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									<identifier>oai:www.peertechzpublications.org:10.17352/2581-5407.000056</identifier>
									<datestamp>2026-05-29</datestamp>
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									<oai_dc:dc xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:mml="http://www.w3.org/1998/Math/MathML" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
										<dc:title>
										Beyond Troponins: Emerging Biomarkers for Early Detection of Chemotherapy-Induced Cardiotoxicity in Breast Cancer
										</dc:title><dc:creator>Themelidi Vasiliki</dc:creator><dc:creator> Vlachou Maria</dc:creator><dc:creator> Varvarelis Orfeas-Petros</dc:creator><dc:creator> Ioakeim Kalliopi</dc:creator><dc:creator> Kampouroglou Effrosyni</dc:creator><dc:creator>Tsekoura Dorothea</dc:creator><dc:description>&lt;p&gt;Although modern breast cancer therapies have significantly improved long-term survival, reliable tools for the early detection and prediction of Cancer Therapy-Related Cardiac Dysfunction (CTRCD) remain essential. Cardiovascular toxicity encompasses a broad spectrum of manifestations, ranging from asymptomatic myocardial dysfunction to heart failure, ischemic heart disease, valvular abnormalities, arrhythmias, hypertension, and thromboembolic events.&lt;/p&gt;&lt;p&gt;Anthracyclines and radiation therapy are the most well-established cardiotoxic treatments. Anthracycline-induced cardiotoxicity demonstrates a dose-dependent and often irreversible pattern (Type I cardiotoxicity), primarily mediated by oxidative stress and mitochondrial injury. In contrast, HER-2 targeted therapies are associated with reversible myocardial dysfunction (Type II cardiotoxicity), mainly through the disruption of the ErbB2 signaling pathway. Newer therapies, including anti-VEGF agents and endocrine therapies combined with CDK4/6 inhibitors, further expand the spectrum of cardiovascular risks.&lt;/p&gt;&lt;p&gt;Current guidelines support the use of left ventricular ejection fraction, troponins, and natriuretic peptides for cardiotoxicity monitoring. However, emerging biomarkers, including myeloperoxidase, matrix metalloproteinases, galectin-3, inflammatory markers, and microRNAs, have shown potential for the early detection of myocardial injury.&amp;nbsp;&lt;/p&gt;&lt;p&gt;This review summarizes the current evidence regarding the mechanisms, clinical features, and risk factors of cardiotoxicity associated with breast cancer therapy. It further evaluates both established and novel biomarkers and highlights the clinical value of integrating them with advanced imaging modalities to improve the early detection and monitoring of cardiac remodeling. Further research is required to validate these approaches for clinical use (Graphical abstract).&lt;/p&gt;&lt;p&gt;&lt;img src="https://www.cancerresgroup.us/articles/figures/GJCT-12-156-g001i.gif" alt=""&gt;&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Graphical abstract: &lt;/strong&gt;Integrated multimodal approach for the early detection of Cancer Therapy-Related Cardiac Dysfunction. Cancer therapies trigger myocardial injury through multiple mechanisms. Combined use of cardiac biomarkers and advanced imaging modalities, particularly global longitudinal strain, enables detection of subclinical dysfunction before a decline in left ventricular ejection fraction. Early identification allows for timely cardioprotective interventions and prevention of progression to heart failure.&lt;/p&gt;&lt;br&gt;</dc:description>
										<dc:publisher>Global Journal of Cancer Therapy - Peertechz Publications</dc:publisher>
										<dc:date>2026-05-29</dc:date>
										<dc:type>Research Article</dc:type>
										<dc:identifier>https://doi.org/10.17352/2581-5407.000056</dc:identifier>
										<dc:language>en</dc:language>
										<dc:rights>Copyright © Themelidi Vasiliki et al.</dc:rights>
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