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Updated: Jul 16, 2025

A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
Published on: June 7, 2018
Clonal Hematopoiesis as a Molecular Risk Factor for Doxorubicin-Induced Cardiotoxicity: A Proof-of-Concept Study
Jamila Mammadova1, Christelle Colin-Leitzinger2, Diep Nguyen3
1Morsani College of Medicine, University of South Florida, Tampa, FL.
Clonal hematopoiesis (CH) increases the risk of doxorubicin-induced cardiotoxicity (DIC) in cancer patients. Identifying CH may help predict and prevent heart damage from chemotherapy.
Area of Science:
- Oncology
- Cardiology
- Genetics
Background:
- Anthracyclines, like doxorubicin, are potent chemotherapy agents but can cause dose-limiting cardiotoxicity.
- Clonal hematopoiesis (CH), characterized by somatic mutations in hematopoietic stem cells, is linked to cardiovascular risks.
- The relationship between CH and doxorubicin-induced cardiotoxicity (DIC) is not well understood.
Purpose of the Study:
- To investigate the hypothesis that clonal hematopoiesis (CH) increases the risk of doxorubicin-induced cardiotoxicity (DIC).
Main Methods:
- A retrospective cohort study of 100 cancer patients treated with doxorubicin.
- Patients experiencing symptomatic heart failure, reduced ejection fraction, or arrhythmia were identified (n=25).
- Clonal hematopoiesis (CH) was detected using DNA from peripheral blood and tumor samples.
Main Results:
- High cumulative doxorubicin dose (>240 mg/m²), clonal hematopoiesis (CH), and a history of smoking were significantly associated with doxorubicin-induced cardiotoxicity (DIC).
- After adjusting for confounding factors, CH remained a strong predictor (OR, 8.58; P = .0033).
Conclusions:
- Clonal hematopoiesis (CH) shows preliminary evidence as a predictive risk factor for doxorubicin-induced cardiotoxicity (DIC).
- CH may serve as a valuable precision medicine biomarker for cancer patients undergoing anthracycline treatment.
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