Evidence map›Paper›PMID 38542207›Full record

ReviewInternational journal of molecular sciences2024

Targeting BTK in B Cell Malignancies: From Mode of Action to Resistance Mechanisms.

Samir Mouhssine, Nawar Maher, Bassam Francis Matti, Alaa Fadhil Alwan, Gianluca Gaidano

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
11.8field-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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 27 citations in OpenAlex.

  1. Experimental and therapeutic medicine · 2026
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  6. Fingertip Fissures Associated with Ibrutinib in an Elderly Patient with Mantle Cell LymphomaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Samir MouhssineDivision of Hematology, Department of Translational Medicine, Università del Piemonte Orientale and Azienda Ospedaliero-Universitaria Maggiore della Carità, 28100 Novara, Italy.ORCID 0000-0002-0389-3268
Nawar MaherDivision of Hematology, Department of Translational Medicine, Università del Piemonte Orientale and Azienda Ospedaliero-Universitaria Maggiore della Carità, 28100 Novara, Italy.ORCID 0009-0007-9307-1965
Bassam Francis MattiDepartment of Hematology and Bone Marrow Transplant, Hematology and Bone Marrow Transplant Center, Medical City, Baghdad 00964, Iraq.ORCID 0009-0009-6981-7426
Alaa Fadhil AlwanDepartment of Hematology and Bone Marrow Transplant, Hematology and Bone Marrow Transplant Center, Medical City, Baghdad 00964, Iraq.
Gianluca GaidanoDivision of Hematology, Department of Translational Medicine, Università del Piemonte Orientale and Azienda Ospedaliero-Universitaria Maggiore della Carità, 28100 Novara, Italy.ORCID 0000-0002-4681-0151
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITBaghdad Medical City · IQMustansiriyah University · IQ

Funding

Associazione Italiana Contro le Leucemie Linfomi e Mieloma Novara 2022Italian Association for Cancer Research 5 x 1000 No. 21198Ministero della Salute PNRR-MAD-2022-12375673Ministero della Salute RF-2018-12365790University of Eastern Piedmont Amadeo Avogadro AGING Project
6 · The paper itself

Abstract

The B cell receptor (BCR) signaling pathway plays a crucial role in B cell development and contributes to the pathogenesis of B cell neoplasms. In B cell malignancies, the BCR is constitutively active through both ligand-dependent and ligand-independent mechanisms, resulting in continuous Bruton tyrosine kinase (BTK) signaling activation, which provides a survival and proliferation advantage to the neoplastic clone. Among B cell malignancies, those in which the most significant results were obtained by treatment with BTK inhibitors (BTKi) include chronic lymphocytic leukemia, mantle cell lymphoma, lymphoplasmacytic lymphoma, and diffuse large B cell lymphoma. Covalent BTKi (namely ibrutinib, acalabrutinib, and zanubrutinib) functions by irreversibly blocking BTK through covalent binding to the cysteine residue 481 (Cys-481) in the ATP-binding domain. Despite the high efficacy and safety of BTKi treatment, a significant fraction of patients affected by B cell malignancies who are treated with these drugs experience disease relapse. Several mechanisms of resistance to covalent BTKi, including Cys-481 mutations of BTK, have been investigated in B cell malignancies. Non-covalent BTKi, such as pirtobrutinib, have been developed and proven effective in patients carrying both Cys-481-mutated and unmutated BTK. Moreover, targeting BTK with proteolysis-targeting chimeras (PROTACs) represents a promising strategy to overcome resistance to BTKi in B cell neoplasms.

Indexed as

Leukemia, Lymphocytic, Chronic, B-CellLymphoma, Large B-Cell, DiffuseAdultAgammaglobulinaemia Tyrosine KinaseHumansLigandsProtein Kinase InhibitorsAgammaglobulinaemia Tyrosine KinaseLigandsProtein Kinase InhibitorsBruton tyrosine kinaseBTK degraderschronic lymphocytic leukemiadiffuse large B cell lymphomalymphoplasmacytic lymphomamantel cell lymphoma

Identifiers

PMID38542207
PMCPMC10970225
OpenAlexW4392698975

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.