ArticleScientific reports2019
Bruton's tyrosine kinase is at the crossroads of metabolic adaptation in primary malignant human lymphocytes.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Metabolic vulnerabilities and therapeutic opportunities in diffuse large B-cell lymphoma.Oncogenesis · 2026Review
- Article
- Impact of therapeutic inhibition of oncogenic cell signaling tyrosine kinase on cell metabolism: in vivo-detectable metabolic biomarkers of inhibition.Journal of translational medicine · 2024Article
- Impaired Cardiac AMPK (5'-Adenosine Monophosphate-Activated Protein Kinase) and CaJournal of the American Heart Association · 2024Article
- Epidemiology, clinical characteristics and potential mechanism of ibrutinib-induced ventricular arrhythmias.Frontiers in pharmacology · 2024Review
- Targeting metabolic reprogramming in chronic lymphocytic leukemia.Experimental hematology & oncology · 2022Review
- BTK inhibition limits B-cell-T-cell interaction through modulation of B-cell metabolism: implications for multiple sclerosis therapy.Acta neuropathologica · 2022Article
- Dual BTK/SYK inhibition with CG-806 (luxeptinib) disrupts B-cell receptor and Bcl-2 signaling networks in mantle cell lymphoma.Cell death & disease · 2022Article
- Lipid metabolism in autoimmune rheumatic disease: implications for modern and conventional therapies.The Journal of clinical investigation · 2022Review
- Review
- Acute Effects of Ibrutinib on Ventricular Arrhythmia in Spontaneously Hypertensive Rats.JACC. CardioOncology · 2020Article
- Deciphering the Electrophysiological Mechanisms for Ibrutinib-Induced Ventricular Arrhythmias.JACC. CardioOncology · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this work we explored metabolic aspects of human primary leukemic lymphocytes that hold a potential impact on the treatment of Bruton tyrosine kinase (BTK)-driven diseases. Our results suggest that there is crosstalk between Bruton tyrosine kinase (BTK) signaling and bioenergetic stress responses. In primary chronic lymphocytic leukemia (CLL) lymphocytes, pharmacological interference with mitochondrial ATP synthesis or glucose metabolism affects BTK activity. Conversely, an inhibitor of BTK used clinically (ibrutinib) induces bioenergetic stress responses that in turn affect ibrutinib resistance. Although the detailed molecular mechanisms are still to be defined, our work shows for the first time that in primary B cells, metabolic stressors enhance BTK signaling and suggest that metabolic rewiring to hyperglycemia affects ibrutinib resistance in TP53 deficient chronic lymphocytic leukemia (CLL) lymphocytes.
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