Evidence map›Paper›PMID 32498335›Full record

ReviewJournal of clinical medicine2020

Genetic Factors Involved in Cardiomyopathies and in Cancer.

María Sabater-Molina, Marina Navarro-Peñalver, Carmen Muñoz-Esparza, Ángel Esteban-Gil, Juan Jose Santos-Mateo, Juan R Gimeno

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 26% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
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

6 authors at 3 institutions in 2 countries.

María Sabater-MolinaUnidad de Cardiopatías Hereditarias, Servicio de Cardiología, Hospital Universitario Virgen dela Arrixaca, El Palmar, 30120 Murcia, Spain.
Marina Navarro-PeñalverUnidad de Cardiopatías Hereditarias, Servicio de Cardiología, Hospital Universitario Virgen dela Arrixaca, El Palmar, 30120 Murcia, Spain.ORCID 0000-0002-6254-6039
Carmen Muñoz-EsparzaUnidad de Cardiopatías Hereditarias, Servicio de Cardiología, Hospital Universitario Virgen dela Arrixaca, El Palmar, 30120 Murcia, Spain.
Ángel Esteban-GilBiomedical Informatics & Bioinformatics Platform, Institute for Biomedical Research of Murcia (IMIB)/Foundation for Healthcare Training & Research of the Region of Murcia (FFIS), 30003 Murcia, Spain.
Juan Jose Santos-MateoUnidad de Cardiopatías Hereditarias, Servicio de Cardiología, Hospital Universitario Virgen dela Arrixaca, El Palmar, 30120 Murcia, Spain.ORCID 0000-0003-3546-4350
Juan R GimenoUnidad de Cardiopatías Hereditarias, Servicio de Cardiología, Hospital Universitario Virgen dela Arrixaca, El Palmar, 30120 Murcia, Spain.ORCID 0000-0001-5818-1754
Instituto de Salud Carlos III · ESERN GUARD-Heart · NLComunidad Autónoma de la Región de Murcia · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer therapy-induced cardiomyopathy (CCM) manifests as left ventricular (LV) dysfunction and heart failure (HF). It is associated withparticular pharmacological agents and it is typically dose dependent, but significant individual variability has been observed. History of prior cardiac disease, abuse of toxics, cardiac overload conditions, age, and genetic predisposing factors modulate the degree of the cardiac reserve and the response to the injury. Genetic/familial cardiomyopathies (CMY) are increasingly recognized in general populations with an estimated prevalence of 1:250. Association between cardiac and oncologic diseases regarding genetics involves not only the toxicity process, but pathogenicity. Genetic variants in germinal cells that cause CMY (LMNA, RAS/MAPK) can increase susceptibility for certain types of cancer. The study of mutations found in cancer cells (somatic) has revealed the implication of genes commonly associated with the development of CMY. In particular, desmosomal mutations have been related to increased undifferentiation and invasiveness of cancer. In this article, the authors review the knowledge on the relevance of environmental and genetic background in CCM and give insights into the shared genetic role in the pathogenicity of the cancer process and development of CMY.

Indexed as

arrithmogenic cardiomyopathycancercardiomyopathycardiotoxicitydilated cardiomayopathygenetic

Identifiers

PMID32498335
PMCPMC7356401
OpenAlexW3034037300

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.