Prostatic intraepithelial neoplasia and atypical adenomatous hyperplasia. Relationship to pathologic parameters, volume and spatial distribution of carcinoma of the prostate.
OBJECTIVE
To summarize studies that have investigated the morphologic, spatial and volumetric relationship between prostate cancer and its putative precursors, high grade prostatic intraepithelial neoplasia (HGPIN) and atypical adenomatous hyperplasia (AAH).


METHODS
Studies addressing the relationship between morphologic parameters of prostate cancer (i.e., stage, grade, volume and anatomic distribution) and both HGPIN and AAH are reviewed. Similar data based on our institutional experience with surgical and autopsy series of step-sectioned, totally embedded prostate glands are also presented.


RESULTS
Most investigators have demonstrated significant associations between HGPIN and carcinoma in terms of coexistence, "zonal" origin and physical proximity. The two lesions have a high tendency to be present simultaneously; both originate predominantly in the peripheral zone and are often found within the same microscopic field. Reports on the relationship between HGPIN and the stage of prostate cancer are less consistent, and the associations of this lesion with cancer grade and volume are exceedingly complex. HGPIN appears to be associated with moderately to poorly differentiated, smaller, often-multifocal tumors and is less frequent in large, high grade cancers. There are data suggesting a trend-of a reciprocal relationship between more extensive and diffuse HGPIN and large-volume prostate cancers. Conversely, there is a wide spectrum of volume distribution of the two lesions in glands harboring smaller tumors. Similar data concerning AAH are limited.


CONCLUSIONS
There are strong and consistent data supporting various aspects of the morphologic associations between HGPIN and prostate cancer. The indications that glands harboring larger tumors tend to contain less extensive HGPIN could raise the hypothesis that as carcinoma becomes larger, it may replace areas of the gland previously occupied by HGPIN. Alternatively, prostate cancer can evolve from ducts with HGPIN and gradually overgrow their precursor. There is a relative dearth of similar information concerning AAH.
Sakr
W A
WA
Department of Pathology, Harper Hospital, Wayne State University, Detroit, Michigan 48201, USA.
Grignon
D J
DJ
D000236:Adenoma / Q000473:pathology*; D006801:Humans; D006965:Hyperplasia; D008297:Male; D011467:Prostate / Q000473:pathology*; D019048:Prostatic Intraepithelial Neoplasia / Q000175:diagnosis / Q000473:pathology*; D011471:Prostatic Neoplasms / Q000175:diagnosis / Q000473:pathology*