Evidence map›Paper›PMID 30768178›Full record

ReviewCardiovascular research2019

Personalized medicine in cardio-oncology: the role of induced pluripotent stem cell.

Nazish Sayed, Mohamed Ameen, Joseph C Wu

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review
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

3 authors at 2 institutions in 1 country.

Nazish SayedStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA.
Mohamed AmeenStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA.
Joseph C WuStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA.
Cardiovascular Institute of the South · USStanford University · US

Funding

T32 Training Program in Mechanisms and Innovation in Vascular DiseaseT32HL098049 · NHLBI · STANFORD UNIVERSITY · PI Nicholas James Leeper, Philip S Tsao · 2010 to 2026
$6.3M
Modeling Tyrosine Kinase Inhibitor-Induced Vascular Dysfunction Using Human iPSCsR01HL141851 · NHLBI · STANFORD UNIVERSITY · PI WONG, WING H., WU, JOSEPH C. · 2018 to 2025
$5.7M
Modeling Susceptibility to Chemotherapy-Induced Cardiotoxicity Using Human iPSCsR01HL123968 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS, WU, JOSEPH C. · 2014 to 2021
$4.8M
Assessment of Low-Dose Radiation Risk and Mechanisms of Individual RadiosensitivityR01HL132875 · NHLBI · STANFORD UNIVERSITY · PI WU, JOSEPH C. · 2016 to 2019
$1.9M
Modeling Endothelial Dysfunction in LMNA-related Dilated CardiomyopathyK01HL135455 · NHLBI · STANFORD UNIVERSITY · PI SAYED, NAZISH · 2017 to 2021
$828k
NHLBI NIH HHS K01 HL135455NHLBI NIH HHS R01 HL123968NHLBI NIH HHS R01 HL132875NHLBI NIH HHS R01 HL141851
6 · The paper itself

Abstract

Treatment of cancer has evolved in the last decade with the introduction of new therapies. Despite these successes, the lingering cardiotoxic side-effects from chemotherapy remain a major cause of morbidity and mortality in cancer survivors. These effects can develop acutely during treatment, or even years later. Although many risk factors can be identified prior to beginning therapy, unexpected toxicity still occurs, often with lasting consequences. Specifically, cardiotoxicity results in cardiac cell death, eventually leading to cardiomyopathy and heart failure. Certain risk factors may predispose an individual to experiencing adverse cardiovascular effects, and when unexpected cardiotoxicity occurs, it is generally managed with supportive care. Animal models of chemotherapy-induced cardiotoxicity have provided some mechanistic insights, but the precise mechanisms by which these drugs affect the heart remains unknown. Moreover, the genetic rationale as to why some patients are more susceptible to developing cardiotoxicity has yet to be determined. Many genome-wide association studies have identified genomic variants that could be associated with chemotherapy-induced cardiotoxicity, but the lack of validation has made these studies more speculative rather than definitive. With the advent of human induced pluripotent stem cell (iPSC) technology, researchers not only have the opportunity to model human diseases, but also to screen drugs for their efficacy and toxicity using human cell models. Furthermore, it allows us to conduct validation studies to confirm the role of genomic variants in human diseases. In this review, we discuss the role of iPSCs in modelling chemotherapy-induced cardiotoxicity.

Indexed as

CardiologyMedical OncologyPrecision MedicineAnimalsAntineoplastic AgentsCardiotoxicityGenetic Predisposition to DiseaseHeart DiseasesHumansInduced Pluripotent Stem CellsMolecular Targeted TherapyNeoplasmsPharmacogenomic VariantsPhenotypeRisk AssessmentRisk FactorsAntineoplastic AgentsCardio-oncologyChemotherapyInduced pluripotent stem cellsPharmacogenomicsPrecision medicine

Identifiers

PMID30768178
PMCPMC6933506
OpenAlexW2913357915

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.