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INTERNATIONAL CONGRESS OF

CancerGenetics

• GLS1 Inhibition and Glutamine Addiction in MYC-Driven Burkitt Lymphoma: A Systematic Review

• Alireza Pourrahim,^1,* Mohammad Mahdi Pourrahim,² Omid Raiesi,³ Alireza Vasiee,⁴
  1. Student Research Committee, Faculty of Medicine, Ilam University of Medical Sciences, Ilam, Iran
  2. Student Research Committee, Faculty of Medicine, Ilam University of Medical Sciences, Ilam, Iran
  3. Omid Raiesi
  4. Department of Nursing, Faculty of Nursing and Midwifery, Ilam University of Medical Sciences, Ilam, Iran
  
  
  
• Introduction: Burkitt lymphoma is characterized by MYC oncogene overexpression, which drives glutamine addiction through upregulation of glutaminase 1 (GLS1). Pharmacologic GLS1 inhibition represents a targeted strategy to starve tumor cells of glutamine, induce apoptosis, and suppress tumor growth. We systematically reviewed preclinical evidence quantifying the efficacy of GLS1 inhibitors in MYC-driven Burkitt lymphoma models.
• Methods: We searched PubMed, EMBASE, Web of Science, and Cochrane Library databases from inception through June 2025 using (“Burkitt lymphoma” AND “GLS1” OR “glutaminase”) AND (“inhibitor” OR “inhibition”). Eligible studies were in vitro or in vivo investigations of GLS1 inhibitors (e.g., CB-839, BPTES) in MYC-overexpressing Burkitt lymphoma cell lines or xenograft models. Two reviewers independently screened titles/abstracts, extracted data on half-maximal inhibitory concentration (IC50), cell viability reduction, apoptosis induction, tumor volume change, and survival metrics. Study quality was assessed with SYRCLE’s risk-of-bias tool for animal models and a modified Cochrane checklist for cell-based assays.
• Results: Across six preclinical studies including 12 MYC-driven Burkitt lymphoma cell lines and 84 xenografted mice, the pooled half-maximal inhibitory concentration (IC₅₀) for GLS1 inhibitors was 1.8 ± 0.5 μM. Treatment at 5 μM reduced cell viability by 62% (95% CI 55–69%) and induced a 3.2-fold increase in apoptosis (95% CI 2.5–3.8). In murine models, mean tumor volume was suppressed by 58% (95% CI 50–66%) at 21 days post-treatment, and median survival improved by 45% (HR 0.55; 95% CI 0.42–0.71). Off-target effects were minimal, with < 5% mean body weight loss and no organ histopathology abnormalities.
• Conclusion: Preclinical evidence demonstrates that GLS1 inhibition in MYC-driven Burkitt lymphoma significantly lowers cell viability, induces apoptosis, suppresses tumor growth, and prolongs survival with an acceptable safety profile. These aggregated findings support advancing GLS1 inhibitors into early-phase clinical trials for MYC-overexpressing Burkitt lymphoma.
• Keywords: Burkitt lymphoma; GLS1 inhibition; glutamine addiction; CB-839; xenograft