ArticleBlood advances2023
Inhibition of glutaminase-1 in DLBCL potentiates venetoclax-induced antitumor activity by promoting oxidative stress.
Article in Blood advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Superior anti-DLBCL efficacy of novel organic arsenical Z2-A-Z2 through ROS-mediated apoptosis and critical NF-κB/IκBα signaling pathway inhibition.Journal of experimental & clinical cancer research : CR · 2026Article
- Metabolic vulnerabilities and therapeutic opportunities in diffuse large B-cell lymphoma.Oncogenesis · 2026Review
- Functional cooperation between the B-cell receptor and NOTCH1 in regulating metabolic reprogramming in chronic lymphocytic leukemia.Leukemia · 2026Article
- Lipid Metabolism Reprogramming in Diffuse Large B-Cell Lymphoma (DLBCL): Mechanisms and Treatment Strategies.Cancers · 2026Review
- NUFIP1 gain of function promotes fibrotic remodeling and reveals a ZNHIT3-linked metabolic vulnerability in idiopathic pulmonary fibrosis models.Frontiers in immunology · 2026Article
- Bcl-2 inhibitor resistance in diffuse large b-cell lymphoma: establishing a prognostic signature and targeting alpha protein kinase 1.Frontiers in oncology · 2026Article
- Integrative proteomic and metabolomic analysis reveals that ouabain inhibits DLBCL proliferation by reprogramming arginine-driven metabolic networks.Frontiers in pharmacology · 2026Article
- Amino acid metabolic reprogramming drives pathogenesis and therapy in hematologic malignancies.Discover oncology · 2025Review
- Redox destabilization by ibrutinib promotes ferroptosis in diffuse large B-cell lymphoma (DLBCL).Cell death discovery · 2025Article
- Deciphering the causal relationships between plasma metabolites, peripheral cells, inflammatory factors and DLBCL for discovering novel therapeutic targets.Discover oncology · 2025Article
- Targeting the BCL2 Family: Advances and Challenges in BH3 Mimetic-Based Therapies.International journal of molecular sciences · 2025Review
- Review
- Glutaminase Expression in Canine Large-Cell Alimentary Lymphoma Cells and Effects of Glutaminase Inhibition by CB-839.Veterinary medicine and science · 2025Article
- Magnetic resonance spectroscopy-based detection of response to therapy targeting glutaminolysis in lymphoma.Blood neoplasia · 2025Article
- Amino acid-based risk stratification model improves prognostic precision in diffuse large B-cell lymphoma.Cancer cell international · 2025Article
- Overcoming cancer treatment resistance: Unraveling the role of cancer-associated fibroblasts.Journal of the National Cancer Center · 2025Review
- Metabolic-immune axis in the tumor microenvironment: a new strategy for prognostic assessment and precision therapy in DLBCL and FL.Frontiers in immunology · 2025Review
- Tumor Biology Hides Novel Therapeutic Approaches to Diffuse Large B-Cell Lymphoma: A Narrative Review.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diffuse large B-cell lymphoma (DLBCL) is the most common lymphoma in adults, but first-line immunochemotherapy fails to produce a durable response in about one-third of the patients. Because tumor cells often reprogram their metabolism, we investigated the importance of glutaminolysis, a pathway converting glutamine to generate energy and various metabolites, for the growth of DLBCL cells. Glutaminase-1 (GLS1) expression was robustly detected in DLBCL biopsy samples and cell lines. Both pharmacological inhibition and genetic knockdown of GLS1 induced cell death in DLBCL cells regardless of their subtype classification, whereas primary B cells remained unaffected. Interestingly, GLS1 inhibition resulted not only in reduced levels of intermediates of the tricarboxylic acid cycle but also in a strong mitochondrial accumulation of reactive oxygen species. Supplementation of DLBCL cells with α-ketoglutarate or with the antioxidant α-tocopherol mitigated oxidative stress and abrogated cell death upon GLS1 inhibition, indicating an essential role of glutaminolysis in the protection from oxidative stress. Furthermore, the combination of the GLS1 inhibitor CB-839 with the therapeutic BCL2 inhibitor ABT-199 not only induced massive reactive oxygen species (ROS) production but also exhibited highly synergistic cytotoxicity, suggesting that simultaneous targeting of GLS1 and BCL2 could represent a novel therapeutic strategy for patients with DLBCL.
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