Tag results:
acute myeloid leukemia
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.
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.
Cell Therapy News
piggyBac System to Co-Express NKG2D CAR and IL-15 to Augment the In Vivo Persistence and Anti-AML Activity of Human Peripheral Blood NK Cells
[Molecular Therapy-Methods & Clinical Development] Using a non-viral piggyBac transposon technology and human peripheral blood derived primary natural killer (NK) cells, scientists generated CAR-NK cells to target NKG2D ligands.
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.
Hematopoiesis News
Asxl1loss Cooperates with Oncogenic Nras in Mice to Reprogram Immune Microenvironment and Drive Leukemic Transformation
[Blood] Investigators showed that concurrent ASXL1 and NRAS mutations defined a population of chronic myelomonocytic leukemia patients with shorter leukemia-free survival than those with ASXL1 mutation only.
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.