ArticleCancer drug resistance (Alhambra, Calif.)2019
Glutaminase inhibition in renal cell carcinoma therapy.
Article in Cancer drug resistance (Alhambra, Calif.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Inhibition of glutamine metabolism blocks tumor growth and sensitizes ccRCC to immune checkpoint blockade.Journal of translational medicine · 2026Article
- Unraveling autophagy-metabolism crosstalk in cancer: Molecular insights and therapeutic strategies.Theranostics · 2026Review
- FOXO1 links KRAS G12D and G12V alleles to glutamine and nitrogen metabolism in colorectal cancer.EMBO reports · 2026Article
- Energy Metabolism and Cancer Pain: A Pathway to Innovative Treatment Strategies.Current topics in medicinal chemistry · 2026Review
- Targeting the Glutaminolysis Pathway in Glaucoma-Associated Fibrosis.International journal of molecular sciences · 2025Review
- TKT drives renal cell carcinoma progression through metabolic reprogramming and synergistic interaction with PKM2.Cell death discovery · 2025Article
- The pathogenesis and therapeutic implications of metabolic reprogramming in renal cell carcinoma.Cell death discovery · 2025Review
- The perspective of targeting cancer cell metabolism: combination therapy approaches.Molecular biology reports · 2025Review
- Metabolic crossroads: unravelling immune cell dynamics in gastrointestinal cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Glutamine's double-edged sword: fueling tumor growth and offering therapeutic hope.Frontiers in immunology · 2025Review
- MtDNA copy number enrichment is associated with poor prognosis and eosinophilic morphology in clear cell renal cell carcinoma.Pathology oncology research : POR · 2025Article
- Metabolic reprogramming and immunosenescence in colorectal cancer: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Pyruvate metabolism dictates fibroblast sensitivity to GLS1 inhibition during fibrogenesis.JCI insight · 2024Article
- Electron transport chain and mTOR inhibition synergistically decrease CD40 signaling and counteract venetoclax resistance in chronic lymphocytic leukemia.Haematologica · 2024Article
- Characterization of a fluorescence imaging probe that exploits metabolic dependency of ovarian clear cell carcinoma.Scientific reports · 2023Article
- FASN multi-omic characterization reveals metabolic heterogeneity in pancreatic and prostate adenocarcinoma.Journal of translational medicine · 2023Article
- CD133-Functionalized Gold Nanoparticles as a Carrier Platform for Telaglenastat (CB-839) against Tumor Stem Cells.International journal of molecular sciences · 2022Article
- Clinical development of metabolic inhibitors for oncology.The Journal of clinical investigation · 2022Review
- Inhibition of glutaminolysis in combination with other therapies to improve cancer treatment.Current opinion in chemical biology · 2021Review
- A facile and sensitive method of quantifying glutaminase binding to its inhibitor CB-839 in tissues.Journal of genetics and genomics = Yi chuan xue bao · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Receptor tyrosine kinase inhibitors have been a standard first-line therapy for renal cell carcinoma (RCC) for over a decade. Although they stabilize the disease, they are unable to remove all tumor cells, leading to relapse. Moreover, both intrinsic and acquired resistance to therapy are a significant health burden. In order to overcome resistance, several combination therapies have been recently approved by the FDA. Another approach takes advantage of altered metabolism in tumor cells, which switch to alternative metabolic pathways to sustain their rapid growth and proliferation. CB-839 is a small molecule inhibitor of kidney type glutaminase (GLS). GLS is often upregulated in glutamine addicted cancers, enhancing glutamine metabolism for the production of energy and the biosynthesis of various cellular building blocks. CB-839 is currently in clinical trials for several tumors, including clear cell (cc)RCC, both as monotherapy and in combination with the approved therapeutic agents everolimus, cabozantinib and nivolumab. Early results of Phase 1/2 clinical trials look promising, especially for CB-839 plus cabozantinib, and all combinations seem to be well tolerated. However, cancer cells can activate compensatory pathways to overcome glutaminolysis inhibition. Therefore, genetic and metabolomic studies are crucial for the successful implementation of CB-839 alone or in combination in subgroups of ccRCC patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.