Journal ArticleDOI
Anthracycline-Induced Cardiotoxicity: A Review of Pathophysiology, Diagnosis, and Treatment
TLDR
Progress made over the past two decades in understanding the molecular and genetic basis of anthracycline-induced cardiotoxicity is reviewed; detecting and monitoring myocardial dysfunction; using adjunct cardioprotectant therapies; and improvingCardioprotection with agents such as liposomal and pegylated doxorubicin are reviewed.Abstract:
Anthracyclines have been widely used in children and adults to treat hematologic malignancies, soft-tissue sarcomas, and solid tumors However, anthracyclines come with both short- and long-term cardiotoxic effects, ranging from occult changes in myocardial structure and function to severe cardiomyopathy and heart failure that may result in cardiac transplantation or death Here, we review the progress made over the past two decades in understanding the molecular and genetic basis of anthracycline-induced cardiotoxicity; detecting and monitoring myocardial dysfunction; using adjunct cardioprotectant therapies, such as dexrazoxane; and improving cardioprotection with agents such as liposomal and pegylated doxorubicin Despite this increased understanding, preventing drug-induced cardiotoxicity while maintaining oncologic efficacy to achieve the highest quality of life over a lifespan remain cornerstones of successful anthracycline chemotherapy during childhoodread more
Citations
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Journal ArticleDOI
Anticancer drug nanomicelles formed by self-assembling amphiphilic dendrimer to combat cancer drug resistance
Tuo Wei,Chao Chen,Juan Liu,Cheng Liu,Paola Posocco,Xiaoxuan Liu,Qiang Cheng,Shuaidong Huo,Zicai Liang,Maurizio Fermeglia,Sabrina Pricl,Xing-Jie Liang,Palma Rocchi,Ling Peng +13 more
TL;DR: An innovative drug delivery system based on a self-assembling amphiphilic dendrimer, which can generate supramolecular nanomicelles with large void space in their core to encapsulate anticancer drugs with high loading capacity, was established.
Journal ArticleDOI
Doxorubicin induces cardiotoxicity through upregulation of death receptors mediated apoptosis in cardiomyocytes.
Liqun Zhao,Baolin Zhang +1 more
TL;DR: Investigation of doxorubicin-induced cytotoxicity in human induced pluripotent stem cells-derived cardiomyocytes shows that the induction of death receptors in carduomyocytes is likely a critical mechanism by which doxorbicin causes cardiotoxicity.
Journal ArticleDOI
Doxorubicin-induced cardiotoxicity: An update on the molecular mechanism and novel therapeutic strategies for effective management
TL;DR: In this paper, the authors provided a detailed review on the current understanding of the pathological mechanisms behind the well-known Dox-induced cardiotoxicity and provided some of the most plausible pharmacological strategies which have been tested against doxorubicin-induced Cardiotoxicity.
Journal ArticleDOI
Immunogenic cell death in anticancer chemotherapy and its impact on clinical studies.
TL;DR: Recent progress in identifying and classifying ICD inducers; concepts and molecular mechanisms of ICD; and the impact and potential applications of I CD in clinical studies are summarized.
Journal ArticleDOI
Use of biomarkers for the assessment of chemotherapy-induced cardiac toxicity.
TL;DR: Biomarkers represent an exciting potential complement or replacement for echocardiographic monitoring of chemotherapy related cardiac toxicity which may allow for earlier realization of the degree of cardiac damage occurring during treatment, creating the opportunity for more timely modulation of therapy.
References
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Journal ArticleDOI
Risk factors for doxorubicin-induced congestive heart failure.
TL;DR: There was a continuum of increasing risk as the cumulative amount of administered drug increased, and a weekly dose schedule of doxorubicin was associated with a significantly lower incidence of congestive heart failure than was the usually employed every 3-week schedule.
Journal ArticleDOI
Congestive heart failure in patients treated with doxorubicin: a retrospective analysis of three trials.
TL;DR: Doxorubicin is a highly effective and widely used cytotoxic agent with application that is limited by cardiotoxicity related to the cumulative dose of the drug, which is reflected in the incidence in the broader clinical oncology setting.
Journal ArticleDOI
Identification of the molecular basis of doxorubicin-induced cardiotoxicity
Sui Zhang,Xiaobing Liu,Xiaobing Liu,Tasneem Bawa-Khalfe,Long Sheng Lu,Yi Lisa Lyu,Leroy-Fong Liu,Edward T.H. Yeh,Edward T.H. Yeh +8 more
TL;DR: Cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-IIβ) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis and ROS formation.
Journal ArticleDOI
Late Cardiac Effects of Doxorubicin Therapy for Acute Lymphoblastic Leukemia in Childhood
Steven E. Lipshultz,Steven D. Colan,Richard D. Gelber,Antonio R. Perez-Atayde,Stephen E. Sallan,Stephen P. Sanders +5 more
TL;DR: Doxorubicin therapy in childhood impairs myocardial growth in a dose-related fashion and results in a progressive increase in left ventricular afterload sometimes accompanied by reduced contractility, hypothesized to result in inadequateleft ventricular mass and clinically important heart disease in later years.
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