AIM: To investigate the expression of the KIT/stem cell factor (SCF) axis in different renal cell carcinoma subtypes with regard to targeted therapies. MATERIALS AND METHODS: The expression of KIT and SCF were immunhistochemically assessed in 40 clear cell (ccRCC), 25 papillary (pRCC) and 19 chromophobe carcinomas (chRCC); 27 oncocytomas and 32 benign kidney parenchyma specimens differentiated into distal tubules (DT) and proximal tubules (PT). RESULTS: The expression of KIT was significantly higher in chRCC and oncocytoma compared to ccRCC and pRCC. All tumours exhibited a significant increase of membranous to cytoplasmic KIT expression, with the highest in ccRCC and pRCCs. SCF was expressed in all tumour subgroups, with the highest in oncocytomas and pRCC. SCF correlated positively with the cytoplasmic expression of KIT. A higher tumour stage correlated to lower KIT expression in ccRCC. CONCLUSION: Simultaneous expression of SCF and KIT in renal tumours, which seems to undergo a shift from the cytoplasm to the cell membrane, suggests paracrine and autocrine mechanisms in KIT activation, with different, as yet unknown, regulatory mechanisms in the different tumour entities.
AIM: To investigate the expression of the KIT/stem cell factor (SCF) axis in different renal cell carcinoma subtypes with regard to targeted therapies. MATERIALS AND METHODS: The expression of KIT and SCF were immunhistochemically assessed in 40 clear cell (ccRCC), 25 papillary (pRCC) and 19 chromophobe carcinomas (chRCC); 27 oncocytomas and 32 benign kidney parenchyma specimens differentiated into distal tubules (DT) and proximal tubules (PT). RESULTS: The expression of KIT was significantly higher in chRCC and oncocytoma compared to ccRCC and pRCC. All tumours exhibited a significant increase of membranous to cytoplasmic KIT expression, with the highest in ccRCC and pRCCs. SCF was expressed in all tumour subgroups, with the highest in oncocytomas and pRCC. SCF correlated positively with the cytoplasmic expression of KIT. A higher tumour stage correlated to lower KIT expression in ccRCC. CONCLUSION: Simultaneous expression of SCF and KIT in renal tumours, which seems to undergo a shift from the cytoplasm to the cell membrane, suggests paracrine and autocrine mechanisms in KIT activation, with different, as yet unknown, regulatory mechanisms in the different tumour entities.