AI Article Synopsis
- Atypical adenomatous hyperplasia (AAH) is identified as a possible precursor to pulmonary adenocarcinoma, with the roles of COX-2, Fas, and Fas ligand (FasL) under investigation.
- In a study of 40 tissue samples (31 adenocarcinoma and 9 AAH), COX-2 was significantly more expressed in adenocarcinoma (65%) compared to AAH (22%).
- The results indicate that COX-2 expression could be linked to the progression from AAH to adenocarcinoma, with minimal expression of Fas and FasL in both types.
Article Abstract
Background: Atypical adenomatous hyperplasia (AAH) has been reported to be a precancerous lesion of pulmonary adenocarcinoma. Cyclooxygenase-2 (COX-2), Fas and Fas ligand (FasL) are believed to be involved in the pathogenesis and progression of cancer.
Patients And Methods: We examined the expression of COX-2, Fas and FasL in 31 tissue specimens of adenocarcinoma and 9 of AAH using an immunohistochemical method.
Results: COX-2 staining was observed in 20 (65%) specimens of adenocarcinoma and 2 (22%) of AAH. There was a significant difference in incidence of expression between these two groups (p = 0.025). All tumor specimens obtained from three patients with simultaneous multiple adenocarcinoma showed positive COX-2 staining. In two patients having both adenocarcinoma and AAH, COX-2 expression was detected in adenocarcinoma but not in AAH. Fas was expressed in 5 (16%) adenocarcinoma and 2 (22%) AAH specimens. FasL was detected in 3 (9.7%) adenocarcinoma and 1 (11%) AAH specimen.
Conclusion: These findings suggest that COX-2 might play a role in the progression from AAH to adenocarcinoma.
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