biostudies-literatureDwivedi PNational Institute of Environmental Health SciencesNCRR NIH HHSNIEHS NIH HHSNational Cancer InstituteNCI NIH HHSNational Institutes of HealthNIH HHSe1900144https://www.ebi.ac.uk/biostudies/studies/S-EPMC7492401biostudies-literatureUnknown14(5)<h4>Purpose</h4>To evaluate cellular protein changes in response to treatment with an approved drug, ibrutinib, in cells expressing normal or mutated granulocyte-colony stimulating factor receptor (G-CSFR). G-CSFR mutations are associated with some hematological malignancies. Previous studies show the efficacy of ibrutinib (a Bruton's tyrosine kinase inhibitor) in mutated G-CSFR leukemia models but do not address broader signaling mechanisms.<h4>Experimental design</h4>A label-free quantitative proteomics workflow to evaluate the cellular effects of ibrutinib treatment is established. This includes three biological replicates of normal and mutated G-CSFR expressed in a mouse progenitor cell (32D cell line) with and without ibrutinib treatment.<h4>Results</h4>The proteomics dataset shows abProteomics. Clinical applicationsSWATH-Proteomics of Ibrutinib's Action in Myeloid Leukemia Initiating Mutated G-CSFR Signaling.PMC74924011S10 RR027015‐01CA196658R01 CA196658ES007250S10 RR0270151S10 RR027015-01P30 ES006096T32 ES007250Grimes HLMuench DEChutipongtanate SGreis KDDwivedi PAzam MfalseSWATH-Proteomics of Ibrutinib's Action in Myeloid Leukemia Initiating Mutated G-CSFR Signaling.<h4>Purpose</h4>To evaluate cellular protein changes in response to treatment with an approved drug, ibrutinib, in cells expressing normal or mutated granulocyte-colony stimulating factor receptor (G-CSFR). G-CSFR mutations are associated with some hematological malignancies. Previous studies show the efficacy of ibrutinib (a Bruton's tyrosine kinase inhibitor) in mutated G-CSFR leukemia models but do not address broader signaling mechanisms.<h4>Experimental design</h4>A label-free quantitative proteomics workflow to evaluate the cellular effects of ibrutinib treatment is established. This includes three biological replicates of normal and mutated G-CSFR expressed in a mouse progenitor cell (32D cell line) with and without ibrutinib treatment.<h4>Results</h4>The proteomics dataset shows ab2020-01-01T00:00:00Z2020 Sep2026-05-07T15:20:04.364Z2022-02-11T10:00:15.66ZS-EPMC74924013231921710.1002/prca.201900144