and trafficking” or “SMART” model, which has been developed based on data derived from studies of HSCs as the most well-characterized stem cell type.
[Science China-Life Sciences] |
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| Trillium Therapeutics, Inc. announced that it has dosed the first TP53-mutated acute myeloid leukemia patient with TTI-622, an investigational checkpoint inhibitor of the innate immune system, in combination with azacitidine.
[Trillium Therapeutics, Inc.] |
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| January 12 – 14, 2022
Shanghai, China |
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| | Baylor College of Medicine – Houston, Texas, United States |
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| | The Scripps Research Institute – La Jolla, California, United States |
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| | University of California, San Francisco – San Francisco, California, United States |
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| | University of Gothenburg – Gothenburg, Sweden |
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| | Dalhousie University – Halifax, Nova Scotia, Canada |
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