Arterial thrombosis and cancer: insights from observations in myeloproliferative neoplasms and CHIP

Cardiovascular diseases and cancer are the leading global causes of morbidity and mortality and are increasingly recognized as biologically interconnected rather than independent conditions. Growing epidemiological and mechanistic evidence supports a bidirectional relationship between thrombosis-related cardiovascular events and cancer development [ 1 ]. In particular, major arterial thrombosis (AT) has been associated with an increased risk of subsequent solid tumors, suggesting a shared pathogenic substrate rather than simple comorbidity [ 2 ]. Within this framework, atherosclerosis emerges as a central pathogenic hub. As a chronic inflammatory disease, it not only precipitates acute arterial events but also sustains a pro-inflammatory and pro-oxidative systemic milieu that may favor carcinogenesis and tumor progression [ 2 ].