ReviewExperimental hematology & oncology2022
Bruton tyrosine kinase inhibitors in B-cell lymphoma: beyond the antitumour effect.
Review in Experimental hematology & oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 23 citations in OpenAlex.
- Advances in molecular pathobiology of PCNSL - towards clinical implementation of novel diagnostics and therapeutics.Biomarker research · 2026Review
- Mechanisms, optimization strategies, and salvage options for CAR-T cell therapy.Biomarker research · 2026Review
- Review
- Pharmacophore-targeted fluorescence sensing of ibrutinibRSC advances · 2026Article
- Zanubrutinib enhances CD19 CAR T killing of B-cell lymphoma by inhibiting BTK phosphorylation, regulating PI3K/AKT/mTOR pathway, and promoting autophagy.Blood science (Baltimore, Md.) · 2026Article
- Review
- Aberrant glycosylation in hematologic malignancies: mechanisms, immune evasion, and therapeutic targeting.Blood cancer journal · 2026Review
- Targeting Bruton's Tyrosine Kinase (BTK) in Autoimmunity: Achievements, Opportunities and Challenges.Drug design, development and therapy · 2026Review
- GNA15 as a regulator of tumor-immune crosstalk: oncogenic signaling, microenvironmental remodeling, and implications for targeted immunotherapy.Frontiers in immunology · 2026Review
- Article
- Microsecond simulations to investigate the structural mechanism of super-resistant double mutations in BTK to the covalent inhibitor ibrutinib in multiple leukemia.Scientific reports · 2025Article
- Expanded CD16Scientific reports · 2025Article
- The EBV-Positive Tumor Methylome Is Distinct from EBV-Negative in Diffuse Large B-Cell Lymphoma.Cancers · 2025Article
- Targeted protein degradation with small molecules for cancer immunotherapy.Asian journal of pharmaceutical sciences · 2025Review
- Investigation of the mechanism of hypertension caused by BTKi in the treatment of hematologic diseases.Frontiers in pharmacology · 2025Review
- Bruton's Tyrosine Kinase Inhibitors: A Versatile Therapeutic Approach for Cancer, Autoimmune Disorders, GVHD and COVID-19.Mini reviews in medicinal chemistry · 2025Review
- Navigating the changing landscape of BTK-targeted therapies for B cell lymphomas and chronic lymphocytic leukaemia.Nature reviews. Clinical oncology · 2024Review
- Ion Trap LC/MS reveals the generation of reactive intermediates in acalabrutinib metabolism: phase I metabolic profiling and bioactivation pathways elucidation.RSC advances · 2024Article
- Unraveling the Role of the NLRP3 Inflammasome in Lymphoma: Implications in Pathogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- An Ultrafast UPLC-MS/MS Method for Characterizing the In Vitro Metabolic Stability of Acalabrutinib.Molecules (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Targeting B-cell receptor signalling using Bruton tyrosine kinase (BTK) inhibitors (BTKis) has become a highly successful treatment modality for B-cell malignancies, especially for chronic lymphocytic leukaemia. However, long-term administration of BTKis can be complicated by adverse on- and/or off-target effects in particular cell types. BTK is widely expressed in cells of haematopoietic origin, which are pivotal components of the tumour microenvironment. BTKis, thus, show broad immunomodulatory effects on various non-B immune cell subsets by inhibiting specific immune receptors, including T-cell receptor and Toll-like receptors. Furthermore, due to the off-target inhibition of other kinases, such as IL-2-inducible T-cell kinase, epidermal growth factor receptor, and the TEC and SRC family kinases, BTKis have additional distinct effects on T cells, natural killer cells, platelets, cardiomyocytes, and other cell types. Such mechanisms of action might contribute to the exceptionally high clinical efficacy as well as the unique profiles of adverse effects, including infections, bleeding, and atrial fibrillation, observed during BTKi administration. However, the immune defects and related infections caused by BTKis have not received sufficient attention in clinical studies till date. The broad involvement of BTK in immunological pathways provides a rationale to combine BTKis with specific immunotherapies, such as immune checkpoint inhibitor or chimeric antigen receptor-T-cell therapy, for the treatment of relapsed or refractory diseases. This review discusses and summarises the above-mentioned issues as a reference for clinicians and researchers.
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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 Socratic graph.