Evidence map›Paper›PMID 35492830›Full record

ReviewJACC. CardioOncology2022

Mechanistic and Clinical Overview Cardiovascular Toxicity of BRAF and MEK Inhibitors:

Claire Glen, Yun Yi Tan, Ashita Waterston, Thomas R Jeffry Evans, Robert J Jones, Mark C Petrie, Ninian N Lang

Open access · goldAbstract readReview
In one paragraph

Review in JACC. CardioOncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.9field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Advances in the management of pediatric low-grade glioma.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
  6. Review
  7. RAS/MAPK inhibition in pediatric gliomas.Neuro-oncology advances · 2026
    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

7 authors at 3 institutions in 1 country.

Claire GlenInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.
Yun Yi TanBeatson West of Scotland Cancer Centre, NHS Greater Glasgow and Clyde, Glasgow, United Kingdom.
Ashita WaterstonBeatson West of Scotland Cancer Centre, NHS Greater Glasgow and Clyde, Glasgow, United Kingdom.
Thomas R Jeffry EvansBeatson West of Scotland Cancer Centre, NHS Greater Glasgow and Clyde, Glasgow, United Kingdom.
Robert J JonesBeatson West of Scotland Cancer Centre, NHS Greater Glasgow and Clyde, Glasgow, United Kingdom.
Mark C PetrieInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.
Ninian N LangInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.
NHS Greater Glasgow and Clyde · GBUniversity of Glasgow · GBBeatson West of Scotland Cancer Centre · GB

Funding

Cancer Research UK 11650Cancer Research UK 20409
6 · The paper itself

Abstract

Rapidly accelerated fibrosarcoma B-type (BRAF) and mitogen-activated extracellular signal-regulated kinase (MEK) inhibitors have revolutionized melanoma treatment. Approximately half of patients with melanoma harbor a BRAF gene mutation with subsequent dysregulation of the RAF-MEK-ERK signaling pathway. Targeting this pathway with BRAF and MEK blockade results in control of cell proliferation and, in most cases, disease control. These pathways also have cardioprotective effects and are necessary for normal vascular and cardiac physiology. BRAF and MEK inhibitors are associated with adverse cardiovascular effects including hypertension, left ventricular dysfunction, venous thromboembolism, atrial arrhythmia, and electrocardiographic QT interval prolongation. These effects may be underestimated in clinical trials. Baseline cardiovascular assessment and follow-up, including serial imaging and blood pressure assessment, are essential to balance optimal anti-cancer therapy while minimizing cardiovascular side effects. In this review, an overview of BRAF/MEK inhibitor-induced cardiovascular toxicity, the mechanisms underlying these, and strategies for surveillance, prevention, and treatment of these effects are provided.

Indexed as

ACE, angiotensin-converting enzymeAF, atrial fibrillationBRAF inhibitorBRAF, rapidly accelerated fibrosarcoma B-typecardio-oncologycardiovascular toxicityCVAE, cardiovascular adverse eventEGFR, epidermal growth factor receptorERK, extracellular signal-regulated kinasehypertensionleft ventricular systolic dysfunctionLVSD, left ventricular systolic dysfunctionMEK inhibitorMEK, mitogen-activated extracellular signal-regulated kinasemelanomaRAF, rapidly accelerated fibrosarcomaVEGF, vascular endothelial growth factor

Identifiers

PMID35492830
PMCPMC9040125
OpenAlexW4220814338

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.