Evidence map›Paper›PMID 32470534›Full record

ReviewInternational journal of cardiology2020

Cardiotoxicity of the BCR-ABL1 tyrosine kinase inhibitors: Emphasis on ponatinib.

Anand Prakash Singh, Prachi Umbarkar, Sultan Tousif, Hind Lal

Open access · bronzeAbstract readReview
In one paragraph

Review in International journal of cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  12. Chronic Myeloid Leukemia and the T315IInternational journal of molecular sciences · 2025
    Review
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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 at 1 institution in 1 country.

Anand Prakash SinghDivision of Cardiovascular Disease, UAB | The University of Alabama at Birmingham, Birmingham, AL 35294-1913, USA. Electronic address: apsingh@uabmc.edu.
Prachi UmbarkarDivision of Cardiovascular Disease, UAB | The University of Alabama at Birmingham, Birmingham, AL 35294-1913, USA.
Sultan TousifDivision of Cardiovascular Disease, UAB | The University of Alabama at Birmingham, Birmingham, AL 35294-1913, USA.
Hind LalDivision of Cardiovascular Disease, UAB | The University of Alabama at Birmingham, Birmingham, AL 35294-1913, USA. Electronic address: hindlal@uabmc.edu.
University of Alabama at Birmingham · US

Funding

Signaling Mechanisms Governing Myocardial Fibrosis in Diseased HeartR01HL133290 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Hind Lal · 2017 to 2026
$3.6M
Project-002R01HL143074 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Hind Lal · 2019 to 2026
$3.4M
Heart Failure in Cancer PatientsR01HL119234 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LAL, HIND · 2014 to 2017
$1.6M
NHLBI NIH HHS R01 HL119234NHLBI NIH HHS R01 HL133290NHLBI NIH HHS R01 HL143074
6 · The paper itself

Abstract

The advent of tyrosine kinase inhibitors (TKIs) targeted therapy revolutionized the treatment of chronic myeloid leukemia (CML) patients. However, cardiotoxicity associated with these targeted therapies puts the cancer survivors at higher risk. Ponatinib is a third-generation TKI for the treatment of CML patients having gatekeeper mutation T315I, which is resistant to the first and second generation of TKIs, namely, imatinib, nilotinib, dasatinib, and bosutinib. Multiple unbiased screening from our lab and others have identified ponatinib as most cardiotoxic FDA approved TKI among the entire FDA approved TKI family (total 50+). Indeed, ponatinib is the only treatment option for CML patients with T315I mutation. This review focusses on the cardiovascular risks and mechanism/s associated with CML TKIs with a particular focus on ponatinib cardiotoxicity. We have summarized our recent findings with transgenic zebrafish line harboring BNP luciferase activity to demonstrate the cardiotoxic potential of ponatinib. Additionally, we will review the recent discoveries reported by our and other laboratories that ponatinib primarily exerts its cardiotoxicity via an off-target effect on cardiomyocyte prosurvival signaling pathways, AKT and ERK. Finally, we will shed light on future directions for minimizing the adverse sequelae associated with CML-TKIs.

Indexed as

Antineoplastic AgentsCardiotoxicityAnimalsDrug Resistance, NeoplasmHumansImidazolesProtein Kinase InhibitorsPyridazinesZebrafishAntineoplastic AgentsImidazolesponatinibProtein Kinase InhibitorsPyridazinesCardio-oncologyCardiotoxicityPonatinibTyrosine kinase inhibitor

Identifiers

PMID32470534
PMCPMC8095092
OpenAlexW3029527842

What OpenQuestion holds

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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.