IMMUNOHISTOCHEMICAL STUDY OF TUMOR CELL-ASSOCIATED PLASMINOGEN ACTIVATORS AND PLASMINOGEN-ACTIVATOR INHIBITORS IN LUNG CARCINOMAS

Study objective: To compare the expression of plasminogen activators ( PA) and plasminogen activator inhibitors (PAI) in normal lung mucosa a nd lung carcinomas. Design: Immunohistochemical localization of urokin ase-type PA (uPA), tissue-type PA (tPA), type 1 PAI (PAI-1), and type 2 PAI (PAI-2) in four normal lung biopsy specimens and in four adenoca rcinomas (AC), four squamous carcinomas (SC), two large-cell carcinoma s (LCC), and ten small-cell carcinomas (SCC) biopsy specimens. Qualita tive immunostaining scoring system. Results: tPA and uPA immunostainin g scores from all specimens were statistically similar. The cellular s taining for uPA and tPA was generally constant (normal epithelial laye rs, AC cells, SC cells) except for LCC cells (inconstant uPA staining, p<10(-3)). Both PAIs were detected in cells of the normal epithelial layer. The four carcinoma cell types stained for PAI in a statisticall y different pattern (p<10(-3). Cells of the peripheral cords of SCC we re inconstantly PAI-1 and PAI-2 positive (p<10(-3)). LCC were PAI-2 ne gative and inconstantly stained for PAI-1. SCC cells were PAI-1 and PA I-2 negative. Conclusion: Lung carcinomas of worst clinical prognosis no longer express PAI reactivity. The imbalance of the plasminogen act ivation pathway may favor the spreading of the more invasive histologi c types of bronchogenic carcinomas.