ReviewOncogene2017
From identification of the BTK kinase to effective management of leukemia.
Review in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 57 citations in OpenAlex.
- Phase I/II Clinical Trial-Based Early Economic Evaluation of Acalabrutinib for Relapsed Chronic Lymphocytic Leukaemia.Applied health economics and health policy · 2019Trial
- Covalent and Non-Covalent BTK Inhibition in Chronic Lymphocytic Leukemia Treatment.Current treatment options in oncology · 2025Review
- In silico analysis of atrial fibrillation and hypertension mechanism of action secondary to ibrutinib/acalabrutinib in chronic lymphocytic leukemia.Scientific reports · 2025Article
- Estimating the Number of Polygenic Diseases Among Six Mutually Exclusive Entities of Non-Tumors and Cancer.International journal of molecular sciences · 2024Review
- Enzyme Is the Name-Adapter Is the Game.Cells · 2024Review
- Targeted small molecule therapy and inhibitors for lymphoma.Future medicinal chemistry · 2024Review
- Revealing the Role of the Arg and Lys in Shifting Paradigm from BTK Selective Inhibition to the BTK/HCK Dual Inhibition - Delving into the Inhibitory Activity of KIN-8194 against BTK, and HCK in the Treatment of MutatedAnti-cancer agents in medicinal chemistry · 2024Article
- Recent Advances in Small Molecule Inhibitors for the Treatment of Osteoarthritis.Journal of clinical medicine · 2023Review
- Battling BTK mutants with noncovalent inhibitors that overcome Cys481 and Thr474 mutations in Waldenström macroglobulinemia therapy: structural mechanistic insights on the role of fenebrutinib.Journal of molecular modeling · 2022Article
- Review
- Selecting the optimal BTK inhibitor therapy in CLL: rationale and practical considerations.Therapeutic advances in hematology · 2022Review
- Article
- p65BTK Is a Novel Biomarker and Therapeutic Target in Solid Tumors.Frontiers in cell and developmental biology · 2021Review
- Comparative Analysis of BTK Inhibitors and Mechanisms Underlying Adverse Effects.Frontiers in cell and developmental biology · 2021Review
- The evolving role of Bruton's tyrosine kinase inhibitors in chronic lymphocytic leukemia.Therapeutic advances in hematology · 2021Review
- Resistance Mutations to BTK Inhibitors Originate From the NF-κB but Not From the PI3K-RAS-MAPK Arm of the B Cell Receptor Signaling Pathway.Frontiers in immunology · 2021Review
- BTK Inhibitors in Chronic Lymphocytic Leukemia: Biological Activity and Immune Effects.Frontiers in immunology · 2021Review
- Differential impact of BTK active site inhibitors on the conformational state of full-length BTK.eLife · 2020Article
- Novel mouse model resistant to irreversible BTK inhibitors: a tool identifying new therapeutic targets and side effects.Blood advances · 2020Article
- Noncovalent inhibitors reveal BTK gatekeeper and auto-inhibitory residues that control its transforming activity.JCI insight · 2019Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BTK is a cytoplasmic protein-tyrosine kinase, whose corresponding gene was isolated in the early 1990s. BTK was initially identified by positional cloning of the gene causing X-linked agammaglobulinemia and independently in a search for new kinases. Given the phenotype of affected patients, namely lack of B-lymphocytes and plasma cells with the ensuing inability to mount humoral immune responses, BTK inhibitors were anticipated to have beneficial effects on antibody-mediated pathologies, such as autoimmunity. In contrast to, for example, the SRC-family of cytoplasmic kinases, there was no obvious way in which structural alterations would yield constitutively active forms of BTK, and such mutations were also not found in leukemias or lymphomas. In 2007, the first efficient inhibitor, ibrutinib, was reported and soon became approved both in the United States and in Europe for the treatment of three B-cell malignancies, mantle cell lymphoma, chronic lymphocytic leukemia and Waldenström's macroglobulinemia. Over the past few years, additional inhibitors have been developed, with acalabrutinib being more selective, and recently demonstrating fewer clinical adverse effects. The antitumor mechanism is also not related to mutations in BTK. Instead tumor residency in lymphoid organs is inhibited, making these drugs highly versatile. BTK is one of the only 10 human kinases that carry a cysteine in the adenosine triphosphate-binding cleft. As this allows for covalent, irreversible inhibitor binding, it provides these compounds with a highly advantageous character. This quality may be crucial and bodes well for the future of BTK-modifying medicines, which have been estimated to reach annual multi-billion dollar sales in the future.
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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.