Platelet activation and eicosanoid signaling in ovarian cancer: implications for biomarker development

Ovarian cancer remains one of the most lethal gynecological malignancies worldwide due to late-stage diagnosis, poor prognosis, and frequent chemoresistance. The limited sensitivity and specificity of current diagnostic approaches, particularly for early-stage disease, highlight the urgent need for improved biomarkers and diagnostic strategies. Nowadays, ovarian cancer diagnostics are based mainly on the established biomarkers CA125 and HE4, which in some countries most commonly combined in the Risk of Ovarian Malignancy Algorithm (ROMA). Despite their widespread clinical use, these biomarkers are of limited specificity and sensitivity, particularly in early-stage disease, underscoring the need for more efficient screening and diagnostic approaches. This review summarizes current evidence on the molecular mechanisms linking oxidative stress, inflammation, and platelet activation with ovarian cancer progression and discusses the diagnostic and prognostic potential of related biomarkers. Oxidative stress and inflammation contribute to dysregulated signaling pathways and tumor progression, providing a mechanistic basis for the identification of novel biomarkers. Increasing evidence indicates that platelet activation contributes to tumor growth, angiogenesis, and metastasis. This justifies the strategy of exploring platelet-derived mediators, including thromboxane B 2 and other eicosanoids, as potential biomarkers of ovarian cancer. Overall, current evidence indicates that oxidative stress-, inflammation-, and platelet-associated molecular pathways represent promising sources of novel biomarkers and potential therapeutic targets in ovarian cancer.