title: Epidermal growth factor receptor (EGFR) expression in prostatic adenocarcinoma after hormonal therapy: a fluorescence in situ hybridization and immunohistochemical analysis.
abstract: BACKGROUND
  The progression of normal prostatic epithelium to androgen-dependent cancer and, eventually, hormone-refractory prostate cancer is a complex process involving many different growth regulatory signals. Activation of epidermal growth factor receptor (EGFR) has been implicated in prostate cancer cell growth.
  
  
  METHODS
  This study was undertaken to investigate both amplification of EGFR gene by fluorescence in situ hybridization (FISH) and over-expression of EGFR by immunohistochemical staining in prostate tissue from 71 patients treated by hormonal therapy.
  
  
  RESULTS
  EGFR gene amplification was present in 1 of 71 tumors, and polysomy of chromosome 7 was present in 24 of 71 tumors. Immunohistochemically, EGFR expression was demonstrable in 57 of 71 tumors. Membranous immunostaining for EGFR was observed in >75% of tumor cells in 11% of cases, in 51-75% of tumor cells in 20% of cases, in 26-50% of tumor cells in 21% of cases, in 11-25% of tumor cells in 21% of cases, and in 1-10% of tumor cells in 7% of cases. No immunostaining for EGFR was seen in 20% of cases. There was no correlation between EGFR protein expression and gene amplification. There was also no correlation between EGFR expression and clinicopathological characteristics or clinical outcome.
  
  
  CONCLUSIONS
  We found that EGFR gene expression was detectable in 35% of this large series of hormone-treated prostate cancer, and that EGFR protein is frequently expressed in tissue from these patients. EGFR over-expression may serve as a reasonable target for therapeutic intervention in this otherwise difficult to treat subset of prostate cancer.
authors.affiliation: Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Marks
authors.forename: Shaobo
authors.initials: S
authors.lastname: Zhang
authors.forename: Rodolfo
authors.initials: R
authors.lastname: Montironi
authors.forename: Ryan P
authors.initials: RP
authors.lastname: McCarthy
authors.forename: Gregory T
authors.initials: GT
authors.lastname: MacLennan
authors.forename: Antonio
authors.initials: A
authors.lastname: Lopez-Beltran
authors.forename: Zhong
authors.initials: Z
authors.lastname: Jiang
authors.forename: Honghong
authors.initials: H
authors.lastname: Zhou
authors.forename: Suqin
authors.initials: S
authors.lastname: Zheng
authors.forename: Darrell D
authors.initials: DD
authors.lastname: Davidson
authors.forename: Lee Ann
authors.initials: LA
authors.lastname: Baldridge
authors.forename: Liang
authors.initials: L
authors.lastname: Cheng
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics; D000368:Aged; D000369:Aged, 80 and over; D000726:Androgen Antagonists / Q000627:therapeutic use*; D004273:DNA, Neoplasm / Q000737:chemistry / Q000235:genetics; D066246:ErbB Receptors / Q000096:biosynthesis* / Q000235:genetics; D005784:Gene Amplification; D006801:Humans; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D008875:Middle Aged; D009376:Neoplasms, Hormone-Dependent / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics; D011471:Prostatic Neoplasms / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics
chemical_list: D000726:Androgen Antagonists; D004273:DNA, Neoplasm; D066246:ErbB Receptors