title: Neuroendocrine cells in benign prostatic hyperplasia and prostatic carcinoma: effect of hormonal treatment.
abstract: The present study was undertaken to analyze the changes in neuroendocrine cells of the human prostate induced by neoplasms and the effect of hormonal treatment. Samples of human prostate (n = 47) were obtained during surgery or removal of organs for transplantation. The cases analyzed represent normal prostates (n = 4); benign prostatic hyperplasias (n = 10; prostatic carcinomas with Gleason scores of 2-4 (n = 5), 5-7 (n = 10), and 8-10 (n = 3), and prostatic carcinomas treated with hormonal therapy (n = 15). Immunohistochemistry for chromogranin A was performed, and the density of neuroendocrine cells as well as the intensity of the immunostaining within their cytoplasms were evaluated using image analysis. Neuroendocrine cells showing chromogranin A immunoreactivity were identified in all cases studied. They were localized scattered in the acini, and no differences in their morphology were observed among groups. Interestingly, chromogranin A immunoreactivity was also present in typical epithelial cells of prostatic cancer with Gleason scores ranging from 8 to 10. The density of chromogranin A immunoreactive cells was higher in neoplastic tissue with respect to the normal prostate, reaching maximal values in prostatic carcinomas with Gleason scores of 8-10 which were hormonally treated. Regarding the intensity of immunostaining in the prostatic carcinomas with Gleason scores of 8-10 only, a significant increase in relation to the other groups was found. The present results demonstrate that the neuroendocrine cells have similar morphological features and distribution in normal prostate, benign prostatic hyperplasia, and prostatic carcinoma. Their density in prostatic cancer increases following hormonal therapy and varies in relation to the tumoral degree or histological evaluation, suggesting a role of neuroendocrine cells in human prostatic cancer.
authors.affiliation: Department of Urology, San Agustin Hospital, Avilés, Spain.
authors.forename: J L
authors.initials: JL
authors.lastname: Guate
authors.forename: S
authors.initials: S
authors.lastname: Escaf
authors.forename: C L
authors.initials: CL
authors.lastname: Menendez
authors.forename: M
authors.initials: M
authors.lastname: del Valle
authors.forename: J A
authors.initials: JA
authors.lastname: Vega
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use*; D014408:Biomarkers, Tumor; D002452:Cell Count / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D053379:Chromogranin A; D002864:Chromogranins / Q000378:metabolism; D005485:Flutamide / Q000627:therapeutic use*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009490:Neurosecretory Systems / Q000378:metabolism* / Q000473:pathology; D011467:Prostate / Q000378:metabolism; D011470:Prostatic Hyperplasia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D011471:Prostatic Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology
chemical_list: D018931:Antineoplastic Agents, Hormonal; D014408:Biomarkers, Tumor; D053379:Chromogranin A; D002864:Chromogranins; D005485:Flutamide