Ductal carcinomas of the prostate: a clinicopathological and immunohistochemical study

Objectives To confirm the expression of prostate specific antigen (PSA) and prostatic acid phosphatase (PAP) in ductal carcinomas of the prostate, and to analyse p53, Ki67, oestrogen (ER) and androgen (AR) receptors in these tumours. Materials and methods Paraffin‐embedded samples from 12 patients with ductal carcinoma of the prostate were assessed for pattern, mitotic count and the presence of a microacinar carcinoma component. There were six pure ductal and six mixed microacinar and ductal carcinomas. Sections were stained immunohistochemically for the expression of PSA, PAP, Ki67, p53, AR and ER. Clinical data were obtained from case notes. Results Six of the ductal tumours had a papillary pattern whilst the others had a cribriform appearance. The mitotic rates in the ductal areas were high in the tumours from eight of the 12 patients. PSA and PAP immunohistochemistry were positive in all the cases. No ER immunoreactivity was found in any of the patients. Ten of the ductal tumours showed strong reactivity with AR, the other two were weakly positive; two of the tumours were strongly positive for p53 protein. All the ductal carcinomas expressed Ki67, three having >25% nuclear marking. One patient who was strongly positive for p53 and had a high Ki67 score survived only one year after diagnosis. Survival ranged from 1 to 13 years after diagnosis. Conclusion This study confirms the expression of PSA and PAP in ductal carcinomas of the prostate. The percentage of tumours expressing p53 was similar to that published for high‐grade microacinar carcinomas. The results for Ki67 suggest that ductal tumours have higher scores than microacinar tumours, but further studies are required to ascertain if this is significantly different. As half the patients with ductal tumours had co‐existent microacinar tumours, we advise transrectal prostatic biopsies in patients diagnosed with pure ductal carcinomas on transurethral resection specimens, to exclude high‐grade microacinar carcinomas. The presence of AR and the lack of ER in all the ductal carcinomas confirms that these tumours are prostatic in origin and should be treated with anti‐androgen therapy.