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By Wen G Jiang; R E Mansel

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Induction of MMP-9 leads to destruction of the inhibitor thus unleashing the elastase that cleaves the epithelial-dermal contacts leading to the skin blistering characteristic of bullous pemphigoid. MMP-9 can also affect the inflammatory response in other ways since it has enzymatic activity allowing the degradation of some inflammatory cytokines and activates interleukin-8 by cleaving it to a smaller more active form (Van Den Steen et al, 2000). 6. MMP-9 AND TUMOR PROGRESSION Evidence of the effects of these gelatinases on tumor progression and metastasis comes both from studies in vitro, in tumor models and in knock out mice.

APMIS 1999; 107: 120–127. de Groot FMH, van Berkom LWA, Scheeren HW. Synthesis and biological evaluation of 2′carbamate-linked and 2′-carbonate-linked prodrugs of paclitaxel: Selective activation by the tumor-associated protease plasmin. J Med Chem 2000; 43: 3093–3102. Deng G, Curriden SA, Wang S, Rosenberg S, Loskutoff DJ. Is plasminogen activator inhibitor1 the molecular switch that governs urokinase receptor-mediated cell adhesion and release? J Cell Biol 1996; 134: 1–9. Deng G, Waltz DA, Navaneetha R, Drummond RJ, Rosenberg S, Chapman HA.

Recent data suggest that uPAR is an integrin ligand rather than, or in addition to, an integrin-associated protein (Tarui et al, 2001). 2. CLINICAL RELEVANCE OF THE PLASMINOGEN/PLASMIN 2. SYSTEM Many studies have shown that upregulation of uPA, uPAR and PAI-1 in malignant tumors is associated with increased malignancy [for review, see (Reuning et al, 1998; Andreasen et al, 1997; Frankenne et al, 1999; Brunner et al, 1999; Schmitt et al, 2000). These proteolytic factors are very good prognostic markers, suited to identify cancer patients at risk to develop metastases (Schmitt et al, 2000).

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