Evaluating Bruton Tyrosine Kinase Inhibition in T-Cell Leukemia and Lymphoma Models 2258370

Abstract

Abstract Introduction Bruton’s Tyrosine Kinase (BTK) is a cytoplasmic kinase best known for its role in B-cell receptor signaling, but aberrant activation of related kinase pathways has also been observed in T-cell malignancies. Targeting BTK and associated signaling nodes represents a potential therapeutic approach for T-cell cancers. This study investigates the effects of BTK inhibition on two T-cell models, Jurkat (human T-cell leukemia) and EL4 (mouse T-cell lymphoma), to assess cross-species responses and therapeutic relevance. Methods Jurkat and EL4 cells were cultured under standard conditions and treated with a selective BTK inhibitor. Cell proliferation was measured using colorimetric viability assays, and ELISA was used to evaluate phosphorylation of downstream signaling proteins. SDS-PAGE was performed to assess changes in protein expression patterns following inhibitor treatment. Results BTK inhibition decreased proliferation in both Jurkat and EL4 cells compared with controls. ELISA data indicated reduced phosphorylation of signaling intermediates associated with cell survival, and SDS-PAGE analysis revealed distinct shifts in protein banding consistent with suppression of kinase-dependent pathways. Conclusion These results suggest that BTK-related signaling contributes to proliferation in T-cell leukemia and lymphoma models. Continued experiments will further define the pathways affected by BTK inhibition and evaluate its potential as a therapeutic target in T-cell malignancies. Funding Source n/a Topic Categories Translational and Interventional Immunology (TI)