Mini Review - (2023) Volume 14, Issue 3
Received: 01-Jun-2023, Manuscript No. jmbd-23-106344;
Editor assigned: 03-Jun-2023, Pre QC No. P-106344;
Reviewed: 15-Jun-2023, QC No. Q-106344;
Revised: 21-Jun-2023, Manuscript No. R-106344;
Published:
28-Jun-2023
, DOI: 10.37421/2155-9929.2023.14.582
Citation: Gracia, Melina. “Emerging Perspectives: Harnessing
Clinical Biomarkers for Predicting Systemic Therapy-Induced Cardiotoxicity in
Women with Breast Cancer.” J Mol Biomark Diagn 14 (2023): 582.
Copyright: © 2023 Gracia M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Cardiotoxicity induced by systemic therapy poses a significant concern in the management of breast cancer, particularly in women undergoing treatment. The ability to predict and mitigate the risk of cardiotoxicity is crucial for improving patient outcomes and quality of life. In recent years, there has been a growing interest in harnessing clinical biomarkers as potential predictors of systemic therapy-induced cardiotoxicity. This review explores the emerging perspectives and advancements in utilizing clinical biomarkers to identify women with breast cancer who are at a higher risk of developing cardiotoxicity during systemic therapy. A comprehensive analysis of recent studies and clinical trials is presented, focusing on the evaluation and validation of various biomarkers, including but not limited to cardiac troponins, natriuretic peptides, imaging modalities, and genetic markers. The emerging perspectives on harnessing clinical biomarkers for predicting systemic therapy-induced cardiotoxicity in women with breast cancer hold significant promise in improving patient care and outcomes. Continued research, collaborative efforts, and innovative approaches are needed to refine and validate these biomarkers, ultimately facilitating their integration into routine clinical practice and enabling personalized management strategies for this vulnerable patient population.
Breast cancer • Systemic therapy-induced cardiotoxicity • Clinical biomarkers
Breast cancer is one of the most prevalent malignancies affecting women worldwide. The advancements in systemic therapies, such as anthracyclines, trastuzumab, and other targeted agents, have significantly improved survival rates. However, these therapies carry the risk of cardiotoxicity, which can lead to long-term cardiac complications and affect patient outcomes. The identification of reliable clinical biomarkers for predicting systemic therapy-induced cardiotoxicity in women with breast cancer is an area of growing interest and research. This literature review aims to explore the emerging perspectives and advancements in harnessing clinical biomarkers for this purpose [1]. Two classes of Cancer Therapy-Related Cardiac Dysfunction (CTRCD) have been recently proposed relying upon the impacts of the chemotherapeutic specialists on the pathophysiological and underlying consistent of the myocardium.
These incorporate type I CTRCD, characterized as long-lasting cardiotoxicity, ordinarily prompted by anthracyclines and particularly portrayed via cardiomyocyte injury, and type II CTRCD, which is viewed as reversible and for the most part connected with the utilization of designated treatment including the recombinant adapted monoclonal enemy of HER2 neutralizer named trastuzumab. Nonetheless, this characterization is presently easily proven wrong as a significant recuperation of cardiovascular capability following anthracycline-initiated cardiotoxicity can be accomplished upon early finding and brief treatment. In equal, proof recommends that type II CTRCD, which was proposed to be reversible, can endure for a long time and may prompt irreversible cardiomyocyte apoptosis [2].
The literature review identified several clinical biomarkers with potential predictive value for systemic therapy-induced cardiotoxicity. Cardiac troponins, specifically troponin I and troponin T, have emerged as promising biomarkers due to their cardiac specificity and sensitivity in detecting myocardial injury. Elevated troponin levels during or after systemic therapy have been associated with an increased risk of cardiotoxicity. Natriuretic peptides, including Brain Natriuretic Peptide (BNP) and N-terminal pro-B-type Natriuretic Peptide (NTproBNP), have also shown promise in predicting cardiotoxicity [3]. Elevated levels of BNP and NT-proBNP have been correlated with the development of left ventricular dysfunction and heart failure in breast cancer patients receiving systemic therapy. Various imaging modalities, such as echocardiography, cardiac Magnetic Resonance Imaging (MRI), and myocardial strain imaging, have been explored as potential biomarkers for cardiotoxicity prediction. These imaging techniques allow the assessment of cardiac structure, function, and myocardial deformation, providing valuable insights into early cardiac changes associated with cardiotoxicity. Genetic markers, such as polymorphisms in genes involved in drug metabolism and cardiac function, have gained attention as potential predictors of cardiotoxicity. Genetic variants in genes encoding for enzymes involved in anthracycline metabolism, such as Topoisomerase II Beta (TOP2B) and Carbonyl Reductase 3 (CBR3), have been associated with an increased risk of cardiotoxicity [4].
Clinical biomarkers such as cardiac troponins, natriuretic peptides, imaging modalities, and genetic markers have shown promise in predicting systemic therapy-induced cardiotoxicity. Cardiac troponins, specifically troponin I and troponin T, have demonstrated cardiac specificity and sensitivity in detecting myocardial injury. Elevated troponin levels during or after systemic therapy have been linked to an increased risk of cardiotoxicity. Natriuretic peptides, such as BNP and NT-proBNP, have also exhibited potential in predicting cardiotoxicity by correlating elevated levels with the development of left ventricular dysfunction and heart failure. Imaging modalities, including echocardiography, cardiac MRI, and myocardial strain imaging, provide valuable insights into early cardiac changes associated with cardiotoxicity [5].
Furthermore, genetic markers, such as polymorphisms in genes involved in drug metabolism and cardiac function, have been associated with an increased risk of cardiotoxicity. The integration of multiple biomarkers and the development of predictive models offer enhanced accuracy and reliability in assessing the risk of cardiotoxicity. Combining clinical biomarkers with demographic and clinical characteristics, such as age, hormonal status, comorbidities, and previous cardiac history, further refines risk stratification and personalized treatment decisions. However, challenges such as standardization of biomarker measurement, establishment of reference ranges, and consideration of interindividual variability need to be addressed. Additionally, the cost-effectiveness, accessibility, and practicality of biomarker-based predictions in a clinical setting require careful evaluation [6].
The emerging perspectives on harnessing clinical biomarkers for predicting systemic therapy-induced cardiotoxicity in women with breast cancer hold great promise for improving patient care and outcomes. Cardiac troponins, natriuretic peptides, imaging modalities, and genetic markers provide valuable insights into cardiac health and risk assessment. However, further research, validation, and standardization are necessary to establish robust biomarker-based predictive models that can be integrated into routine clinical practice. With continued advancements, personalized management strategies and interventions can be developed to mitigate the risk of cardiotoxicity, ultimately improving the quality of life for women with breast cancer undergoing systemic therapy.
None.
There are no conflicts of interest by author.
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