title: Progesterone receptor expression in human prostate cancer: correlation with tumor progression.
abstract: BACKGROUND
  The recent discovery of the classical estrogen receptor alpha (ERalpha) in metastatic and recurrent prostatic adenocarcinoma suggests that estrogens are implicated in prostate cancer progression.
  
  
  METHODS
  To get more insight into estrogen signaling in prostate cancer tissue, the current study has examined the immunoprofile of the estrogen-inducible progesterone receptor (PR), and evaluated its relation to ERalpha gene expression.
  
  
  RESULTS
  In primary tumors, the PR was detectable in 36% of primary Gleason grade 3 (5 of 14 cases), 33% of primary Gleason grade 4 (5 of 15 cases), and in 58% of primary Gleason grade 5 tumors (7 of 12 cases). None of the 41 primary tumors investigated revealed significant PR expression in more than 50% of tumor cells. Conversely, moderate to strong receptor expression was observed in 60% of metastatic lesions (9 of 15 cases), and in 54% of androgen-insensitive tumors (38 of 71 cases). Irrespective of grades and stages, the presence of the PR was invariably associated with high steady state levels of ERalpha mRNA, whereas the ERalpha protein was undetectable by immunohistochemistry (IHC) in a significant number of cases (58 of 97 cases).
  
  
  CONCLUSIONS
  The progressive emergence of the PR during tumor progression obviously reflects the ability of metastatic and androgen-insensitive tumors to use estrogens through a ERalpha-mediated pathway. The present data provide a theoretical background for studying the efficiency of antiestrogens and antigestagens in the medical treatment of advanced prostate cancer.
authors.affiliation: Institute of Pathology, University of the Saarland, Homburg/Saar, Germany. pahbon@med-rz.uni-sb.de
authors.forename: H
authors.initials: H
authors.lastname: Bonkhoff
authors.forename: T
authors.initials: T
authors.lastname: Fixemer
authors.forename: I
authors.initials: I
authors.lastname: Hunsicker
authors.forename: K
authors.initials: K
authors.lastname: Remberger
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism* / Q000556:secondary; D001859:Bone Neoplasms / Q000235:genetics / Q000378:metabolism / Q000556:secondary; D018450:Disease Progression; D047628:Estrogen Receptor alpha; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008198:Lymph Nodes / Q000378:metabolism; D008297:Male; D009364:Neoplasm Recurrence, Local / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis / Q000235:genetics; D011960:Receptors, Estrogen / Q000096:biosynthesis* / Q000235:genetics; D011980:Receptors, Progesterone / Q000032:analysis / Q000096:biosynthesis*; D018709:Statistics, Nonparametric
chemical_list: D047628:Estrogen Receptor alpha; D012333:RNA, Messenger; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone