Literature DB >> 1712748

Microcarcinoma in the prostate: its association with duct-acinar dysplasia.

J E McNeal1, A Villers, E A Redwine, F S Freiha, T A Stamey.   

Abstract

In a series of 100 prostatectomy specimens obtained for adenocarcinoma, 107 additional incidental microscopic (less than 0.05 cm3) carcinomas were identified. Their morphologic features including location, histologic grade, and associated premalignant changes were documented. In 51 cases there was strong evidence of transition between microcarcinoma and the premalignant lesion, duct-acinar dysplasia. Invasive cancer was usually related to dysplasia through a characteristic intermediate morphologic stage of transitive glands. These glands were smaller than prostatic ducts; they appeared to arise by budding from dysplastic duct walls and showed the same distinctive lining epithelium. They were distinguished from invasive glands by their pseudo-stratified epithelial lining and by consistent association with a sparse, discontinuous basal cell layer. Cytoplasmic differentiation at the point of junction of invasive cancer with transitive or dysplastic glands was studied by immunohistochemical staining for the differentiation markers prostate-specific antigen and pepsinogen II, and staining for mucin. Markedly reduced cytoplasmic differentiation was common in dysplastic and transitive glands. Invasion often coincided with an abrupt increase in cytoplasmic differentiation with expression of ectopic differentiation products. This sequence of biologic changes should be tested in other carcinomas where the exact point of invasion can be identified.

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Year:  1991        PMID: 1712748     DOI: 10.1016/0046-8177(91)90286-x

Source DB:  PubMed          Journal:  Hum Pathol        ISSN: 0046-8177            Impact factor:   3.466


  14 in total

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2.  Transient neonatal estrogen exposure to estrogen-deficient mice (aromatase knockout) reduces prostate weight and induces inflammation in late life.

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Review 3.  Molecular alterations in prostate cancer as diagnostic, prognostic, and therapeutic targets.

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4.  Differential expression of cytokeratin mRNA and protein in normal prostate, prostatic intraepithelial neoplasia, and invasive carcinoma.

Authors:  Y Yang; J Hao; X Liu; B Dalkin; R B Nagle
Journal:  Am J Pathol       Date:  1997-02       Impact factor: 4.307

Review 5.  Precursor lesions for prostate cancer.

Authors:  M R Feneley; C Busch
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6.  Heterogeneous clinicopathological features of intraductal carcinoma of the prostate: a comparison between "precursor-like" and "regular type" lesions.

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Review 7.  The significance of atypical adenomatous hyperplasia and prostatic intraepithelial neoplasia for the development of prostate carcinoma. An update.

Authors:  B G Helpap; D G Bostwick; R Montironi
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Review 8.  Precursor lesions to prostatic adenocarcinoma.

Authors:  Jonathan I Epstein
Journal:  Virchows Arch       Date:  2008-12-02       Impact factor: 4.064

9.  Molecular evidence that invasive adenocarcinoma can mimic prostatic intraepithelial neoplasia (PIN) and intraductal carcinoma through retrograde glandular colonization.

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10.  Integrin alpha 5 beta 1 expression negatively regulates cell growth: reversal by attachment to fibronectin.

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