QUANTITATIVE-EVALUATION OF APOPTOSIS AND PROLIFERATION IN RENAL-CELL CARCINOMA - CORRELATION TO TUMOR SUBTYPE, CYTOLOGICAL GRADE ACCORDING TO THOENES-CLASSIFICATION AND THE OCCURRENCE OF METASTASIS

Citation
W. Hindermann et al., QUANTITATIVE-EVALUATION OF APOPTOSIS AND PROLIFERATION IN RENAL-CELL CARCINOMA - CORRELATION TO TUMOR SUBTYPE, CYTOLOGICAL GRADE ACCORDING TO THOENES-CLASSIFICATION AND THE OCCURRENCE OF METASTASIS, Pathology research and practice, 193(1), 1997, pp. 1-7
Citations number
56
Categorie Soggetti
Pathology
ISSN journal
03440338
Volume
193
Issue
1
Year of publication
1997
Pages
1 - 7
Database
ISI
SICI code
0344-0338(1997)193:1<1:QOAAPI>2.0.ZU;2-C
Abstract
To analyse growth characteristics of human renal cell tumors, 66 renal cell carcinomas and one oncocytoma were investigated concerning the p roliferative activity by immunohistochemical demonstration of the Ki-6 7 antigen (clone MIB1) and the apoptotic rate using the terminal deoxy nucleotidyl-transferase mediated dUTP-fluorescin nick end labelling (T UNEL) method. The TUNEL method indicates DNA double strand breaks cons idered as a hallmark of programmed cell death (apoptosis). Apoptotic c ells were observed in 57 of 67 cases. The apoptotic rate (percentage o f stained tumor cells) varied from O% to 54.1%. GI carcinomas possesse d a statistically significant higher apoptotic rate than GII/GIII car- cinemas. The proliferation index (percentage of Ki-67 labelled cells) ranged from 0.09% to 22.3%. The well differentiated carcinomas (GI) sh owed statistically lower proliferative activity than moderate and poor ly differentiated carcinomas (GII/GII). The clear cell variant of rena l cell carcinoma expressed a higher apoptotic rate than the chromophil ic variant. A statistical correlation between apoptosis/proliferation and occurrence of metastasis could not be established. In progression from well to less differentiated renal cell carcinoma the decrease of apoptotic rate, as well as the increase of the proliferative activity, contributes to a rapid tumor growth.