Sex differences influence cancer incidence and susceptibility to cardiovascular toxicity, with females experiencing more treatment-related adverse events such as cardiac dysfunction.
This review highlights the importance of integrating sex-specific surveillance and multi-omic risk stratification to predict and prevent cancer therapy-related cardiotoxicity.
Sex differences influence cancer incidence, treatment response, and susceptibility to cardiovascular toxicity. Males exhibit higher rates and poorer outcomes in most non-sex-specific cancers, while females more frequently experience treatment-related adverse events, including cancer therapy-related cardiac dysfunction. Biological factors such as hormonal status, genetic polymorphisms, immune responses, and pharmacokinetics contribute to these disparities. In cardio-oncology, women—particularly premenopausal or with specific genotypes—may be at increased risk for cardiotoxicity after treatment with anthracyclines, immune checkpoint inhibitors or radiotherapy. Clonal hematopoiesis and certain germline genetic variants such as single nucleotide polymorphisms (e.g., RARG rs2229774, HAS3 rs2232228) are emerging as potential sex-informed biomarkers for predicting cardiotoxicity risk. Despite growing evidence, sex remains insufficiently integrated into clinical trials and guideline development in cardio-oncology. This review highlights the importance of sex-specific surveillance, prevention, and multi-omic risk stratification to advance precision cardio-oncology and support better outcomes for patients across the cancer care continuum.
Keramida et al. (Fri,) conducted a review in Cancer and Cardiotoxicity. Sex differences influence cancer incidence and susceptibility to cardiovascular toxicity, with females experiencing more treatment-related adverse events such as cardiac dysfunction.
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