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Pathologica. 1994 Apr;86(2):128-41.

A theoretical rationale on the histogenesis of premalignant lesions and early carcinoma of the prostate.

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  • 1Dipartimento di Patologia Umana ed Ereditaria, Universit√† degli Studi di Pavia.


Several localized non-malignant and dysplastic glandular proliferations of the prostate mimick well-differentiated invasive prostatic microcarcinoma (PMC). However, the basal cell layer (BCL) is intact and evident in benign hyperplasias and lacking in PMC; consequently, immunohistochemical reactions for BCL, by means of keratin 903 antibody, are essential for distinguishing PMC from cribriform clear cell hyperplasia (CCCH), typical tubular hyperplasia and tubular transitional metaplasia, tubular, microtubular and cribriform basal cell hyperplasias, post-undeveloped prepuberal (PUPPUH), florid (FH) and mesonephric remnant hyperplasias. Moreover, the hyperplastic basal cells are also immunostained for prostatic specific antigen (PSA). The identification of myoepithelial cells (positive for keratin 903, actin and S100 protein antibodies) allow the diagnosis of prostatic sclerosing adenosis. Basement membrane (BM) and BCL are focally absent in post-atrophic hyperplasia (PAH), PUPPUH, FH and in extratubulo-alveolar gemmations of dysplasic lesions such as prostatic intraepithelial neoplasia (PIN), adenomatous atypical hyperplasia (AAH) and adenosis, where hypercromatic nuclei and enlarged nucleoli are the most important cytological criteria for defining malignant changes. Two putative oncogenic stages have been identified in the present work on these morphological grounds by critically examining the histogenetic hypoteses given in the literature on PMC precursors. The first is characterized by precancerous conditions such as PAH, PUPPUH, CCCH and FH that may become dysplastic though not necessarily; the second includes precancerous lesions, namely atypical tubulo-alveolar budding-in or budding-off as PIN and AAH, respectively, that may evolve towards PMC. The histogenesis of rare prostatic carcinomas are also considered. Basal cell and adenoid-cyst carcinomas seem to originate from atypical basal cell proliferations and metaplastic (transitional, adenosquamous, mucinous) carcinomas from basal and columnar-cells. Transitional and endometrioid carcinomas affect the mesonephric part of the prostate. Prostatic endocrine cells may give rise to carcinoid tumors, whereas some well-differentiated or anaplastic carcinomas may present more or less numerous endocrine cells and/or Paneth-like cells by means of a prosoplastic and ketaplastic process from neoplastic elements that underwent a stem cell backward differentiation.

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