Tag results:
leukemia cells
Hematopoiesis News
The GPI-Anchored Protein CD109 Protects Hematopoietic Progenitor Cells from Undergoing Erythroid Differentiation Induced by TGF-β
[Leukemia] Investigators found that CD109 suppressed TGF-β signaling in hematopoietic stem progenitor cells (HSPCs), and increased the sensitivity of PIGA-mutated HSPCs to TGF-β, leading to the preferential commitment of erythroid progenitor cells to mature red blood cells in immune-mediated bone marrow failure.
Hematopoiesis News
TCP1 Increases Drug Resistance in Acute Myeloid Leukemia by Suppressing Autophagy via Activating AKT/mTOR Signaling
[Cell Death & Disease] Scientists discovered that the T-complex protein 1 (TCP1) expression was elevated in acute myeloid leukemia patients and high TCP1 expression was associated with low complete response rate along with poor overall survival.
Hematopoiesis News
Demethylating Therapy Increases Anti-CD123 CAR T Cell Cytotoxicity against Acute Myeloid Leukemia
[Nature Communications] Investigators indicated that 5′-Azacitidine increased the immunogenicity of acute myeloid leukemia cells, enhancing recognition and elimination of malignant cells by highly efficient CTLA-4negative anti-CD123 chimeric antigen receptor (CAR) T cells.
Cell Therapy News
Demethylating Therapy Increases Anti-CD123 CAR T Cell Cytotoxicity against Acute Myeloid Leukemia
[Nature Communications] The authors developed third-generation anti-CD123 CAR T cells with a humanized CSL362-based ScFv and a CD28-OX40-CD3ζ intracellular signaling domain.
Immune Regulation News
Targeting eIF4F Translation Complex Sensitizes B-ALL Cells to Tyrosine Kinase Inhibition
[Scientific Reports] In cellular models of Philadelphia Chromosome-positive B-ALL, mTOR kinase inhibitors that inhibit both mTOR-complex-1and mTOR-complex-2 enhanced the cytotoxicity of tyrosine kinase inhibitors such as dasatinib.
Hematopoiesis News
DNMT3A Harboring Leukemia-Associated Mutations Directs Sensitivity to DNA Damage at Replication Forks
[Clinical Cancer Research] Investigators showed that DNMT3A mutations underlied a defect in recovery from replication fork arrest with subsequent accumulation of unresolved DNA damage, which may have therapeutic tractability.