Posters
Academic Level (Author 1)
Faculty
Discipline/Specialty (Author 1)
Neuroscience
Academic Level (Author 2)
Medical Student
Discipline Track
Biomedical Science
Abstract
Upon exposure to oxidative stress, acute myeloid leukemia (AML) cells have higher levels of ROS compared to normal hematopoietic cells, which are thought to be due to NOX2 activity. Phenomena of altered ROS metabolism has been associated with therapy resistance and relapse in AML which opened avenues for ROS-targeted therapeutic strategies. When mitochondrial fusion is inhibited in AML cells, this suppresses ROS levels as well as caspase-dependent cell cycle arrest at the level of G0/G1 transition. In AML cells, apoptosis via the endoplasmic reticulum stress pathway is ROS-mediated via the G protein-coupled estrogen receptor agonist LNS8801; therapy would presumably follow. RUNX dysregulation enhances oxidative stress and DNA damage in leukemia, particularly pediatric AML driven by RUNX1-ETO fusion. The role of ROS in cancer cells stresses the fine line antioxidant therapies must walk in cancer treatment, which may make resistant cells more sensitive or resistant to treatment. This review highlights the ROS metabolism in AML pathogenesis with an interesting horizon in the search for new therapeutic approaches. It emphasizes the need for individualized approaches in cancer treatment to improve response rates.
Presentation Type
Poster
Recommended Citation
Zuo, Alex and Alanis, Anthony, "Oxidative Stress in Leukemia: A Double-Edged Sword" (2024). Research Colloquium. 20.
https://scholarworks.utrgv.edu/colloquium/2024/posters/20
Included in
Oxidative Stress in Leukemia: A Double-Edged Sword
Upon exposure to oxidative stress, acute myeloid leukemia (AML) cells have higher levels of ROS compared to normal hematopoietic cells, which are thought to be due to NOX2 activity. Phenomena of altered ROS metabolism has been associated with therapy resistance and relapse in AML which opened avenues for ROS-targeted therapeutic strategies. When mitochondrial fusion is inhibited in AML cells, this suppresses ROS levels as well as caspase-dependent cell cycle arrest at the level of G0/G1 transition. In AML cells, apoptosis via the endoplasmic reticulum stress pathway is ROS-mediated via the G protein-coupled estrogen receptor agonist LNS8801; therapy would presumably follow. RUNX dysregulation enhances oxidative stress and DNA damage in leukemia, particularly pediatric AML driven by RUNX1-ETO fusion. The role of ROS in cancer cells stresses the fine line antioxidant therapies must walk in cancer treatment, which may make resistant cells more sensitive or resistant to treatment. This review highlights the ROS metabolism in AML pathogenesis with an interesting horizon in the search for new therapeutic approaches. It emphasizes the need for individualized approaches in cancer treatment to improve response rates.
