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. 2025 Nov 11:12:1624023.
doi: 10.3389/fcvm.2025.1624023. eCollection 2025.

Soluble suppression of tumorigenicity-2 changes during cardiotoxic cancer treatment: a systematic review and meta-analysis

Luca Fazzini  1 , Simone Angius  1 , Nicola Campana  1 , Luca Pascalis  1 , Martino Deidda  1 , Giordano Maria Pugliesi  2   3 , Vincenzo Quagliariello  4 , Nicola Maurea  4 , Carlo Gabriele Tocchetti  5   6   7   8 , Pietro Ameri  9   10 , Christian Cadeddu Dessalvi  1
Affiliations

Soluble suppression of tumorigenicity-2 changes during cardiotoxic cancer treatment: a systematic review and meta-analysis

Luca Fazzini et al. Front Cardiovasc Med. .

Abstract

Background: Soluble suppression of tumorigenicity-2 (sST2) is a promising biomarker of cardiovascular disease and heart failure. Data about the changes in sST2 concentrations during cancer treatment and the relationship with cancer treatment-related cardiotoxicity are sparse.

Methods: We conducted a systematic review and meta-analysis to explore longitudinal changes in sST2 levels at three time points (T0 baseline, T1 post-chemotherapy, and T2 follow-up) in cancer patients treated with cardiotoxic therapies and compared these changes to traditional biomarkers of cardiac injury, i.e., troponin and NT-proBNP. Using random-effects models, mean differences (MD), and standardized MD (SMD), we analyzed (i) ST2 longitudinal changes, (ii) the association between ST2 and cardiotoxicity [defined through left ventricular ejection fraction (LVEF)] providing pooled estimates of correlations, and (iii) the SMD variations among biomarkers.

Results: Eight studies were included, comprising 433 patients treated with anthracycline and/or HER2-directed antibodies. There was a trend toward increased sST2 levels from T0 to T2 (MD 1.86, 95% CI -0.97 to 4.68, p = 0.200) and decreased levels from T1 to T2 (MD -1.96, 95% CI -4.28 to 0.37, p = 0.100). A pooled analysis showed a negative correlation between sST2 levels and LVEF (r -0.29, 95% CI, -0.49- -0.05, p < 0.010). Comparisons with Troponin and NT-proBNP showed a significantly higher Troponin SMD at T0-T1 (p = 0.027), while no significant differences were observed for NT-proBNP.

Conclusion: sST2 showed dynamic changes during cardiotoxic therapy correlating with cardiotoxicity. Troponin was demonstrated to have greater longitudinal variations. Further research is needed to evaluate longitudinal sST2 levels in patients who develop cardiotoxicity vs. those who do not.

Keywords: ST2; biomarker; cardioncology; cardiotoxcity; cardiotoxic adverse effect.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Forest plot showing the sST2 mean difference between T0 and T2 (panel A), between T0 and T1 (panel B), and between T1 and T2 (panel C).
Figure 2
Figure 2
Forest plot showing the meta-analysis of correlations between sST2 and cardiotoxicity.
Figure 3
Figure 3
Comparison of troponin and sST2 standard mean differences between T0 and T2 (panel A), and T0 and T1 (panel B).
Figure 4
Figure 4
Comparison of NT-proBNP and sST2 standard mean differences between T0 and T2 (panel A), and T0 and T1 (panel B).
See this image and copyright information in PMC

References

    1. Camilli M, Cipolla CM, Dent S, Minotti G, Cardinale DM. Anthracycline cardiotoxicity in adult cancer patients. JACC: CardioOncology. (2024) 6(5):655–77. 10.1016/j.jaccao.2024.07.016 - DOI - PMC - PubMed
    1. Bloom MW, Hamo CE, Cardinale D, Ky B, Nohria A, Baer L, et al. Cancer therapy–related cardiac dysfunction and heart failure. Circ Heart Fail. (2016) 9(1):e002661. 10.1161/CIRCHEARTFAILURE.115.002661 - DOI - PMC - PubMed
    1. Carver JR, Shapiro CL, Ng A, Jacobs L, Schwartz C, Virgo KS, et al. American society of clinical oncology clinical evidence review on the ongoing care of adult cancer survivors: cardiac and pulmonary late effects. J Clin Oncol. (2007) 25(25):3991–4008. 10.1200/JCO.2007.10.9777 - DOI - PubMed
    1. Patnaik JL, Byers T, DiGuiseppi C, Dabelea D, Denberg TD. Cardiovascular disease competes with breast cancer as the leading cause of death for older females diagnosed with breast cancer: a retrospective cohort study. Breast Cancer Res. (2011) 13(3):R64. 10.1186/bcr2901 - DOI - PMC - PubMed
    1. Lyon AR, Dent S, Stanway S, Earl H, Brezden-Masley C, Cohen-Solal A, et al. Baseline cardiovascular risk assessment in cancer patients scheduled to receive cardiotoxic cancer therapies: a position statement and new risk assessment tools from the cardio-oncology study group of the heart failure association of the European society of cardiology in collaboration with the international cardio-oncology society. Eur J Heart Fail. (2020) 22(11):1945–60. 10.1002/ejhf.1920 - DOI - PMC - PubMed

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