Evidence map›Paper›PMID 39042344›Full record

ReviewCurrent cardiology reports2024

Cardiovascular Toxicity in Cancer Therapy: Protecting the Heart while Combating Cancer.

Amit Manhas, Dipti Tripathi, Dilip Thomas, Nazish Sayed

Abstract readReview
In one paragraph

Review in Current cardiology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

4 authors.

Amit ManhasStanford Cardiovascular Institute, Stanford, CA, 94305, USA.
Dipti TripathiStanford Cardiovascular Institute, Stanford, CA, 94305, USA.
Dilip ThomasStanford Cardiovascular Institute, Stanford, CA, 94305, USA.
Nazish SayedStanford Cardiovascular Institute, Stanford, CA, 94305, USA. sayedns@stanford.edu.

Funding

Deciphering the Endothelial Cell-Cardiomyocyte Crosstalk in LMNA CardiomyopathyR01HL158641 · NHLBI · STANFORD UNIVERSITY · PI SAYED, NAZISH · 2021 to 2025
$2.2M
Unraveling the role of endothelium in chemotherapy-induced cardiotoxicityR01HL161002 · NHLBI · STANFORD UNIVERSITY · PI SAYED, NAZISH · 2022 to 2025
$1.6M
Unraveling Adverse Effects of Checkpoint Inhibitors Using iPSC-derived Cardiac OrganoidsK99HL163443 · NHLBI · STANFORD UNIVERSITY · PI THOMAS, DILIP · 2023 to 2024
$249k
American Heart Association 23POST1020812American Heart Association SFRN grant 869015NHLBI NIH HHS K99 HL163443NHLBI NIH HHS R01 HL158641NHLBI NIH HHS R01 HL161002NIH HHS NIH K99 HL163443-01A1NIH HHS R01 HL158641, R01 HL161002
6 · The paper itself

Abstract

purpose of reviewThis review explores the cardiovascular toxicity associated with cancer therapies, emphasizing the significance of the growing field of cardio-oncology. It aims to elucidate the mechanisms of cardiotoxicity due to radiotherapy, chemotherapy, and targeted therapies, and to discuss the advancements in human induced pluripotent stem cell technology (hiPSC) for predictive disease modeling. RECENT

findingsRecent studies have identified several chemotherapeutic agents, including anthracyclines and kinase inhibitors, that significantly increase cardiovascular risks. Advances in hiPSC technology have enabled the differentiation of these cells into cardiovascular lineages, facilitating more accurate modeling of drug-induced cardiotoxicity. Moreover, integrating hiPSCs into clinical trials holds promise for personalized cardiotoxicity assessments, potentially enhancing patient-specific therapeutic strategies. Cardio-oncology bridges oncology and cardiology to mitigate the cardiovascular side-effects of cancer treatments. Despite advancements in predictive models using hiPSCs, challenges persist in accurately replicating adult heart tissue and ensuring reproducibility. Ongoing research is essential for developing personalized therapies that balance effective cancer treatment with minimal cardiovascular harm.

Indexed as

Antineoplastic AgentsCardiotoxicityInduced Pluripotent Stem CellsNeoplasmsAnthracyclinesCardiovascular DiseasesHumansRadiotherapyAnthracyclinesAntineoplastic Agents3D modelsCardiotoxicityChemotherapyiPSCsPharmacogenomics

Identifiers

PMID39042344
PMCPMC12243937

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.