ArticleMolecular & cellular proteomics : MCP2020
Phosphotyrosine-based Phosphoproteomics for Target Identification and Drug Response Prediction in AML Cell Lines.
Article in Molecular & cellular proteomics : MCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
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- Kinase activities in pancreatic ductal adenocarcinoma with prognostic and therapeutic avenues.Molecular oncology · 2024Article
- Application of omics in the diagnosis, prognosis, and treatment of acute myeloid leukemia.Biomarker research · 2024Review
- Illuminating phenotypic drug responses of sarcoma cells to kinase inhibitors by phosphoproteomics.Molecular systems biology · 2024Article
- Candidate biomarkers for treatment benefit from sunitinib in patients with advanced renal cell carcinoma using mass spectrometry-based (phospho)proteomics.Clinical proteomics · 2023Article
- Advancing wide implementation of precision oncology: A liquid nitrogen-free snap freezer preserves molecular profiles of biological samples.Cancer medicine · 2023Article
- Proteomic Characterization of Acute Myeloid Leukemia for Precision Medicine.Molecular & cellular proteomics : MCP · 2023Review
- Principles of phosphoproteomics and applications in cancer research.The Biochemical journal · 2023Article
- Recent Advances in the Development of Anti-FLT3 CAR T-Cell Therapies for Treatment of AML.Biomedicines · 2022Review
- Phosphoproteomic Analysis of FLCN Inactivation Highlights Differential Kinase Pathways and Regulatory TFEB Phosphoserines.Molecular & cellular proteomics : MCP · 2022Article
- Proteomic and phosphoproteomic measurements enhance ability to predict ex vivo drug response in AML.Clinical proteomics · 2022Article
- FLT3-ITD transduces autonomous growth signals during its biosynthetic trafficking in acute myelogenous leukemia cells.Scientific reports · 2021Article
- Phosphoproteomics: a valuable tool for uncovering molecular signaling in cancer cells.Expert review of proteomics · 2021Review
- Quantitative Analysis of Tyrosine Phosphorylation from FFPE Tissues Reveals Patient-Specific Signaling Networks.Cancer research · 2021Article
- Phosphoproteomic Characterization of Primary AML Samples and Relevance for Response Toward FLT3-inhibitors.HemaSphere · 2021Article
- Combining Mass Spectrometry-Based Phosphoproteomics with a Network-Based Approach to Reveal FLT3-Dependent Mechanisms of Chemoresistance.Proteomes · 2021Review
- Drug ranking using machine learning systematically predicts the efficacy of anti-cancer drugs.Nature communications · 2021Article
- Focal adhesion kinase inhibition synergizes with nab-paclitaxel to target pancreatic ductal adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2021Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a clonal disorder arising from hematopoietic myeloid progenitors. Aberrantly activated tyrosine kinases (TK) are involved in leukemogenesis and are associated with poor treatment outcome. Kinase inhibitor (KI) treatment has shown promise in improving patient outcome in AML. However, inhibitor selection for patients is suboptimal.In a preclinical effort to address KI selection, we analyzed a panel of 16 AML cell lines using phosphotyrosine (pY) enrichment-based, label-free phosphoproteomics. The Integrative Inferred Kinase Activity (INKA) algorithm was used to identify hyperphosphorylated, active kinases as candidates for KI treatment, and efficacy of selected KIs was tested.Heterogeneous signaling was observed with between 241 and 2764 phosphopeptides detected per cell line. Of 4853 identified phosphopeptides with 4229 phosphosites, 4459 phosphopeptides (4430 pY) were linked to 3605 class I sites (3525 pY). INKA analysis in single cell lines successfully pinpointed driver kinases (PDGFRA, JAK2, KIT and FLT3) corresponding with activating mutations present in these cell lines. Furthermore, potential receptor tyrosine kinase (RTK) drivers, undetected by standard molecular analyses, were identified in four cell lines (FGFR1 in KG-1 and KG-1a, PDGFRA in Kasumi-3, and FLT3 in MM6). These cell lines proved highly sensitive to specific KIs. Six AML cell lines without a clear RTK driver showed evidence of MAPK1/3 activation, indicative of the presence of activating upstream RAS mutations. Importantly, FLT3 phosphorylation was demonstrated in two clinical AML samples with a
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