Evidence map›Paper›PMID 30701101›Full record

ReviewJournal of thoracic disease2018

Molecular mechanisms underlying cardiotoxicity of novel cancer therapeutics.

Simon Braumann, Stephan Baldus, Roman Pfister

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of thoracic disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Simon BraumannDepartment of Cardiology, Heart Center, University of Cologne, Cologne Cardiovascular Research Center, Cologne, Germany.
Stephan BaldusDepartment of Cardiology, Heart Center, University of Cologne, Cologne Cardiovascular Research Center, Cologne, Germany.
Roman PfisterDepartment of Cardiology, Heart Center, University of Cologne, Cologne Cardiovascular Research Center, Cologne, Germany.
University Hospital Cologne · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Novel cancer therapeutics contribute to a steadily declining cancer mortality. However, several of these new therapies target pathways also involved in the cardiovascular system thus causing cardiotoxic side effects such as chemotherapy-induced heart failure (CIHF). This might limit the applicability of these effective treatments in a relevant number of patients. Furthermore, given the improving cancer survival rates, chemotherapy-induced cardiotoxic complications receive increasing attention given their potential impact on long-term morbidity and mortality. The understanding of molecular mechanisms that underlie CIHF is crucial for future improvement of pharmacodynamics of these therapeutics but also for developing specific interventions to prevent CIHF. Here, we discuss molecular mechanisms underlying CIHF of novel cancer therapeutics including a short synopsis on clinical management of patients suffering from CIHF.

Indexed as

cardiotoxicityChemotherapyheart failure (HF)targeted therapy

Identifiers

PMID30701101
PMCPMC6328392
OpenAlexW2897191232

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.