Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To explore mechanisms of coagulation activation in adenocarcinoma of the prostate, the occurrence and distribution of components of coagulation and fibrinolysis pathways in situ were studied by means of immunohistochemical techniques applied to frozen sections of fresh malignant and benign hyperplastic prostatic tissue obtained at transurethral resection. Fibrinogen was distributed throughout the perivascular and tumor connective tissue in both malignant and benign disease but was not present in adjacent areas of normal prostate. Antibodies specific for fibrin and D-dimer crosslink sites stained vascular endothelium focally in both malignant and benign tissues. Both neoplastic cells and benign hyperplastic glandular epithelial cells stained weakly and in a patchy distribution for tissue factor and focally for low-molecular-weight urokinase-type plasminogen activator. Focal staining of vascular endothelium was also observed for tissue plasminogen activator and plasmin-antiplasmin complex neoantigen. By contrast, no tissue staining was observed for factor VII, factor X, factor XIII "a" subunit, high-molecular-weight urokinase-type plasminogen activator, plasminogen activator inhibitors 1 to 3, protein C, and protein S. Thus, the similarity in findings between benign hyperplastic and neoplastic prostate tissue, the lack of either an intact tumor cell-associated coagulation pathway or fibrin formation, and the presence of fibrin on vascular endothelium are consistent with the concept that coagulation activation in prostatic cancer may not be due to a direct effect of the tumor cells on the clotting mechanism. Rather, such activation may be induced by a soluble tumor product that activates procoagulant activity on certain host (for example, vascular endothelial) cells. These findings, together with the lack of effect of warfarin anticoagulation on the clinical course of patients with prostatic cancer, contrast with findings in certain other tumor types and suggest that coagulation activation may not contribute to progression of adenocarcinoma of the prostate.
 ...
PMID:Fibrin formation on vessel walls in hyperplastic and malignant prostate tissue. 170 19

The association between cancer and hypercoagulability states is well known. It usually presents as a complication of gastrointestinal tract adenocarcinomas. We present the case of patient diagnosed of prostatic adenocarcinoma who was admitted because of pain and inflammation in the left side of the neck. The ultrasound study showed a jugular vein thrombosis. In the bibliographic review (MEDLINE 1990-1995), we have not found any similar reports Jugular vein thrombosis is a rare complication and usually is secondary to central vein catheter insertion, although it has been also described with ovarian hyperstimulation syndrome, infections, head and neck tumors and rarely in other neoplastic diseases. The physiopathologic process is not well known, although it is known that neoplastic cells interact with the thrombin and plasmin generating systems and that there is also a decrease in coagulation inhibitors, all of which leads to prothrombin activation in the absence of the corresponding increases in thrombin inhibitor complexes.
 ...
PMID:[Jugular thrombosis and adenocarcinoma of the prostate: a state of hypercoagulability?]. 1068 25