Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Prostate-specific antigen, prostate cancer, and disorders of hemostasis. 2001 32

Hypercoagulable states are common disorders with high risk of thrombosis associated with cardiovascular and malignant diseases. The pathogenesis of hypercoagulability is multifactorial. The basic physiological mechanism is the imbalance between anticoagulant activities and procoagulant activities in hemostatic system. In this review, we discuss the correlation between apoptosis and thrombogenesis in hypercoagulable states. Some cell-associated cofactors in coagulation system, including phosphatidylserine, tissue factor, thrombomodulin and cancer procoagulant, are regulated during apoptosis of various cell types. Vascular endothelial cells may act as one of the most important aspects affecting the balance of anticoagulant and procoagulant activities. When endothelial cells are activated or induced to undergo apoptosis by a number of physiological factors, such as inflammatory cytokines and bacterial lipopolysaccharide, the procoagulant activities of endothelial cells are enhanced. Other cell types such as apoptotic vascular smooth muscle cells, monocytes and macrophages may also contribute to the pathogenesis in atherosclerosis. Apoptotic tumor cells, which express high level of procoagulant activities, may act as a direct trigger for coagulation activation.
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PMID:The Pathogenetic Role of Apoptosis in Hypercoagulable States. 2741 81