STUDY OBJECTIVE: To compare the expression of plasminogen activators (PA) and plasminogen activator inhibitors (PAI) in normal lung mucosa and lung carcinomas. DESIGN: Immunohistochemical localization of urokinase-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 adenocarcinomas (AC), four squamous carcinomas (SC), two large-cell carcinomas (LCC), and ten small-cell carcinomas (SCC) biopsy specimens. Qualitative immunostaining scoring system. RESULTS: tPA and uPA immunostaining scores from all specimens were statistically similar. The cellular staining for uPA and tPA was generally constant (normal epithelial layers, 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 statistically different pattern (p < 10(-3)). Cells of the peripheral cords of SCC were inconstantly PAI-1 and PAI-2 positive (p < 10(-3)). LCC were PAI-2 negative and inconstantly stained for PAI-1. SCC cells were PAI-1 and PAI-2 negative. CONCLUSION: Lung carcinomas of worst clinical prognosis no longer express PAI reactivity. The imbalance of the plasminogen activation pathway may favor the spreading of the more invasive histologic types of bronchogenic carcinomas.
STUDY OBJECTIVE: To compare the expression of plasminogen activators (PA) and plasminogen activator inhibitors (PAI) in normal lung mucosa and lung carcinomas. DESIGN: Immunohistochemical localization of urokinase-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 adenocarcinomas (AC), four squamous carcinomas (SC), two large-cell carcinomas (LCC), and ten small-cell carcinomas (SCC) biopsy specimens. Qualitative immunostaining scoring system. RESULTS:tPA and uPA immunostaining scores from all specimens were statistically similar. The cellular staining for uPA and tPA was generally constant (normal epithelial layers, 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 statistically different pattern (p < 10(-3)). Cells of the peripheral cords of SCC were inconstantly PAI-1 and PAI-2 positive (p < 10(-3)). LCC were PAI-2 negative and inconstantly stained for PAI-1. SCC cells were PAI-1 and PAI-2 negative. CONCLUSION:Lung carcinomas of worst clinical prognosis no longer express PAI reactivity. The imbalance of the plasminogen activation pathway may favor the spreading of the more invasive histologic types of bronchogenic carcinomas.