PMID- 18302229
OWN - NLM
STAT- MEDLINE
DCOM- 20080620
LR  - 20181201
IS  - 0270-4137 (Print)
IS  - 0270-4137 (Linking)
VI  - 68
IP  - 8
DP  - 2008 Jun 1
TI  - Gene amplification and mutation analysis of epidermal growth factor receptor in 
      hormone refractory prostate cancer.
PG  - 803-8
LID - 10.1002/pros.20743 [doi]
AB  - BACKGROUND: Amplification and mutation of the epidermal growth factor receptor 
      (EGFR) and Her-2 genes were analyzed in both hormone sensitive and hormone 
      refractory prostate cancer (HRPC). METHODS: Gene amplifications of EGFR and Her-2 
      were analyzed by fluorescence in situ hybridization (FISH) with direct 
      sequencing. Studies were performed on a total of 10 patients; tissues were 
      sampled at the time of initial diagnosis and after the conversion to HRPC (a 
      total of 20 tissue samples). Direct sequencing was performed on exons 18-24 of 
      EGFR and exons 19 and 20 of Her-2. Amplification and mutation were compared with 
      clinicopathologic features. RESULTS: Gene amplification of EGFR was observed in 6 
      (30%) out of 20 samples. A total of six EGFR mutations in exons 18 and 19 were 
      detected in three pairs of tissues (three patients). One patient, with hormone 
      refractory status, had a novel deletion mutation in EGFR exon 19. EGFR mutations 
      were associated with the acinar type of prostate cancer but were not associated 
      with the ductal type. No significant correlation was found between mutation 
      change and hormone sensitive or refractory status. However, the time to convert 
      to HRPC was significantly shorter in the patients with a mutation in the EGFR 
      gene (P = 0.017). There were no Her-2 gene amplifications or mutations found in 
      any of the samples. CONCLUSIONS: EGFR gene mutation and amplification occurred 
      frequently in advanced prostate cancer cases. EGFR mutations do not appear to 
      play a significant role in the hormone refractory pathway but are associated with 
      prognosis.
CI  - (c) 2008 Wiley-Liss, Inc.
FAU - Cho, Kang Su
AU  - Cho KS
AD  - Department of Urology & Urological Science Institute, Yonsei University College 
      of Medicine, Seoul, Korea.
FAU - Lee, Joong Shik
AU  - Lee JS
FAU - Cho, Nam Hoon
AU  - Cho NH
FAU - Park, Kyeongmee
AU  - Park K
FAU - Ham, Won Sik
AU  - Ham WS
FAU - Choi, Young Deuk
AU  - Choi YD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Prostate
JT  - The Prostate
JID - 8101368
RN  - 0 (Antineoplastic Agents, Hormonal)
RN  - EC 2.7.10.1 (ErbB Receptors)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Antineoplastic Agents, Hormonal/therapeutic use
MH  - DNA Mutational Analysis
MH  - ErbB Receptors/*genetics
MH  - *Gene Amplification
MH  - Genes, erbB-2
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Mutation
MH  - Neoplasms, Hormone-Dependent/drug therapy/*genetics
MH  - Prognosis
MH  - Prostatic Neoplasms/diagnosis/drug therapy/*genetics
EDAT- 2008/02/28 09:00
MHDA- 2008/06/21 09:00
CRDT- 2008/02/28 09:00
PHST- 2008/02/28 09:00 [pubmed]
PHST- 2008/06/21 09:00 [medline]
PHST- 2008/02/28 09:00 [entrez]
AID - 10.1002/pros.20743 [doi]
PST - ppublish
SO  - Prostate. 2008 Jun 1;68(8):803-8. doi: 10.1002/pros.20743.