D J Grignon1, W A Sakr. 1. Department of Pathology, Harper Hospital, Karmanos Cancer Institute, Detroit, Mich., USA.
Abstract
AIMS: The aim of this report is to review the literature concerning atypical adenomatous hyperplasia (AAH) with specific regard to evidence in support of or refuting its role as a precursor lesion for prostatic adenocarcinoma. METHODS: The available literature was collected and critically reviewed. In addition, recently reported (abstract) but as yet unpublished data were included. Particular attention was focused on biological studies. RESULTS: There is considerable morphologic evidence suggesting that AAH is associated with low-grade (Gleason patterns 1 and 2) adenocarcinoma arising in the transition zone. Only limited biologic studies have been performed. There is weak and limited data to indicate that AAH has a proliferation rate higher than hyperplasia but lower than adenocarcinoma. AAH is diploid, as are most examples of low-grade adenocarcinoma. A few markers (blood group antigens, peanut agglutinin) show similar patterns of expression in AAH and adenocarcinoma while others (carbohydrate D-galactose-N-acetyl-D-galactosamine) do not. Recent cytogenetic analyses have detected abnormalities of chromosome 8 in a very small proportion (4-6%) of cases of AAH studied. CONCLUSIONS: Presently, the only strong evidence linking AAH to adenocarcinoma is morphologic. The few biologic and molecular/cytogenetic studies performed have not provided convincing evidence to support or refute this possibility. Additional studies are required. Finally, in comparative studies of AAH with adenocarcinoma, the latter should include low-grade transition zone tumors.
AIMS: The aim of this report is to review the literature concerning atypical adenomatous hyperplasia (AAH) with specific regard to evidence in support of or refuting its role as a precursor lesion for prostatic adenocarcinoma. METHODS: The available literature was collected and critically reviewed. In addition, recently reported (abstract) but as yet unpublished data were included. Particular attention was focused on biological studies. RESULTS: There is considerable morphologic evidence suggesting that AAH is associated with low-grade (Gleason patterns 1 and 2) adenocarcinoma arising in the transition zone. Only limited biologic studies have been performed. There is weak and limited data to indicate that AAH has a proliferation rate higher than hyperplasia but lower than adenocarcinoma. AAH is diploid, as are most examples of low-grade adenocarcinoma. A few markers (blood group antigens, peanut agglutinin) show similar patterns of expression in AAH and adenocarcinoma while others (carbohydrate D-galactose-N-acetyl-D-galactosamine) do not. Recent cytogenetic analyses have detected abnormalities of chromosome 8 in a very small proportion (4-6%) of cases of AAH studied. CONCLUSIONS: Presently, the only strong evidence linking AAH to adenocarcinoma is morphologic. The few biologic and molecular/cytogenetic studies performed have not provided convincing evidence to support or refute this possibility. Additional studies are required. Finally, in comparative studies of AAH with adenocarcinoma, the latter should include low-grade transition zone tumors.