IMMUNOMORPHOLOGICAL CHARACTERISTICS OF RENAL-CELL CARCINOMA

Immunomorphological characteristics of 27 renal cell carcinoma (RCC): 18 clear cell, 6 granular (chromophilic), 2 chromophobe, 1 spindle cel l (sarcomatoid) as well as of 1 oncocytoma, were analyzed. The investi gation was performed on cryostat sections by immunoperoxidase techniqu e applying a panel of monoclonal antibodies which defined: proximal (T NE3, TN5, 5D9) and distal (TN8, TN9, 7C2) tubular antigens; intercellu lar adhesion molecule I (ICAM1); HLA class LI (-DQ, -DR and -DP) antig ens, intermediary filaments (cytokeratin and vimentin); and antigens o n tumour infiltrating mononuclear leucocytes (TT1, TT2 and LeuM3 for C D4, CD8 and CD14 antigens, respectively). All RCC with exception of ch romophobe co-expressed cytokeratin and vimentin. In addition, they wer e usually positive for all proximal and two distal tubular markers (TN 8, TN9) indicating primitive cells which could differentiate into the epithelium of both parts of tubule system as the most probable origina tors of in RCC. Almost all RCC but the chromophobe aberrantly expresse d HLA class II antigens which great variability from case to case. The presence of HLA-DR antigens was more intensive and widespread than of HLA-DQ and-DP antigens. Expression of ICAM1 mostly correlated with pr esence of HLA class II antigens, particularly with -DR on tumour cells of RCC. HLA-DR antigen expression was always more prominent than mono nuclear cell infiltrate (among which macrophages prevailed over T cell s) which could suggest that increased histocompatibility antigen expre ssion precedes mononuclear cell influx. In contrast to all other RCC, chromophobe tumours had quite distinct features revealing the most int ense reaction with 7C2 (MAb that produced the weakest reaction with ot her tumour types), absence of vimentin and very weak reaction with ant ibodies for HLA class II Ag and ICAM1. Since oncocytoma has similar im munohistological properties it could be supposed that both tumours hav e common histogenesis.