Multiple Immunoperoxidase Markers in Benign Hyperplasia and Adenocarcinoma of the Prostate

Abstract

A series of 60 cases of prostatic adenocarcinoma and 34 cases of benign prostatic hyperplasia were examined quantitatively after immunoperoxidase staining for prostate-specific antigen (PSA), prostate-specific acid phosphatase (PSAP), carcino-embryonic antigen (CEA), epithelial membrane antigen (EMA), alpha fetoprotein (AFP), and human chorionic gonadotrophin (HCG). The tumors were graded I to IV according to the MDAH grading system recently proposed. Fifty-nine of the 60 tumors were positive for PSA and 58 were positive for PSAP. The one PSA and PSAP negative case was CEA negative and weakly EMA positive. Grade I to III tumors stained more tumor cells and more diffusely for PSA and PSAP than grade IV tumors. There was no significant difference in the intensity or extent of staining between grade I and grade II-III tumors for PSA and PSAP. A comparison of PSA and PSAP showed that PSA stained more intensely and more extensively than PSAP. Benign prostatic tissue and low-grade prostatic tumors did not stain for CEA but three of the 20 grade IV tumors and one of the 23 grade II-III tumors did. Staining for EMA was focal and showed no relation to tumor grade. Benign and malignant lesions failed to stain for AFP and HCG.

Immunophenotypic Characterization of Benign and Malignant Prostatic Lesions

“…Immunophenotyping revealed strong PSA staining for benign lesions as reported by others [8]. In atrophic glands and foci of inflammation, negativity may raise the possibility of carcinoma but morphological correlation solves the issue.…”

“…The diagnosis of the spectrum of preneoplastic and neoplastic lesions is being rendered more objective by the use of immunohistochemistry for phenotyping and prognosticating biologic behaviour. These include markers of differentiation like prostate specific antigen (PSA) and chromogranin, functional alterations (transglutaminase), loss of basal cell layer around glands (high molecular weight cytokeratin HMWCK), proliferative potential (cell-cycle associated proteins like proliferating cell nuclear antigen (PCNA) [8,9], cell death (apoptosis)) and tumour microvasculature (CD 34) [10]. This study was undertaken to assess the pathologic features and determinants of prostate cancer in Indian patients that would provide an insight into its appearance and behaviour.…”

Outcomes in patients with Gleason score 8–10 prostate cancer: relation to preoperative PSA level

“…Thus, a growing tumour does not substantially increase serum PSA levels [19]. As such, high‐grade CaP stains for PSA less intensely than lower‐grade cancers [18,20–23], and the intensity of PSA staining correlates inversely with histological grade of the tumour ( P < 0.001) [18].…”

The monoclonal antibody 7E12H12 can differentiate primary adenocarcinoma of the bladder and prostate

“…Immunohistochemical localization of PSA has proved effective both for detecting normal and neoplastic prostatic epithelial cells, but has also been shown to be useful for the identification of metastatic prostatic tumours whose origin cannot be confirmed by histological criteria alone [ 15]. However, it has been estimated that 5–10% of poorly differentiated prostate adenocarcinomas that show no glandular formation will be negative for PSA or PSAP [ 16, 17]. Furthermore, some of these will show only focal positivity, and when limited samples are obtained, such as by transurethral resection, false‐negatives may result.…”