Prostate cancer is the most prevalent
malignancy in men and the third leading cause of
cancer deaths worldwide. Disorders of hemostasis are commonplace in patients with
prostate cancer and include
disseminated intravascular coagulation,
venous thromboembolism,
acute coronary syndrome, and postsurgical
bleeding. These
hemostatic disorders contribute to the mortality and morbidity of
prostate cancer. The leading mechanisms proposed to underlie
prostate cancer-related coagulopathies are thought to be a hyperexpression of
tissue factor,
cancer procoagulant, and
platelet-activating factor, which is then accompanied by release of large amounts of both prothrombotic and profibrinolytic substances into the bloodstream. Given the generally accepted notion that
prostate-specific antigen (PSA) represents an important
biomarker in
prostate cancer diagnostics, large population screenings were initiated for early detection of
cancer. However, recent clinical and economic drawbacks have been recently raised, including evidence that screening exposes patients to a significant risk of both overdiagnosis and overtreatment. Nevertheless, several lines of evidence suggest that PSA may have
tumor-suppressing activities. Despite being a member of the vast
kallikrein family, which actively interplays with the coagulation cascade, the role of PSA in the pathogenesis of
hemostatic disorders observed in
prostate cancer patients remains circumstantial and speculative. However, observations that the levels of this
cancer marker tend to correlate positively with those of several markers of
thrombin generation, and with postsurgical
bleeding as well as with
coronary atherosclerosis and negative outcomes of
myocardial infarction, raise a new and intriguing scenario regarding the pathophysiological role of this
serine protease.