MODULATION OF PLATELET-ACTIVATING-FACTOR SYNTHESIS BY RECOMBINANT INTERFERON-ALPHA IN HUMAN RENAL-CELL CARCINOMA

Citation
M. Imagawa et al., MODULATION OF PLATELET-ACTIVATING-FACTOR SYNTHESIS BY RECOMBINANT INTERFERON-ALPHA IN HUMAN RENAL-CELL CARCINOMA, Urologia internationalis, 57(1), 1996, pp. 11-16
Citations number
20
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00421138
Volume
57
Issue
1
Year of publication
1996
Pages
11 - 16
Database
ISI
SICI code
0042-1138(1996)57:1<11:MOPSBR>2.0.ZU;2-F
Abstract
Platelet-activating factor (PAF), a potent phospholipid chemical media tor of inflammation, is involved in multiple cellular functions. Since PAF has a strong effect on platelet aggregation and on the enhancemen t of capillary permeability, it is possible that this factor plays an important role in tumor progression. In human renal cell carcinoma (RC C), it has recently been reported that immunotherapy with interferon ( IFN) is effective for the prevention of tumor recurrence and progressi on. To evaluate the role of PAF and the effect of interferon-alpha (IF N-alpha) on PAF production in RCC, we measured PAF content and the act ivity of choline phosphotransferase (CPT), an enzyme involved in the d e novo biosynthesis of PAF, in RCC specimens obtained from 30 patients who had undergone radical nephrectomy for RCC, and in specimens of no rmal renal cortex and normal renal medulla. PAF was present in both RC C and the normal renal tissues. Although CPT activity in RCC was simil ar to that in normal renal cortex, CPT activity in the normal medulla was significantly higher than that in RCC and the normal cortex. No co rrelation was found between CPT activity and the pathological findings in RCC. Although there was no difference in CPT activity in normal re nal tissues between patients treated preoperatively with IFN-alpha and those untreated, CPT activity in RCC was significantly reduced in pat ients who had received IFN-alpha compared with those who had not. Thes e findings suggest that IFN-alpha may modulate the production of PAF i n RCC patients.