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      Variations of circulating cardiac biomarkers during and after anthracycline-containing chemotherapy in breast cancer patients

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          Abstract

          Background

          Over time, the chance of cure after the diagnosis of breast cancer has been increasing, as a consequence of earlier diagnosis, improved diagnostic procedures and more effective treatment options. However, oncologists are concerned by the risk of long term treatment side effects, including congestive heart failure (CHF).

          Methods

          In this study, we evaluated innovative circulating cardiac biomarkers during and after anthracycline-based neoadjuvant chemotherapy (NAC) in breast cancer patients. Levels of cardiac-specific troponins T (cTnT), N-terminal natriuretic peptides (NT-proBNP), soluble ST2 (sST2) and 10 circulating microRNAs (miRNAs) were measured.

          Results

          Under chemotherapy, we observed an elevation of cTnT and NT-proBNP levels, but also the upregulation of sST2 and of 4 CHF-related miRNAs (miR-126-3p, miR-199a-3p, miR-423-5p, miR-34a-5p). The elevations of cTnT, NT-proBNP, sST2 and CHF-related miRNAs were poorly correlated, suggesting that these molecules could provide different information.

          Conclusions

          Circulating miRNA and sST2 are potential biomarkers of the chemotherapy-related cardiac dysfunction (CRCD). Nevertheless, further studies and long-term follow-up are needed in order to evaluate if these new markers may help to predict CRCD and to identify the patients at risk to later develop CHF.

          Electronic supplementary material

          The online version of this article (10.1186/s12885-018-4015-4) contains supplementary material, which is available to authorized users.

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          Most cited references27

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          MicroRNA-34a regulates cardiac ageing and function.

          Reinier A Boon, Kazuma Iekushi, Stefanie Lechner … (2013)
          Ageing is the predominant risk factor for cardiovascular diseases and contributes to a significantly worse outcome in patients with acute myocardial infarction. MicroRNAs (miRNAs) have emerged as crucial regulators of cardiovascular function and some miRNAs have key roles in ageing. We propose that altered expression of miRNAs in the heart during ageing contributes to the age-dependent decline in cardiac function. Here we show that miR-34a is induced in the ageing heart and that in vivo silencing or genetic deletion of miR-34a reduces age-associated cardiomyocyte cell death. Moreover, miR-34a inhibition reduces cell death and fibrosis following acute myocardial infarction and improves recovery of myocardial function. Mechanistically, we identified PNUTS (also known as PPP1R10) as a novel direct miR-34a target, which reduces telomere shortening, DNA damage responses and cardiomyocyte apoptosis, and improves functional recovery after acute myocardial infarction. Together, these results identify age-induced expression of miR-34a and inhibition of its target PNUTS as a key mechanism that regulates cardiac contractile function during ageing and after acute myocardial infarction, by inducing DNA damage responses and telomere attrition.
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            Circulating microRNAs are new and sensitive biomarkers of myocardial infarction

            Yuri D’Alessandra, Paolo Devanna, Federica Limana … (2010)
            Aims Circulating microRNAs (miRNAs) may represent a novel class of biomarkers; therefore, we examined whether acute myocardial infarction (MI) modulates miRNAs plasma levels in humans and mice. Methods and results Healthy donors (n = 17) and patients (n = 33) with acute ST-segment elevation MI (STEMI) were evaluated. In one cohort (n = 25), the first plasma sample was obtained 517 ± 309 min after the onset of MI symptoms and after coronary reperfusion with percutaneous coronary intervention (PCI); miR-1, -133a, -133b, and -499-5p were ∼15- to 140-fold control, whereas miR-122 and -375 were ∼87–90% lower than control; 5 days later, miR-1, -133a, -133b, -499-5p, and -375 were back to baseline, whereas miR-122 remained lower than control through Day 30. In additional patients (n = 8; four treated with thrombolysis and four with PCI), miRNAs and troponin I (TnI) were quantified simultaneously starting 156 ± 72 min after the onset of symptoms and at different times thereafter. Peak miR-1, -133a, and -133b expression and TnI level occurred at a similar time, whereas miR-499-5p exhibited a slower time course. In mice, miRNAs plasma levels and TnI were measured 15 min after coronary ligation and at different times thereafter. The behaviour of miR-1, -133a, -133b, and -499-5p was similar to STEMI patients; further, reciprocal changes in the expression levels of these miRNAs were found in cardiac tissue 3–6 h after coronary ligation. In contrast, miR-122 and -375 exhibited minor changes and no significant modulation. In mice with acute hind-limb ischaemia, there was no increase in the plasma level of the above miRNAs. Conclusion Acute MI up-regulated miR-1, -133a, -133b, and -499-5p plasma levels, both in humans and mice, whereas miR-122 and -375 were lower than control only in STEMI patients. These miRNAs represent novel biomarkers of cardiac damage.
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              Chronic disease in the Childhood Cancer Survivor Study cohort: a review of published findings.

              Lisa Diller, Leslie Robison, E Chow … (2009)
              Article 0 comments Cited 100 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Guy Jerusalem: g.jerusalem@chu.ulg.ac.be
                Journal
                Journal ID (nlm-ta): BMC Cancer
                Journal ID (iso-abbrev): BMC Cancer
                Title: BMC Cancer
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1471-2407
                Publication date (Electronic): 29 January 2018
                Publication date PMC-release: 29 January 2018
                Publication date Collection: 2018
                Volume: 18
                Electronic Location Identifier: 102
                Affiliations
                [1 ]ISNI 0000 0001 0805 7253, GRID grid.4861.b, Department of Medical Oncology, , University Hospital (CHU) and University of Liège, ; Liège, Belgium
                [2 ]ISNI 0000 0001 0805 7253, GRID grid.4861.b, Laboratory of Human Genetics, GIGA Research, , University Hospital (CHU) and University of Liège, ; Liège, Belgium
                [3 ]ISNI 0000 0001 0805 7253, GRID grid.4861.b, GIGA Cardiovascular Sciences, Department of Cardiology, , Heart Valve Clinic, University Hospital (CHU) and University of Liège, ; Liège, Belgium
                [4 ]Gruppo Villa Maria Care and Research, Anthea Hospital, Bari, Italy
                Article
                Publisher ID: 4015
                DOI: 10.1186/s12885-018-4015-4
                PMC ID: 5789542
                PubMed ID: 29378531
                SO-VID: 4ac284e9-761a-4a2a-91dc-2725e92b2472
                Copyright © © The Author(s). 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 3 November 2016
                Date accepted : 22 January 2018
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100003134, Fonds pour la Formation à la Recherche dans l’Industrie et dans l’Agriculture;
                Funded by: Télévie
                Funded by: FIRS
                Funded by: Région Wallone
                Funded by: French Community of Belgium
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: biomarkers,cardiotoxicity,chemotherapy,soluble st2,micrornas
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: biomarkers, cardiotoxicity, chemotherapy, soluble st2, micrornas

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