ArticleGenes & cancer2012
Structure, regulation, signaling, and targeting of abl kinases in cancer.
Article in Genes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 150 citations in OpenAlex.
- Proximity-Induced Rewiring of Oncogenic Kinase Triggers Apoptosis.ACS central science · 2026Article
- Expression, purification, and crystallization of recombinant human ABL-1 kinase for X-ray crystallography.Turkish journal of chemistry · 2026Article
- Identification of bioactive phytoconstituents as promising ABL2 inhibitors using virtual screening and molecular dynamics simulation.Scientific reports · 2025Article
- Laminar CD34+ membranous cells with mechanosensitive properties in subcutaneous fascia of the abdominal midline.Scientific reports · 2025Article
- Autophosphorylation of oncoprotein TEL-ABL in myeloid and lymphoid cells confers resistance to the allosteric ABL inhibitor asciminib.Science signaling · 2025Article
- Structure and Dynamics of the ABL1 Tyrosine Kinase and Its Important Role in Chronic Myeloid Leukemia.Archiv der Pharmazie · 2025Review
- miR-143-3p Promotes TGenes · 2025Article
- Autophagy and Cancer: Insights into Molecular Mechanisms and Therapeutic Approaches for Chronic Myeloid Leukemia.Biomolecules · 2025Review
- Identification of BRCA new prognostic targets and neoantigen candidates from fusion genes.Discover oncology · 2024Article
- ETV6::ABL1 fusion: from overlooked minor clone in myeloproliferative neoplasm to major player in leukemic transformation.Virchows Archiv : an international journal of pathology · 2024Article
- Article
- A Comprehensive Review of Protein Biomarkers for Invasive Lung Cancer.Current oncology (Toronto, Ont.) · 2024Review
- Article
- An Update on Protein Kinases as Therapeutic Targets-Part I: Protein Kinase C Activation and Its Role in Cancer and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- AtypicalACS medicinal chemistry letters · 2023Article
- PARP1 Characterization as a Potential Biomarker forCancers · 2023Article
- Kinase regulation by liquid-liquid phase separation.Trends in cell biology · 2023Review
- Dasatinib for chronic myelomonocytic leukemia with ZMIZ1-ABL1 fusion gene: a case report.International journal of hematology · 2023Article
- Jak2/STAT6/c-Myc pathway is vital to the pathogenicity of Philadelphia-positive acute lymphoblastic leukemia caused by P190Cell communication and signaling : CCS · 2023Article
- Asciminib in the Treatment of Philadelphia Chromosome-Positive Chronic Myeloid Leukemia: Focus on Patient Selection and Outcomes.Cancer management and research · 2023Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abl kinases are prototypic cytoplasmic tyrosine kinases and are involved in a variety of chromosomal aberrations in different cancers. This causes the expression of Abl fusion proteins, such as Bcr-Abl, that are constitutively activated and drivers of tumorigenesis. Over the past decades, biochemical and functional studies on the molecular mechanisms of Abl regulation have gone hand in hand with progression of our structural understanding of autoinhibited and active Abl conformations. In parallel, Abl oncoproteins have become prime molecular targets for cancer therapy, using adenosine triphosphate (ATP)-competitive kinase inhibitors, such as imatinib. Abl-targeting drugs serve as a paradigm for our understanding of kinase inhibitor action, specificity, and resistance development. In this review article, I will review the molecular mechanisms that are responsible for the regulation of Abl kinase activity and how oncogenic Abl fusions signal. Furthermore, past and ongoing efforts to target Abl oncoproteins using ATP-competitive and allosteric inhibitors, as well as future possibilities using combination therapy, will be discussed.
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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.