D. Kamel et al., PROLIFERATING CELL NUCLEAR ANTIGEN BUT NOT P53 OR HUMAN PAPILLOMAVIRUS DNA CORRELATES WITH ADVANCED CLINICAL STAGE IN RENAL-CELL CARCINOMA, Histopathology, 25(4), 1994, pp. 339-347
In this study we investigated 56 renal cell carcinomas immunohistochem
ically for the expression of proliferating cell nuclear antigen (PCNA)
and tumour suppressor protein p53. We also analyzed for the presence
of human papilloma virus (HPV) DNA subtypes 6, 11, 16, 18, 31 and 33 b
y in situ hybridization. In carcinomas which showed more than 10% of P
CNA positive nuclei there were significantly more cases with invasion
(P = 0.032) or metastatic disease (P = 0.047). Nine out of 22 grade II
I-IV tumours (40.9%) but only six out of 30 grade I-II tumours (20%) s
howed more than 10% of PCNA positive cells (P = 0.097). Patients with
10% or more PCNA positive cells in kidney tumours had more advanced di
sease at the time of diagnosis than those showing less PCNA positive c
ells (P = 0.05). Six p53 positive cases were found among 56 tumours (1
1%), but only one case had more than 10% positive cell nuclei. The pre
sence of HPV DNA was found in 29 out of 56 cases (52%). Multiple subty
pes were found in 19 cases (34%). The most commonly occurring subtypes
were 18 and 33. There was no association between PCNA, p53 and the pr
esence of HPV DNA subtypes. Because of the association of PCNA with in
vasion and metastatic disease, it would be worth while to study PCNA f
urther as a possible marker for aggressiveness of renal carcinomas. Bo
th this study and those concentrated on mutational analysis suggest th
at p53 is generally not important for the development of renal cell ca
rcinoma. On the other hand, the presence of HPV DNA in these tumours i
mplicates HPV viral infection in the aetiology of renal cancer.