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MicroRNA Screening Reveals Upregulation of FoxO-Signaling in Relapsed Acute Myeloid Leukemia Patients.
Genes (Basel)
December 2024
Department of Hematology, Cell Therapy, Hemostaseology and Infectiology, University Hospital Leipzig, 04103 Leipzig, Germany.
: AML is an aggressive malignant disease characterized by aberrant proliferation and accumulation of immature blast cells in the patient's bone marrow. Chemotherapeutic treatment can effectively induce remission and re-establish functional hematopoiesis. However, many patients experience chemoresistance-associated relapse and disease progression with a poor prognosis.
View Article and Find Full Text PDFMyeloperoxidase and Thyrotropin-Releasing Hormone Within Leukaemia Stem Cells Increased Chemosensitivity in Acute Myeloid Leukaemia.
J Cell Mol Med
December 2024
Division of Hematology/Medical Oncology, Department of Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
Leukaemia stem cells (LSCs) are major contributors to chemoresistance in acute myeloid leukaemia (AML). Identifying potential biomarkers within LSCs that can predict chemosensitivity in AML is key. This prospective study involved 20 consecutive de novo AML patients who underwent '7 + 3' induction therapy.
View Article and Find Full Text PDFCXCL12 chemokine dimer signaling modulates acute myelogenous leukemia cell migration through altered receptor internalization.
bioRxiv
August 2024
Department of Microbiology & Immunology, Medical College of Wisconsin, Milwaukee WI, USA.
Acute myeloid leukemia (AML) is a malignancy of immature myeloid blast cells with stem-like and chemoresistant cells being retained in the bone marrow through CXCL12-CXCR4 signaling. Current CXCR4 inhibitors mobilize AML cells into the bloodstream where they become more chemosensitive have failed to improve patient survival, likely reflecting persistent receptor localization on target cells. Here we characterize the signaling properties of CXCL12-locked dimer (CXCL12-LD), a bioengineered variant of the dimeric CXCL12 structure.
View Article and Find Full Text PDFPharmacological p38 MAPK inhibitor SB203580 enhances AML stem cell line KG1a chemosensitivity to daunorubicin by promoting late apoptosis, cell growth arrest in S-phase, and miR-328-3p upregulation.
Saudi Pharm J
June 2024
Blood and Cancer Research Department, King Abdullah International Medical Research Center (KAIMRC), King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), Ministry of National Guard-Health Affairs (MNG-HA), Riyadh 11481, Saudi Arabia.
Acute myeloid leukaemia (AML) is characterized by uncontrolled proliferation of myeloid progenitor cells and impaired maturation, leading to immature cell accumulation in the bone marrow and bloodstream, resulting in hematopoietic dysfunction. Chemoresistance, hyperactivity of survival pathways, and miRNA alteration are major factors contributing to treatment failure and poor outcomes in AML patients. This study aimed to investigate the impact of the pharmacological p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 on the chemoresistance potential of AML stem cell line KG1a to the therapeutic drug daunorubicin (DNR).
View Article and Find Full Text PDFGlycolysis Modulation by METTL7B Shapes Acute Lymphoblastic Leukemia Cell Proliferation and Chemotherapy Response.
Hum Cell
March 2024
Department of Geriatric Respiratory Disease, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Acute lymphoblastic leukemia (ALL) is a devastating hematological malignancy characterized by uncontrolled proliferation of immature lymphoid cells. While advances in treatment have improved patient outcomes, challenges remain in enhancing therapeutic efficacy and understanding underlying molecular mechanisms. Methyltransferase-like 7B (METTL7B), known for its methyltransferase activity, has been implicated in various solid tumors, yet its role in ALL remains unexplored.
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