BACKGROUND: Our previous study showed that the growth rate of incidentally found renal cell carcinoma (RCC) varied, and that the initial clinical and pathological features did not predict subsequent growth of the carcinoma. The objective of this study was to determine the relationships between cell proliferation, apoptosis, angiogenesis and the growth rates of these RCC. METHODS: We examined cell proliferation, apoptosis, and angiogenesis in 16 incidentally found cases of RCC. Cell proliferation was assessed by immunohistochemical staining with a Ki-67 antibody. Apoptosis was assessed by the terminal deoxynucleotidyl transferase (TdT) mediated deoxy-UTP biotin nick end labeling (TUNEL) technique. The Ki-67 labeling index (KI) and the apoptotic index (AI) were determined as the ratio of immunohistochemically positive cells per 1000 cancer cells. The KI/AI ratio was also determined. Angiogenesis was evaluated by CD34 immunostaining. Finally, we investigated the correlation between these parameters and the growth rate of primary lesions of incidentally found RCC. RESULTS: The KI ranged from 7 to 73 (median, 20), AI ranged from 6 to 171 (median, 26), and microvessel density (MVD) ranged from 21 to 673 (median, 265) for incidentally found RCC. Ki-67 labeling index, AI and MVD were not closely correlated to each other. Furthermore, these parameters were not associated with growth rates of incidentally found RCC. Only the KI/AI ratio was strongly correlated to the growth rate of incidentally found RCC (r = 0.709; P = 0.0083). CONCLUSION: Our results suggest that the balance between cell proliferation and apoptosis partly determines the growth rate of primary lesions of incidentally found RCC.
BACKGROUND: Our previous study showed that the growth rate of incidentally found renal cell carcinoma (RCC) varied, and that the initial clinical and pathological features did not predict subsequent growth of the carcinoma. The objective of this study was to determine the relationships between cell proliferation, apoptosis, angiogenesis and the growth rates of these RCC. METHODS: We examined cell proliferation, apoptosis, and angiogenesis in 16 incidentally found cases of RCC. Cell proliferation was assessed by immunohistochemical staining with a Ki-67 antibody. Apoptosis was assessed by the terminal deoxynucleotidyl transferase (TdT) mediated deoxy-UTP biotin nick end labeling (TUNEL) technique. The Ki-67 labeling index (KI) and the apoptotic index (AI) were determined as the ratio of immunohistochemically positive cells per 1000 cancer cells. The KI/AI ratio was also determined. Angiogenesis was evaluated by CD34 immunostaining. Finally, we investigated the correlation between these parameters and the growth rate of primary lesions of incidentally found RCC. RESULTS: The KI ranged from 7 to 73 (median, 20), AI ranged from 6 to 171 (median, 26), and microvessel density (MVD) ranged from 21 to 673 (median, 265) for incidentally found RCC. Ki-67 labeling index, AI and MVD were not closely correlated to each other. Furthermore, these parameters were not associated with growth rates of incidentally found RCC. Only the KI/AI ratio was strongly correlated to the growth rate of incidentally found RCC (r = 0.709; P = 0.0083). CONCLUSION: Our results suggest that the balance between cell proliferation and apoptosis partly determines the growth rate of primary lesions of incidentally found RCC.
Authors: Kamila Naxerova; Carol J Bult; Anne Peaston; Karen Fancher; Barbara B Knowles; Simon Kasif; Isaac S Kohane Journal: Genome Biol Date: 2008-07-08 Impact factor: 13.583