Evidence map›Paper›PMID 39972943›Full record

ReviewLeukemia & lymphoma2025

Resistance mechanisms and approach to chronic lymphocytic leukemia after BTK inhibitor therapy.

Christine Gruessner, Adrian Wiestner, Clare Sun

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Leukemia & lymphoma, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Bruton's Tyrosine Kinase (BTK) Mutations in Chronic Lymphocytic Leukemia (CLL): A Clinical View.Mediterranean journal of hematology and infectious diseases · 2025
    Review
  3. Article
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

3 authors.

Christine GruessnerHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Adrian WiestnerHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Clare SunHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0001-8498-4729

Funding

Intramural NIH HHS Z99 HL999999
6 · The paper itself

Abstract

Bruton tyrosine kinase (BTK), an essential component of the B-cell receptor (BCR) signaling pathway, is a validated target in chronic lymphocytic leukemia. Ibrutinib, acalabrutinib, and zanubrutinib are covalent BTK inhibitors (cBTKi) that bind to residue C481, leading to sustained target inhibition. A significant proportion of patients develop resistance to continuous cBTKi therapy, predominantly via mutations in

Indexed as

Agammaglobulinaemia Tyrosine KinaseAntineoplastic AgentsDrug Resistance, NeoplasmLeukemia, Lymphocytic, Chronic, B-CellProtein Kinase InhibitorsHumansMolecular Targeted TherapyMutationPiperidinesReceptors, Antigen, B-CellSignal TransductionTumor MicroenvironmentAgammaglobulinaemia Tyrosine KinaseAntineoplastic AgentsBTK protein, humanPiperidinesProtein Kinase InhibitorsReceptors, Antigen, B-CellBruton tyrosine kinase inhibitorsChronic lymphocytic leukemiaresistance mechanismstargeted therapy

Identifiers

PMID39972943
PMCPMC12221821

What OpenQuestion holds

Textmetadata
LicenceTDM
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.