Posters
Academic Level (Author 1)
Faculty
Discipline/Specialty (Author 1)
Neuroscience
Academic Level (Author 2)
Medical Student
Discipline Track
Biomedical Science
Abstract
Reactive oxygen species (ROS) play a crucial role in the pathogenesis and therapeutic resistance of acute myeloid leukemia (AML). AML cells exhibit heightened ROS levels compared to normal hematopoietic cells, primarily attributed to NOX2 activity. Alterations in ROS metabolism contribute to therapy resistance and relapse in AML, prompting investigations into ROS-targeting therapeutic strategies. Inhibition of mitochondrial fusion reduces ROS production, inducing cell cycle arrest at the G0/G1 transition, underscoring the regulatory role of mitochondrial dynamics in AML progression. Additionally, LNS8801, a G protein-coupled estrogen receptor agonist, induces ROS-mediated apoptosis via the endoplasmic reticulum stress pathway in AML cells, suggesting a potential therapeutic avenue. Dysregulation of RUNX genes exacerbates oxidative stress and DNA damage in leukemia, particularly in pediatric AML driven by RUNX1-ETO fusion, implicating ROS in mutational accumulation. The complex role of ROS in cancer cells underscores the nuanced use of antioxidants in therapy, with divergent effects on cancer cell sensitivity to treatment. While ROS modulation holds promise for AML therapy, further research is imperative to delineate optimal strategies harnessing ROS dynamics for improved treatment outcomes. This synthesis underscores the multifaceted interplay between ROS and AML pathogenesis, offering insights into novel therapeutic avenues and emphasizing the need for tailored approaches in cancer management.
Presentation Type
Poster
Recommended Citation
Zuo, Alex and Alanis, Anthony L., "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
Reactive oxygen species (ROS) play a crucial role in the pathogenesis and therapeutic resistance of acute myeloid leukemia (AML). AML cells exhibit heightened ROS levels compared to normal hematopoietic cells, primarily attributed to NOX2 activity. Alterations in ROS metabolism contribute to therapy resistance and relapse in AML, prompting investigations into ROS-targeting therapeutic strategies. Inhibition of mitochondrial fusion reduces ROS production, inducing cell cycle arrest at the G0/G1 transition, underscoring the regulatory role of mitochondrial dynamics in AML progression. Additionally, LNS8801, a G protein-coupled estrogen receptor agonist, induces ROS-mediated apoptosis via the endoplasmic reticulum stress pathway in AML cells, suggesting a potential therapeutic avenue. Dysregulation of RUNX genes exacerbates oxidative stress and DNA damage in leukemia, particularly in pediatric AML driven by RUNX1-ETO fusion, implicating ROS in mutational accumulation. The complex role of ROS in cancer cells underscores the nuanced use of antioxidants in therapy, with divergent effects on cancer cell sensitivity to treatment. While ROS modulation holds promise for AML therapy, further research is imperative to delineate optimal strategies harnessing ROS dynamics for improved treatment outcomes. This synthesis underscores the multifaceted interplay between ROS and AML pathogenesis, offering insights into novel therapeutic avenues and emphasizing the need for tailored approaches in cancer management.