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Journal of Clinical Pathology logoLink to Journal of Clinical Pathology
. 2000 Sep;53(9):655–665. doi: 10.1136/jcp.53.9.655

Morphological identification of the patterns of prostatic intraepithelial neoplasia and their importance

R Montironi 1, R Mazzucchelli 1, F Algaba 1, A Lopez-Beltran 1
PMCID: PMC1731241  PMID: 11041054

Abstract

High grade prostatic intraepithelial neoplasia (PIN) is the most likely precursor of prostatic carcinoma. PIN has a high predictive value as a marker for carcinoma, and its identification in biopsy specimens warrants repeat biopsy for concurrent or subsequent carcinoma. The only methods of detection are biopsy and transurethral resection; PIN does not greatly raise the concentration of serum prostate specific antigen (PSA) or its derivatives, does not induce a palpable mass, and cannot be detected by ultrasound. Androgen deprivation decreases the prevalence and extent of PIN, suggesting that this form of treatment might play a role in chemoprevention. Radiotherapy is also associated with a decreased incidence of PIN.

Key Words: prostate • prostatic intraepithelial neoplasia • intraductal dysplasia • intraductal carcinoma • atypical adenomatous hyperplasia • prostatic adenocarcinoma • chemoprevention

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Figure 1 Normal prostate. The duct is lined by a two cell layer—for example, the basal cell and the secretory or lumenal cell layers.

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Figure 2 Low grade prostatic intraepithelial neoplasia. The nuclei of the secretory cells are enlarged, vary in size, have a normal or slightly increased chromatin content, and possess small or inconspicuous nucleoli. The basal cell layer is almost intact.

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Figure 3 High grade prostatic intraepithelial neoplasia with cribriform pattern. The perimeter cells show features of clearly dysplastic cells, whereas, going from the periphery towards the centre, the nuclei become smaller and the nucleoli become less apparent ("maturation phenomenon"). The basal cell layer is disrupted.

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Figure 4 Inraductal carcinoma. The glandular unit is filled by a cell mass perforated by crisp, neatly punched out spaces of regular size.

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Figure 5 Transition from normal epithelium to prostate cancer with and without an intermediate morphological stage identifiable as prostatic intraepithelial neoplasia.49 GST, glutathione S-transferase; Rb1, retinoblastoma 1.

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Figure 6 Prostatic intraepithelial neoplasia (PIN) following androgen ablation. Secretory cell type stratification is present. However, crowding is less evident than in untreated high grade PIN. The cells show cytoplasmic clearing and enlargement as a result of the coalescence of vacuoles and the rupture of cell membranes. The nucleoli are inconspicuous.

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Figure 7 High grade prostatic intraepithelial neoplasia with early invasion. Direct invasion into the stroma by a small tubular malignant gland, which appeared to originate abruptly from a dysplastic duct wall (arrow).

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