Stable ACC1 protein expression suppressed the growth-promoting activity and increased ROS levels with the consumption of NADPH in a primary bone marrow culture, and delayed the onset of acute myeloid leukemia with increases in mature myeloid cells in mouse models.
[Journal of Clinical Investigation]
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The authors discussed the effective implementation of available therapeutic measures and appropriate disease monitoring of core binding factor acute myelogenous leukemia.
[Blood Cancer Journal]
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Investigators reported an integrated analysis of 3D genome alterations and differential gene expressions in eighteen newly diagnosed T-lineage acute lymphoblastic leukemia patients and four healthy controls. Patients with HOXA11-A13 expressions, but not other genes in the HOXA cluster, had immature immunophenotype and poor outcomes.
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The authors described a distinct subgroup of acute leukemia with expression of myeloid, T lymphoid and stem cell markers driven by aberrant allele-specific deregulation of BCL11B, a master transcription factor responsible for thymic T-lineage commitment and specification.
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Investigators conducted a multicenter biologic assignment trial comparing reduced-intensity hematopoietic cell transplantation to hypomethylating therapy or best supportive care in subjects 50-75 years of age with intermediate-2 or high-risk de novo myelodysplastic syndromes.
[Journal of Clinical Oncology]
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Scientists showed that Fanconi anemia (FA)-mutated cells were hypersensitive to persistent replication stress and that FA proteins played a role in the break-induced-replication-like pathway for fork restart.
[Nature Structural & Molecular Biology]
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Scientists hypothesized that targeted hyperactivation of the phosphatidylinositol-3-phosphate/AKT (PI3K/AKT)-signaling pathway may have been leveraged to trigger chronic lymphocytic leukemia cell death.
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In AML cell lines, myeloid cell leukemia 1 was downregulated following treatment with fadraciclib, resulting in a rapid induction of apoptosis.
[Cell Death Discovery]
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The authors reported that cabozantinib could promote differentiation in erythroid leukemia cells and found that K562 erythroid leukemia cells treated with 1 μM cabozantinib for 72 hours underwent erythroid lineage differentiation.
[Cancer Gene Therapy]
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Researchers employed mitochondrial single-cell assay for transposase-accessible chromatin with sequencing to profile 163,279 cells from nine patients with chronic lymphocytic leukemia collected across disease course and utilized mitochondrial DNA mutations as natural genetic markers of cancer clones.
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Investigators discovered that FLT3-ITD, one of the most frequent mutations in acute myeloid leukemia, was S-palmitoylated by the ZDHHC6 palmitoyl acyltransferase. Disruption of palmitoylation redirected FLT3-ITD to the plasma membrane and rewired its downstream signaling by activating AKT and ERK pathways in addition to STAT5.
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