ReviewCancers2024
Non-Receptor Tyrosine Kinases: Their Structure and Mechanistic Role in Tumor Progression and Resistance.
Review in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Pigmentary Changes Reported with Tyrosine Kinase Inhibitors: A Narrative Review of Mechanisms and Clinical Implications.Clinical drug investigation · 2026Review
- Advances in the design and discovery of small-molecule tyrosine kinase inhibitors for breast cancer.RSC advances · 2026Review
- FAK and Pyk2: Paralogous Kinases with Opposing Roles in Vasculogenic Mimicry in Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Review
- Role of Src family kinases Fyn and Lyn in arenavirus infection.Journal of virology · 2026Article
- Molecularly Targeted Therapies in Oncology: Mechanisms, Resistance, and Combination Strategies.Molecules (Basel, Switzerland) · 2026Review
- Protein-protein interaction-interfering peptide rescues dysregulated NMDA receptor signaling.JCI insight · 2026Article
- Natural products as kinase inhibitors in lung cancer: molecular mechanisms, therapeutic potential, and clinical trials.Frontiers in pharmacology · 2026Review
- Molecular determinants of differential substrate selection between the Src family kinases Lck and Src.Frontiers in immunology · 2026Article
- Possible Applications of Azurin, a Copper-Containing Protein, in Cancer Treatment: Prospects and Challenges.Current drug targets · 2026Review
- Dasatinib Inhibits Basal B Breast Cancer Through ETS1-Mediated Extracellular Matrix Remodeling.Biomedicines · 2025Article
- Src and Abl as Therapeutic Targets in Lung Cancer: Opportunities for Drug Repurposing.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Untangling the Role of MYC in Sarcomas and Its Potential as a Promising Therapeutic Target.International journal of molecular sciences · 2025Review
- Integrated Artificial Intelligence and Physics-Based Methods for theMedicinal chemistry (Shariqah (United Arab Emirates)) · 2025Article
- Dasatinib induces apoptosis and autophagy by suppressing the PI3K/Akt/mTOR pathway in bladder cancer cells.Investigative and clinical urology · 2024Article
- N-myristoyltransferase 1-mediated Src Myristoylation Promotes Non-receptor Tyrosine Kinase Pathways in Oral Squamous Cell Carcinoma.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein tyrosine kinases (PTKs) function as key molecules in the signaling pathways in addition to their impact as a therapeutic target for the treatment of many human diseases, including cancer. PTKs are characterized by their ability to phosphorylate serine, threonine, or tyrosine residues and can thereby rapidly and reversibly alter the function of their protein substrates in the form of significant changes in protein confirmation and affinity for their interaction with protein partners to drive cellular functions under normal and pathological conditions. PTKs are classified into two groups: one of which represents tyrosine kinases, while the other one includes the members of the serine/threonine kinases. The group of tyrosine kinases is subdivided into subgroups: one of them includes the member of receptor tyrosine kinases (RTKs), while the other subgroup includes the member of non-receptor tyrosine kinases (NRTKs). Both these kinase groups function as an "on" or "off" switch in many cellular functions. NRTKs are enzymes which are overexpressed and activated in many cancer types and regulate variable cellular functions in response to extracellular signaling-dependent mechanisms. NRTK-mediated different cellular functions are regulated by kinase-dependent and kinase-independent mechanisms either in the cytoplasm or in the nucleus. Thus, targeting NRTKs is of great interest to improve the treatment strategy of different tumor types. This review deals with the structure and mechanistic role of NRTKs in tumor progression and resistance and their importance as therapeutic targets in tumor therapy.
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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.