Differential Gene Expression Signatures Predict Survival Outcomes in Acute Myeloid Leukemia: A cBioPortal-Based Transcriptomic Analysis
Seongsu (William) Kim
Chadwick International School, Incheon, South Korea
Publication date: July 10, 2026
Chadwick International School, Incheon, South Korea
Publication date: July 10, 2026
DOI: http://doi.org/10.34614/JIYRC2026I10
ABSTRACT
Acute Myeloid Leukemia (AML) is a malignancy of the bone marrow characterized by uncontrolled proliferation of immature myeloid cells. Although genetic alterations influence prognosis, the transcriptomic patterns linked to survival remain insufficiently defined. This study analyzed RNA-seq expression profiles from cBioPortal, comparing living (n = 1335) and deceased (n = 708) AML patients to identify genes associated with survival outcomes. Differential expression analysis revealed that several HOXA family members—HOXA3, HOXA5, HOXA6, HOXA9, and HOXA10—located at chromosome 7p15.2 were markedly overexpressed in deceased patients, consistent with their roles in maintaining stem-cell–like states and blocking myeloid differentiation. In contrast, survivors demonstrated elevated expression of UGT2B11, MPO, LPO, EPX, and IL5RA (q < 6.94 × 10⁻¹³), genes involved in detoxification, oxidative stress reduction, and immune regulation. Together, these opposing expression programs highlight HOXA-driven aggressiveness versus metabolic–immune resilience, offering potential prognostic biomarkers and therapeutic targets for AML.
Acute Myeloid Leukemia (AML) is a malignancy of the bone marrow characterized by uncontrolled proliferation of immature myeloid cells. Although genetic alterations influence prognosis, the transcriptomic patterns linked to survival remain insufficiently defined. This study analyzed RNA-seq expression profiles from cBioPortal, comparing living (n = 1335) and deceased (n = 708) AML patients to identify genes associated with survival outcomes. Differential expression analysis revealed that several HOXA family members—HOXA3, HOXA5, HOXA6, HOXA9, and HOXA10—located at chromosome 7p15.2 were markedly overexpressed in deceased patients, consistent with their roles in maintaining stem-cell–like states and blocking myeloid differentiation. In contrast, survivors demonstrated elevated expression of UGT2B11, MPO, LPO, EPX, and IL5RA (q < 6.94 × 10⁻¹³), genes involved in detoxification, oxidative stress reduction, and immune regulation. Together, these opposing expression programs highlight HOXA-driven aggressiveness versus metabolic–immune resilience, offering potential prognostic biomarkers and therapeutic targets for AML.
