Cytogenetic alterations and coagulopathy in breast cancer patients: molecular mechanisms and clinical implications.

Breast cancer is characterized by diverse cytogenetic alterations that play a pivotal role in tumor initiation, progression, and therapeutic resistance. These chromosomal abnormalities, including gains, losses, and structural rearrangements, contribute to genomic instability and influence cellular behavior in ways that extend beyond tumor growth. One significant but often overlooked consequence of these cytogenetic changes is their impact on the coagulation system, leading to a hypercoagulable state and increasing the risk of thrombosis in breast cancer patients. Emerging evidence links specific cytogenetic aberrations to the dysregulation of coagulation pathways through molecular mechanisms such as upregulation of tissue factor expression, enhanced release of procoagulant microparticles, and modulation of platelet and endothelial cell activation. These processes collectively foster a prothrombotic environment, exacerbating complications like venous thromboembolism and disseminated intravascular coagulation, which significantly affect patient morbidity and mortality. Moreover, the interplay between chromosomal instability and coagulation dysregulation may also influence tumor progression and metastasis.