作者: Manfred Schmitt , Karin Mengele , Apostolos Gkazepis , Rudolf Napieralski , Viktor Magdolen
DOI: 10.1159/000151737
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摘要: centration of tPA in plasma amounts to 5–10 ng/ml, but varies strongly under different physiological and pathological conditions. Although it was already known before 1970 that plasminogen activator activity may be increased tumour tissues over non-neoplastic tissue, for some time, interest turned away from the possible role activators cancer progression [15–20], particularly because techniques used then did not distinguish between two types activators, uPA [21, 22]. In years following Astedt Holmberg’s observation is released by human ovarian cells, several other authors reported elevated concentrations compared [23–26]. These observations prompted investigators restart detailed analyses especially uPA, tissue blood samples patients. Due refined analytical tools instruments, structure its proteolytic activation pathophysiology stroma degradation spread investigated. This also enhanced fact that, 1985, a cell surface receptor (uPAR; CD87) detected became clear thrombolysis fibrinolysis counterbalanced inhibitors uPAR focal adhesion point localised uPA-mediated proteolysis malignant state [27, 28]. 1966, Brakman et al. [29] described presence inhibitor group patients with an impaired fibrinolytic system, took another 18 PAI-1 isolated [30]. The concentration about 20 ng/ml. inhibitor, PAI-2, first placental [31] therefore named placenta-type inhibitor. Later PAI-2 present various white cells [32]. are usually low, can high (above 35 ng/ml) pregnant women.