Stability of the Glycoprotein A-80 in Prostatic Carcinoma Subsequent to Androgen Deprivation Therapy

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Abstract
Androgen deprivation therapy (ADT) results in profound morphologic changes in the benign and malignant prostatic epithelium, including acinar shrinkage and distortion, cytoplasmic clearing, and nuclear hyperchromatism. Data on the immunophenotype of prostatic carcinoma following ADT are limited. A-80 is an oncodevelopmental, mucinous glycoprotein that is strongly and consistently upregulated in high-grade prostatic intraepithelial neoplasia and adenocarcinoma; its expression following ADT has not been investigated. We applied a monoclonal antibody to A-80 to paraffin sections of 54 prostatic carcinomas surgically removed after ADT (Leupron with or without flutamide) and found immunoreactions in 53 of 54 samples (98%). Intense staining was seen in cancer glands, solid aggregates, single cells, and mucinous pools as well as in poorly defined acini lined by shrunken and distorted cells that were difficult to identify as malignant. Hemangiopericytoma-like areas showed A-80 staining in the lumina. Normal, metaplastic, hyperplastic, and atrophic ducts were not similarly reactive. Our findings indicate that there is remarkable stability of the upregulated A-80 glycoprotein in prostatic adenocarcinoma after ADT, despite severe architectural and cytologic alterations. The A-80-reactive colloid pools may reflect ruptured neoplastic glands and spillage of secreted material into stromal spaces. Strong A-80 staining, combined with sporadic cytokeratin reactions in the lumina of hemagiopericytomatous areas, suggests that these are souvenirs of carcinomatous glands revealed by antigenic relics of their component cells. The persistence of A-80 immunoreactivity provides a useful marker for recognizing and monitoring prostatic carcinoma after ADT.