Chromosome 17p loss and coagulation dysregulation in breast cancer: implications for metastatic risk – a narrative review

Chromosome 17p loss is a frequent genomic alteration observed in aggressive breast cancer subtypes and is strongly associated with poor clinical outcomes. This chromosomal region harbors essential tumor suppressor genes, including TP53, whose inactivation drives genomic instability and tumor progression. Concurrently, breast cancer is characterized by coagulation system dysregulation, which creates a prothrombotic environment supporting tumor cell survival, immune evasion, and metastatic dissemination. Emerging evidence reveals a mechanistic link between 17p deletions and coagulation abnormalities. Loss of functional p53 promotes the upregulation of procoagulant factors such as tissue factor and plasminogen activator inhibitor-1, intensifying thrombin generation and fibrin formation. Additionally, 17p loss indirectly influences platelet activation and tumor–platelet interactions, which protect circulating tumor cells and facilitate their extravasation into distant organs. These processes collectively enhance the metastatic capacity of breast cancer cells.