Targeting FMS-like tyrosine kinase 3 (FLT3) in acute myeloid leukemia: Novel molecular approaches and therapeutic challenges.

Acute myeloid leukemia (AML), a heterogeneous hematologic malignancy, has generally a poor prognosis despite the recent advancements in diagnostics and treatment. Genetic instability, particularly mutations in the FMS-like tyrosine kinase 3 (FLT3) gene, is associated with severe outcomes. Approximately 30 % of AML patients harbor FLT3 mutations, which have been linked to higher relapse and reduced survival rates.

Deficiency of miR-155 in leukemic B-cells results in cell cycle arrest and deregulation of MIR155HG/TP53INP1/CDKN1A/CCND1 network.

Background: Cell cycle progression and leukemia development are tightly regulated processes in which even a small imbalance in the expression of cell cycle regulatory molecules and microRNAs (miRNAs) can lead to an increased risk of cancer/leukemia development. Here, we focus on the study of a ubiquitous, multifunctional, and oncogenic miRNA-hsa-miR-155-5p (miR-155, MIR155HG), which is overexpressed in malignancies including chronic lymphocytic leukemia (CLL). Nonetheless, the precise mechanism of how miR-155 regulates the cell cycle in leukemic cells remains the subject of extensive research.

Surgical results in patients with CNS lymphoma. Comparison of predictive value of intraoperative MRI and intraoperative histological examination for diagnostic biopsy yield.

Introduction: Central nervous system lymphoma poses significant diagnostic challenges, with stereotactic biopsy being the gold standard for diagnosis. Intraoperative magnetic resonance imaging and intraoperative histological examination are utilized to enhance biopsy yield, yet their comparative efficacy remains unclear.

Research Question: This study aims to compare the diagnostic yield of intraoperative magnetic resonance imaging and intraoperative histological examination in stereotactic brain biopsies for central nervous system lymphoma.

Imatinib therapy of chronic myeloid leukemia significantly reduces carnitine cell intake, resulting in adverse events.

Objective: A prominent, safe and efficient therapy for patients with chronic myeloid leukemia (CML) is inhibiting oncogenic protein BCR::ABL1 in a targeted manner with imatinib, a tyrosine kinase inhibitor. A substantial part of patients treated with imatinib report skeletomuscular adverse events affecting their quality of life. OCTN2 membrane transporter is involved in imatinib transportation into the cells.