ArticleCancers2020
Proteome and Phosphoproteome Changes Associated with Prognosis in Acute Myeloid Leukemia.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Application of omics in the diagnosis, prognosis, and treatment of acute myeloid leukemia.Biomarker research · 2024Review
- Monocytic Differentiation of Human Acute Myeloid Leukemia Cells: A Proteomic and Phosphoproteomic Comparison of FAB-M4/M5 Patients with and without Nucleophosmin 1 Mutations.International journal of molecular sciences · 2024Article
- Mass Spectrometry-Based Proteogenomics: New Therapeutic Opportunities for Precision Medicine.Annual review of pharmacology and toxicology · 2024Review
- Mapping the proteogenomic landscape enables prediction of drug response in acute myeloid leukemia.Cell reports. Medicine · 2024Article
- Mitochondrial abnormalities as a target of intervention in acute myeloid leukemia.Frontiers in oncology · 2024Review
- Prediction of acute myeloid leukemia prognosis based on autophagy features and characterization of its immune microenvironment.Frontiers in immunology · 2024Article
- Article
- Vacuolar ATPase Is a Possible Therapeutic Target in Acute Myeloid Leukemia: Focus on Patient Heterogeneity and Treatment Toxicity.Journal of clinical medicine · 2023Article
- Posttranslational splicing modifications as a key mechanism in cytarabine resistance in acute myeloid leukemia.Leukemia · 2023Article
- Review
- Proteomic Characterization of Acute Myeloid Leukemia for Precision Medicine.Molecular & cellular proteomics : MCP · 2023Review
- Article
- Special Issue "Personal Therapy for Blood Disorders".Journal of personalized medicine · 2023Article
- Article
- Mass Spectrometry-Based Proteomics Workflows in Cancer Research: The Relevance of Choosing the Right Steps.Cancers · 2023Review
- Advancements in Oncoproteomics Technologies: Treading toward Translation into Clinical Practice.Proteomes · 2023Review
- Article
- Endocan in Acute Leukemia: Current Knowledge and Future Perspectives.Biomolecules · 2022Review
- Toll-like Receptor 4, Osteoblasts and Leukemogenesis; the Lesson from Acute Myeloid Leukemia.Molecules (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is a hematological cancer that mainly affects the elderly. Although complete remission (CR) is achieved for the majority of the patients after induction and consolidation therapies, nearly two-thirds relapse within a short interval. Understanding biological factors that determine relapse has become of major clinical interest in AML. We utilized liquid chromatography tandem mass spectrometry (LC-MS/MS) to identify the protein changes and protein phosphorylation events associated with AML relapse in primary cells from 41 AML patients at time of diagnosis. Patients were defined as relapse-free if they had not relapsed within a five-year clinical follow-up after AML diagnosis. Relapse was associated with increased expression of RNA processing proteins and decreased expression of V-ATPase proteins. We also observed an increase in phosphorylation events catalyzed by cyclin-dependent kinases (CDKs) and casein kinase 2 (CSK2). The biological relevance of the proteome findings was supported by cell proliferation assays using inhibitors of V-ATPase (bafilomycin), CSK2 (CX-4945), CDK4/6 (abemaciclib) and CDK2/7/9 (SNS-032). While bafilomycin preferentially inhibited the cells from relapse patients, the kinase inhibitors were less efficient in these cells. This suggests that therapy against the upregulated kinases could also target the factors inducing their upregulation rather than their activity. This study, therefore, presents markers that could help predict AML relapse and direct therapeutic strategies.
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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.