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hematopoietic stem cells

CXCL12-Abundant Reticular Cells Are the Major Source of IL-6 upon LPS-Stimulation and Thereby Regulate Hematopoiesis

[Blood Advances] Through a combination of gene expression analysis in prospectively isolated non-hematopoietic bone marrow (BM) cell populations and various mouse models, the authors revealed that BM CXCL12-abundant reticular cells were a major source of systemic and local BM IL-6 levels during emergency hematopoiesis following lipopolysaccharide stimulation.

Venetoclax plus Azacitidine and Donor Lymphocyte Infusion in Treating Acute Myeloid Leukemia Patients Who Relapse after Allogeneic Hematopoietic Stem Cell Transplantation

[Annals of Hematology] Scientists evaluated the efficacy and safety of venetoclax plus azacitidine and donor lymphocyte infusion in treating patients with relapsed acute myeloid leukemia after allogeneic hematopoietic stem cell transplantation.

Spred1 Deficit Promotes Treatment Resistance and Transformation of Chronic Phase CML

[Leukemia] Spred1 knockout, regardless if occurred in HSCs or in endothelial cells, increased miR-126 in Lin−Sca-1+c-Kit+, a population enriched in leukemic stem cells (LSCs), resulting in expansion of LSCs, likely through hyperactivation of the MAPK/ERK pathway that augmented Bcl-2 expression and stability.

Combination of Tyrosine Kinase Inhibitors and the MCL1 Inhibitor S63845 Exerts Synergistic Antitumorigenic Effects on CML Cells

[Cell Death & Disease] Scientists show that combining TKI treatment with the small-molecule MCL1 inhibitor S63845 exerted strong synergistic antiviability and proapoptotic effects on chronic myeloid leukemia (CML) lines and CD34+ stem/progenitor cells isolated from untreated CML patients in chronic phase.

Super-Enhancer Landscape Reveals Leukemia Stem Cell Reliance on X-box Binding Protein 1 as a Therapeutic Vulnerability

[Science Translational Medicine] Disruption of the super-enhancer-associated gene transcription by THZ1, a covalent cyclin-dependent kinase 7 inhibitor, efficiently eradicated leukemia stem cells in retroviral BCR-ABL–driven chronic myelogenous leukemia mice while sparing normal hematopoietic stem cells.

The Megakaryocytic Transcription Factor ARID3A Suppresses Leukemia Pathogenesis

[Blood] The authors reported that post-transcriptional repression of the transcription factor ARID3A by miR-125b was a key event in megakaryoblastic leukemia pathogenesis, and showed that chromosome 21-encoded miR-125b synergized with Gata1s to drive leukemogenesis in this context.

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