ReviewArchiv der Pharmazie2025
Structure and Dynamics of the ABL1 Tyrosine Kinase and Its Important Role in Chronic Myeloid Leukemia.
Review in Archiv der Pharmazie, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed.
- Design, Synthesis and Biological Evaluation of Novel Oleanolic Acid Derivatives as Potential Anti-Leukemic Agents.Life (Basel, Switzerland) · 2026Article
- Discovery of a Novel 4,5-Dihydro-1Biomedicines · 2026Article
- Quantification of Binding of Small Molecules to Native Kinases by Flow Cytometry Reveals Divergence from Biochemical Affinities.Journal of the American Chemical Society · 2026Article
- Non-Classical Binding Mechanisms of Ferrocene-Modified Imatinib and Nilotinib Analogues in BCR-ABL1 Kinase Revealed by Computational Analysis.Molecules (Basel, Switzerland) · 2026Article
- Review
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Targeting ABL Tyrosine Kinase in Chronic Myeloid Leukemia: Design, Synthesis, Biological Evaluation, and Computational Studies of Novel Thiazolone Derivatives.Pharmaceutics · 2026Article
- Long-Term PET-Nanoplastic Exposure Alters DNA Damage Response Capacity in BEAS-2B Human Bronchial Epithelial Cells.International journal of molecular sciences · 2026Article
- Therapeutic Approaches for HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis: Current and Emerging Strategies.Pathogens (Basel, Switzerland) · 2026Review
- Targeting the BCR::ABL1 Kinase: Advances Beyond Imatinib in Chronic Myeloid Leukemia.Current hematologic malignancy reports · 2026Review
- Design, Synthesis, and Biological Evaluation ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Rational Design, Synthesis, and Molecular Docking of Novel Terpene Analogues of Imatinib, and Their Inhibition on Downstream BCR-ABL Signaling.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Expression, purification, and crystallization of recombinant human ABL-1 kinase for X-ray crystallography.Turkish journal of chemistry · 2026Article
- Bibliometric analysis and recent trends on tyrosine kinase inhibitors in leukemia.Discover oncology · 2025Article
- The Inositol-5-Phosphatase SHIP1: Expression, Regulation and Role in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Abelson (ABL1) tyrosine kinase is an essential component of non-receptor tyrosine kinases and is associated with numerous cellular processes, including differentiation and proliferation. The structural features of ABL1 include a distinct N-terminal cap region, a C-terminal tail, a bilobed kinase, SH2, and SH3 domains. These domains enable its engagement in several signaling cascades and dynamic control. The pathophysiology of chronic myeloid leukemia (CML) is mainly driven by the BCR-ABL1 oncoprotein, arising from dysregulation of ABL1 kinase, namely through its fusion to the breakpoint cluster region (BCR) gene. ABL1 is a crucial target in the treatment of CML as the BCR-ABL1 fusion causes uncontrolled cellular proliferation and resistance to apoptosis. Tyrosine kinase inhibitors (TKIs) targeting the ABL1 tyrosine kinase are playing a critical role in the treatment of CML through the inhibition of persistently activated signaling pathways mediated by the BCR-ABL1 fusion protein. The article examines the structural characteristics of ABL1, how they relate to CML, and the interactions between ABL1 and the current FDA-approved TKIs, emphasizing the kinase's critical function in carcinogenesis and its possible target status for tyrosine kinase inhibitors.
Indexed as
Identifiers
What OpenQuestion holds
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.