Evidence map›Paper›PMID 29455639›Full record

ReviewMolecular cancer2018

Role of Bruton's tyrosine kinase in B cells and malignancies.

Simar Pal Singh, Floris Dammeijer, Rudi W Hendriks

Erratum issued Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT05596097 (Clinical Research for Efficacy and Safety of Zanubrutinib in Maintenance Therapy of DLBCL Patients With Initial Remission), which is not on this map. Cited by 407 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
407citing papers in PubMed, 2 pooled it
32.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

NCT05596097 phase2unknown statusnot on this mapstarted 2022, after this paper: background citation

Clinical Research for Efficacy and Safety of Zanubrutinib in Maintenance Therapy of DLBCL Patients With Initial Remission

TypeinterventionalSponsorLanZhou UniversityRan2022 to 2026Enrolled15ConditionsDiffuse Large B-cell Lymphoma (DLBCL)ArmsZanubrutinib
3 · Its place in the literature

Who cites it

407 citing papers in PubMed, 2 syntheses or guidelines pooled it, 683 citations in OpenAlex.

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  19. Two-step mechanism of Bruton's tyrosine kinase membrane recruitment and activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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347 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Simar Pal SinghDepartment of Pulmonary Medicine, Room Ee2251a, Erasmus MC Rotterdam, PO Box 2040, NL 3000, CA, Rotterdam, The Netherlands.
Floris DammeijerDepartment of Pulmonary Medicine, Room Ee2251a, Erasmus MC Rotterdam, PO Box 2040, NL 3000, CA, Rotterdam, The Netherlands.
Rudi W HendriksDepartment of Pulmonary Medicine, Room Ee2251a, Erasmus MC Rotterdam, PO Box 2040, NL 3000, CA, Rotterdam, The Netherlands. r.hendriks@erasmusmc.nl.
Erasmus University Rotterdam · NLErasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bruton's tyrosine kinase (BTK) is a non-receptor kinase that plays a crucial role in oncogenic signaling that is critical for proliferation and survival of leukemic cells in many B cell malignancies. BTK was initially shown to be defective in the primary immunodeficiency X-linked agammaglobulinemia (XLA) and is essential both for B cell development and function of mature B cells. Shortly after its discovery, BTK was placed in the signal transduction pathway downstream of the B cell antigen receptor (BCR). More recently, small-molecule inhibitors of this kinase have shown excellent anti-tumor activity, first in animal models and subsequently in clinical studies. In particular, the orally administered irreversible BTK inhibitor ibrutinib is associated with high response rates in patients with relapsed/refractory chronic lymphocytic leukemia (CLL) and mantle-cell lymphoma (MCL), including patients with high-risk genetic lesions. Because ibrutinib is generally well tolerated and shows durable single-agent efficacy, it was rapidly approved for first-line treatment of patients with CLL in 2016. To date, evidence is accumulating for efficacy of ibrutinib in various other B cell malignancies. BTK inhibition has molecular effects beyond its classic role in BCR signaling. These involve B cell-intrinsic signaling pathways central to cellular survival, proliferation or retention in supportive lymphoid niches. Moreover, BTK functions in several myeloid cell populations representing important components of the tumor microenvironment. As a result, there is currently a considerable interest in BTK inhibition as an anti-cancer therapy, not only in B cell malignancies but also in solid tumors. Efficacy of BTK inhibition as a single agent therapy is strong, but resistance may develop, fueling the development of combination therapies that improve clinical responses. In this review, we discuss the role of BTK in B cell differentiation and B cell malignancies and highlight the importance of BTK inhibition in cancer therapy.

Indexed as

Agammaglobulinaemia Tyrosine KinaseAnimalsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorB-LymphocytesBone MarrowCell DifferentiationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHumansLeukemia, B-CellLymphoma, B-CellLymphopoiesisMolecular Targeted TherapyProtein Kinase InhibitorsReceptors, Antigen, B-CellAgammaglobulinaemia Tyrosine KinaseBiomarkers, TumorProtein Kinase InhibitorsReceptors, Antigen, B-CellB cell developmentB cell receptor signalingBruton’s tyrosine kinaseChemokine receptorChronic lymphocytic leukemiaIbrutinibLeukemiaLymphomaTumor microenvironment

Identifiers

PMID29455639
PMCPMC5817726
OpenAlexW2791299132

What OpenQuestion holds

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LicenceCC BY
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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.