92 kDa matrix metalloproteinase-9 (MMP-9) is believed to play an important role in degrading the matrix and basement membrane, contributing to the invasion and metastasis of malignant solid tumors. However, little is known about its involvement in a malignant fibrous histiocytoma. The aim of this study was to investigate the expression of MMP-9 and to correlate its expression with clinicopathologic parameters in human malignant fibrous histiocytomas.

Archival tumor tissues from 20 patients with a malignant fibrous histiocytoma were analyzed by immunohistochemistry for the expression of MMP-9. Clinical information was obtained through the computerized retrospective database from the tumor registry.

Seventeen of 20 (85%) tumors showed a positive reaction for MMP-9. MMP-9 activity was inversely correlated with patients' survival time (p=.011). There was no significant correlation between the activated MMP-9 expression and all the other clinicopathologic variables.

Our data demonstrate that MMP-9 activation is likely to occur in human malignant fibrous histiocytomas. It is also noteworthy that the expression of MMP-9 may aid in predicting patients' poor prognosis.

c-myc, bcl-2 and p53 are known to regulate apoptosis. There has been growing interest in analyzing their contribution to the pathogenesis and prognosis in a variety of human cancers. This study was undertaken to investigate the expression of these proteins in pulmonary adenocarcinomas and to determine their relationship with clinicopathologic parameters and survival.

Archival tumor tissues from 61 patients with adenocarcinoma of lung were analyzed by immunohistochemistry for the expression of c-myc, bcl-2 and p53 proteins. Clinical information was obtained through the computerized retrospect database from the tumor registry.

Of 61 patients, 32 were men and 29 women with the median age 63 years. 4 had stage I disease, 2 had stage II disease and 55 had stage III disease. The expression of c-myc protein was identified in 13% (8/61) tumors, bcl-2 protein was detected in 1.6% tumors (1/61) and p53 was detected in 77% (47/71) tumors. The association of the expression of c-myc, bcl-2 and p53 was not detected. The survival time was longer in patients expressing c-myc protein than in patients without the c-myc protein expression (p=.045). Neither bcl-2 nor p53 showed the correlation to clinicopathologic variables.

Our data suggest the involvement of p53 alteration in the pathogenesis of lung adenocarcinoma. The c-myc expression in some tumors indicates that c-myc alone may not contribute critically to the development and/or the progression of these tumors. It, however, correlated to the survival time, suggesting the c-myc expression as a favorable prognostic factor possibly through the apoptosis pathway.