Evidence map›Paper›PMID 38137005›Full record

ReviewGenes2023

Resisting the Resistance: Navigating BTK Mutations in Chronic Lymphocytic Leukemia (CLL).

Alexandra Chirino, Skye Montoya, Anita Safronenka, Justin Taylor

Abstract readReview
In one paragraph

Review in Genes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Review
  3. Addition of Ianalumab (VAY736) to Ibrutinib in Patients with Chronic Lymphocytic Leukemia on Ibrutinib Therapy: Results from a Phase Ib Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
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  6. Article
  7. Article
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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

4 authors.

Alexandra ChirinoSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Skye MontoyaSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA.ORCID 0000-0002-2094-6923
Anita SafronenkaSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Justin TaylorSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA.ORCID 0000-0003-4407-6325

Funding

The role of XPO1 in nuclear export of RNAR35GM151109 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Justin Taylor · 2023 to 2026
$1.5M
Defining the Biological and Mechanistic Implications of XPO1 Mutations in Hematologic MalignanciesK08CA230319 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI TAYLOR, JUSTIN · 2018 to 2023
$1.2M
Investigating Resistance Mechanisms to Non-covalent Bruton's Tyrosine Kinase Inhibitors and Therapeutic Approaches to Overcome Resistance for Patients with B-Cell MalignanciesF31CA275378 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MONTOYA, OLIVIA SKYE · 2022 to 2023
$94k
Doris Duke Charitable Foundation CSDANCI NIH HHS F31 CA275378NCI NIH HHS K08 CA230319NIGMS NIH HHS R35 GM151109
6 · The paper itself

Abstract

Bruton's tyrosine kinase (BTK) plays a key role in the B-cell receptor (BCR) signaling pathway and confers anti-apoptotic and proliferative properties to malignant B-cells in chronic lymphocytic leukemia (CLL). Small molecule BTK inhibitors were designed to bind BTK's active site and block downstream signaling. These drugs have now been used in the treatment of thousands of patients with CLL, the most common form of leukemia in the western hemisphere. However, adverse effects of early generations of BTK inhibitors and resistance to treatment have led to the development of newer, more selective and non-covalent BTK inhibitors. As the use of these newer generation BTK inhibitors has increased, novel BTK resistance mutations have come to light. This review aims to discuss previously known and novel BTK mutations, their mechanisms of resistance, and their relationship with patient treatment. Also discussed here are future studies that are needed to investigate the underlying cause allowing these mutations to occur and how they incite resistance. New treatments on the horizon that attempt to maneuver around these resistance mutations can be met with new resistance mutations, creating an unmet need for patients with CLL. Novel therapies and combinations that address all forms of resistance are discussed.

Indexed as

Agammaglobulinaemia Tyrosine KinaseLeukemia, Lymphocytic, Chronic, B-CellHumansMutationSignal TransductionAgammaglobulinaemia Tyrosine KinaseBTK protein, humanBruton’s tyrosine kinasechronic lymphocytic leukemiaresistance mutationstargeted therapy

Identifiers

PMID38137005
PMCPMC10742473

What Socratic 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 Socratic graph.