Evidence map›Paper›PMID 32078113›Full record

ReviewCurrent hematologic malignancy reports2020

Mechanisms of Cardiovascular Toxicity of BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myelogenous Leukemia.

Dakota Gustafson, Jason E Fish, Jeffrey H Lipton, Nazanin Aghel

Open access · hybridAbstract readReview
PubMed Publisher
In one paragraph

Review in Current hematologic malignancy reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  10. miR-497-5p induces apoptosis in K562 cells by downregulating ROCK1.American journal of translational research · 2021
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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 4 institutions in 1 country.

Dakota GustafsonDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Jason E FishDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Jeffrey H LiptonDepartment of Medical Oncology and Hematology, Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, ON, Canada. jeff.lipton@uhn.ca.
Nazanin AghelDivision of Cardiology, Juravinski Cancer Centre, McMaster University, Hamilton, ON, Canada. aghel@hhsc.ca.
McMaster University · CAPrincess Margaret Cancer Centre · CAUniversity Health Network · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewOral tyrosine kinase inhibitors have revolutionized the treatment of chronic myelogenous leukemia, with many patients achieving major clinical and molecular responses without complications. While typically well-tolerated, clinical experience with tyrosine kinase inhibitors (particularly those of the second and third generations) has highlighted unanticipated associations with serious non-cancer adverse effects on various organs, particularly the cardiovascular system. RECENT

findingsHerein, we review the current literature surrounding the major cardiovascular toxicities of BCR-ABL1 tyrosine kinase inhibitors in chronic myelogenous leukemia, discuss potential mechanisms underpinning their development, and suggest future research directions to uncover novel ways to reduce cardiovascular events in patients treated with tyrosine kinase inhibitors. As a whole, while cardiovascular toxicities are well-documented, the mechanistic basis of these clinical observations remains poorly defined. In turn, to provide safe and effective treatment to all patients, it is necessary to close the knowledge gap regarding mechanisms that drive toxicity and elucidate the complex interactions that predispose specific individuals to these toxicities.

Indexed as

AnimalsAntineoplastic AgentsCardiotoxicityCardiovascular DiseasesCardiovascular SystemFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMolecular Targeted TherapyProtein Kinase InhibitorsRisk FactorsSignal TransductionTreatment OutcomeAntineoplastic AgentsBCR-ABL1 fusion protein, humanFusion Proteins, bcr-ablProtein Kinase InhibitorsBiomarkerCardiovascularEndothelialEndotheliumInflammationTyrosine kinase inhibitors

Identifiers

PMID32078113
OpenAlexW3008063389

What OpenQuestion holds

Textmetadata
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.