Summary Extravascular fibrin deposition accompanies diverse types of tissue injury and neoplasia. In the setting of acute and chronic lung injury, the fibrin gel forms a transitional matrix that undergoes remodeling associated with invasion by inflammatory cells and fibroblasts. These cells express procoagulants and fibrinolysins that govern the transformation of the transitional fibrin gel into fibrotic tissue. A similar process accounts for the desmolastic response that surrounds various tumors, including lung cancers and malignant mesothelioma.
Tumors also invade host tissues via remodeling of the transitional fibrin gel.
More recently, we have also studied the role of these processes in the pathogenesis of malignant mesothelioma. We are currently studying how expression of various fibrinolysins, procoagulants and their inhibitors are regulated at the posttranscriptional level and how these molecules influence cellular function via signaling mechanisms. Current Projects Control of the fibrin turnover in pleural disease. Determination of mechanisms that regulate expression of tissue factor and tissue factor pathway inhibitors in lung and pleural disease. Posttranscriptional regulation o f the urokinase receptor and of related molecules.