Epidermal growth factor receptor (EGFR) expression in prostatic adenocarcinoma after hormonal therapy

A fluorescence in situ hybridization and immunohistochemical analysis

Rebecca A. Marks, Shaobo Zhang, Rodolfo Montironi, Ryan P. McCarthy, Gregory T. MacLennan, Antonio Lopez-Beltran, Zhong Jiang, Honghong Zhou, Suqin Zheng, Darrell Davidson, Lee Ann Baldridge, Liang Cheng

Research output: Contribution to journalArticle

27 Citations (Scopus)

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 rumor 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.

Original languageEnglish
Pages (from-to)919-923
Number of pages5
JournalProstate
Volume68
Issue number9
DOIs
StatePublished - Jun 15 2008

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Fluorescence In Situ Hybridization
Epidermal Growth Factor Receptor
Adenocarcinoma
erbB-1 Genes
Neoplasms
Prostatic Neoplasms
Gene Amplification
Therapeutics
Hormones
Chromosomes, Human, Pair 7
Growth
Androgens
Prostate
Proteins
Epithelium
Staining and Labeling
Gene Expression

Keywords

  • Adenocarcinoma
  • Biomarker epidermal growth factor receptor (EGFR)
  • FISH
  • Hormonal therapy
  • Prognosis
  • Prostatic neoplasia

ASJC Scopus subject areas

  • Urology

Cite this

Epidermal growth factor receptor (EGFR) expression in prostatic adenocarcinoma after hormonal therapy : A fluorescence in situ hybridization and immunohistochemical analysis. / Marks, Rebecca A.; Zhang, Shaobo; Montironi, Rodolfo; McCarthy, Ryan P.; MacLennan, Gregory T.; Lopez-Beltran, Antonio; Jiang, Zhong; Zhou, Honghong; Zheng, Suqin; Davidson, Darrell; Baldridge, Lee Ann; Cheng, Liang.

In: Prostate, Vol. 68, No. 9, 15.06.2008, p. 919-923.

Research output: Contribution to journalArticle

Marks, Rebecca A. ; Zhang, Shaobo ; Montironi, Rodolfo ; McCarthy, Ryan P. ; MacLennan, Gregory T. ; Lopez-Beltran, Antonio ; Jiang, Zhong ; Zhou, Honghong ; Zheng, Suqin ; Davidson, Darrell ; Baldridge, Lee Ann ; Cheng, Liang. / Epidermal growth factor receptor (EGFR) expression in prostatic adenocarcinoma after hormonal therapy : A fluorescence in situ hybridization and immunohistochemical analysis. In: Prostate. 2008 ; Vol. 68, No. 9. pp. 919-923.
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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 rumor 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.",
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T1 - Epidermal growth factor receptor (EGFR) expression in prostatic adenocarcinoma after hormonal therapy

T2 - A fluorescence in situ hybridization and immunohistochemical analysis

AU - Marks, Rebecca A.

AU - Zhang, Shaobo

AU - Montironi, Rodolfo

AU - McCarthy, Ryan P.

AU - MacLennan, Gregory T.

AU - Lopez-Beltran, Antonio

AU - Jiang, Zhong

AU - Zhou, Honghong

AU - Zheng, Suqin

AU - Davidson, Darrell

AU - Baldridge, Lee Ann

AU - Cheng, Liang

PY - 2008/6/15

Y1 - 2008/6/15

N2 - 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 rumor 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.

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 rumor 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.

KW - Adenocarcinoma

KW - Biomarker epidermal growth factor receptor (EGFR)

KW - FISH

KW - Hormonal therapy

KW - Prognosis

KW - Prostatic neoplasia

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DO - 10.1002/pros.20715

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JF - Prostate

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