PMID- 18409189
OWN - NLM
STAT- MEDLINE
DCOM- 20080703
LR  - 20181201
IS  - 0270-4137 (Print)
IS  - 0270-4137 (Linking)
VI  - 68
IP  - 9
DP  - 2008 Jun 15
TI  - Epidermal growth factor receptor (EGFR) expression in prostatic adenocarcinoma 
      after hormonal therapy: a fluorescence in situ hybridization and 
      immunohistochemical analysis.
PG  - 919-23
LID - 10.1002/pros.20715 [doi]
AB  - 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.
FAU - Marks, Rebecca A
AU  - Marks RA
AD  - Department of Pathology and Laboratory Medicine, Indiana University School of 
      Medicine, Indianapolis, Indiana, USA.
FAU - Zhang, Shaobo
AU  - Zhang S
FAU - Montironi, Rodolfo
AU  - Montironi R
FAU - McCarthy, Ryan P
AU  - McCarthy RP
FAU - MacLennan, Gregory T
AU  - MacLennan GT
FAU - Lopez-Beltran, Antonio
AU  - Lopez-Beltran A
FAU - Jiang, Zhong
AU  - Jiang Z
FAU - Zhou, Honghong
AU  - Zhou H
FAU - Zheng, Suqin
AU  - Zheng S
FAU - Davidson, Darrell D
AU  - Davidson DD
FAU - Baldridge, Lee Ann
AU  - Baldridge LA
FAU - Cheng, Liang
AU  - Cheng L
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Prostate
JT  - The Prostate
JID - 8101368
RN  - 0 (Androgen Antagonists)
RN  - 0 (DNA, Neoplasm)
RN  - EC 2.7.10.1 (ErbB Receptors)
SB  - IM
MH  - Adenocarcinoma/drug therapy/*enzymology/genetics
MH  - Aged
MH  - Aged, 80 and over
MH  - Androgen Antagonists/*therapeutic use
MH  - DNA, Neoplasm/chemistry/genetics
MH  - ErbB Receptors/*biosynthesis/genetics
MH  - Gene Amplification
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Middle Aged
MH  - Neoplasms, Hormone-Dependent/drug therapy/*enzymology/genetics
MH  - Prostatic Neoplasms/drug therapy/*enzymology/genetics
EDAT- 2008/04/15 09:00
MHDA- 2008/07/04 09:00
CRDT- 2008/04/15 09:00
PHST- 2008/04/15 09:00 [pubmed]
PHST- 2008/07/04 09:00 [medline]
PHST- 2008/04/15 09:00 [entrez]
AID - 10.1002/pros.20715 [doi]
PST - ppublish
SO  - Prostate. 2008 Jun 15;68(9):919-23. doi: 10.1002/pros.20715.