![]() In addition, a second cohort of 30 mice was assigned for early analysis at 5 and 7 months post-irradiation. The Kaplan-Meier estimator was utilized to assess AML free survival. ![]() A total of 86 irradiated B6D2F1 mice with various levels of iron burden were monitored for leukemia development over a period of 70 weeks. Iron overload was introduced via intraperitoneal injection of iron dextran, and iron chelation via oral gavage of deferasirox. We utilized a radiation-induced acute myeloid leukemia (RI-AML) animal model. Conversely, iron chelation therapy (ICT) may reduce AML risk by lowering iron burden in the iron-loaded animals. We hypothesize that iron loading promotes AML development by increasing oxidative stress and disrupting important signaling pathways in the bone marrow cells (BMCs). Multiple RBC transfusions cause secondary iron overload and subsequent excessive generation of reactive oxygen species (ROS), which leads to mutations, cell death, organ failure, and inferior disease outcomes. Patients with myelodysplastic syndrome (MDS) require chronic red blood cell (RBC) transfusion due to anemia.
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