Tag results:
acute myeloid leukemia
Hematopoiesis News
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.
Cell Therapy News
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.
Hematopoiesis News
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.
Hematopoiesis News
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.
Hematopoiesis News
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.
Hematopoiesis News
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.