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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.<\/jats:p>","DOI":"10.1093\/cvr\/cvz024","type":"journal-article","created":{"date-parts":[[2019,2,6]],"date-time":"2019-02-06T07:09:08Z","timestamp":1549436948000},"page":"949-959","source":"Crossref","is-referenced-by-count":48,"title":["Personalized medicine in cardio-oncology: the role of induced pluripotent stem cell"],"prefix":"10.1093","volume":"115","author":[{"given":"Nazish","family":"Sayed","sequence":"first","affiliation":[{"name":"Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA"},{"name":"Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA"},{"name":"Division of Cardiology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed","family":"Ameen","sequence":"additional","affiliation":[{"name":"Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA"},{"name":"Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA"},{"name":"Division of Cardiology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph C","family":"Wu","sequence":"additional","affiliation":[{"name":"Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA, USA"},{"name":"Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA"},{"name":"Division of Cardiology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,2,15]]},"reference":[{"key":"2019122705081132800_cvz024-B1","first-page":"1","article-title":"Deaths: leading causes for 2016","volume":"67","author":"Heron","year":"2018","journal-title":"Natl Vital Stat Rep"},{"key":"2019122705081132800_cvz024-B2","doi-asserted-by":"crossref","first-page":"265.","DOI":"10.1038\/nrc3258","article-title":"Cancer immunotherapy via dendritic cells","volume":"12","author":"Palucka","year":"2012","journal-title":"Nat Rev Cancer"},{"key":"2019122705081132800_cvz024-B3","first-page":"52","article-title":"Advanced targeted therapies in cancer: drug nanocarriers, the future of chemotherapy","volume":"79","author":"Fern Ndez-Medarde","year":"2015","journal-title":"Eur J Pharm Biopharm"},{"key":"2019122705081132800_cvz024-B4","doi-asserted-by":"crossref","first-page":"329","DOI":"10.1038\/clpt.2013.117","article-title":"Clinical approval success rates for investigational cancer drugs","volume":"94","author":"DiMasi","year":"2013","journal-title":"Clin Pharmacol Ther"},{"key":"2019122705081132800_cvz024-B5","doi-asserted-by":"crossref","first-page":"2900","DOI":"10.1200\/JCO.2005.05.827","article-title":"Type II chemotherapy-related cardiac dysfunction: time to recognize a new entity","volume":"23","author":"Ewer","year":"2005","journal-title":"J Clin Oncol"},{"key":"2019122705081132800_cvz024-B6","doi-asserted-by":"crossref","first-page":"475","DOI":"10.7326\/0003-4819-81-4-475","article-title":"Adriamycin cardiotoxicity in man","volume":"81","author":"Rinehart","year":"1974","journal-title":"Ann Intern Med"},{"key":"2019122705081132800_cvz024-B7","first-page":"89","article-title":"Paclitaxel-induced cardiotoxicity. 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