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acute myeloid leukemia

LncRNA BC200/miR-150-5p/MYB Positive Feedback Loop Promotes the Malignant Proliferation of Myelodysplastic Syndrome

[Cell Death & Disease] The authors revealed that the BC200/miR-150-5p/MYB positive feedback loop promoted the proliferation of myelodysplastic syndrome (MDS) cells and was expected to be a potential biomarker and therapeutic target in MDS.

CD38 Knockout Natural Killer Cells Expressing an Affinity Optimized CD38 Chimeric Antigen Receptor Successfully Target Acute Myeloid Leukemia with Reduced Effector Cell Fratricide

[Haematologica] Researchers developed a CD38 CAR-NK cell therapy for acute myeloid leukemia, first by using an NK cell line which had low baseline CD38 expression and subsequently NK cells expanded from healthy donors.

Clinico-Biological Features of T Cell Acute Lymphoblastic Leukemia with Fusion Proteins

[Blood Cancer Journal] An RT-MPLA assay was applied to a consecutive series of 522 adult and pediatric T cell acute lymphoblastic leukemias and identified a fusion transcript in 20% of cases.

Azacitidine-Induced Reconstitution of the Bone Marrow T Cell Repertoire Is Associated with Superior Survival in AML Patients

[Blood Cancer Journal] Since hypomethylating agents possessed immunomodulatory functions that constituted part of their anti-tumor effect, the authors set out to analyze the bone marrow immune environment by next-generation sequencing of T cell receptor beta repertoires in 51 AML patients treated within the RAS-AZIC trial.

Loss of miR-31-5p Drives Hematopoietic Stem Cell Malignant Transformation and Restoration Eliminates Leukemia Stem Cells in Mice

[Science Translational Medicine] Researchers demonstrated a mechanism of HSC malignant transformation through altered energy metabolism and provided a potential therapeutic strategy to treat patients with AML.

An Oncogenic Enhancer Encodes Selective Selenium Dependency in AML

[Cell Stem Cell] By integrating comprehensive pan-cancer enhancer landscapes with genetic dependency mapping, investigators found that AML-enriched enhancers encoded for more selective tumor dependencies.

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