PMID- 16161046
OWN - NLM
STAT- MEDLINE
DCOM- 20060302
LR  - 20220408
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 118
IP  - 5
DP  - 2006 Mar 1
TI  - EGFR protein overexpression and gene amplification in squamous cell carcinomas of 
      the esophagus.
PG  - 1173-80
AB  - Overexpression of epidermal growth factor receptor (EGFR) is observed in many 
      cancers, sometimes accompanied by gene amplification. Recently, several clinical 
      therapies targeting EGFR were developed, but the eligibility criteria for these 
      therapies is not fully established. To develop such eligibility criteria for 
      esophageal squamous cell carcinoma (ESCC), we sought to clarify: (i) the exact 
      frequency of EGFR overexpression, (ii) the relationship between protein 
      overexpression and gene amplification, (iii) the relationship between gene 
      amplification and specific gene mutations and (iv) the correlation between the 
      status of EGFR and clinical or pathological features. Immunohistochemistry 
      revealed that EGFR protein is overexpressed in 53 (50%) of the 106 ESCC examined. 
      Fluorescence in situ hybridization (FISH) indicated clear EGFR gene amplification 
      in 15 of the 53 tumors, somewhat higher EGFR copy in 32 cases, and no increase in 
      6 cases. Gene amplification was significantly associated with high level 
      overexpression. Direct sequencing of exons 19 and 21 of EGFR revealed no 
      mutations in 15 tumors exhibiting gene amplification, and no mutations in 25 
      tumors not exhibiting gene amplification. Overexpression of EGFR was 
      significantly correlated with depth of invasion of the tumor. In conclusion, 
      anti-EGFR therapies may be appropriate for patients with ESCC. We assume that 
      combined analyses by immunohistochemistry/FISH would clarify aberrations in 
      protein and gene function, and could help to identify those patients who may 
      benefit from anti-EGFR therapy.
CI  - (c) 2005 Wiley-Liss, Inc.
FAU - Hanawa, Mitsuhiko
AU  - Hanawa M
AD  - Department of Pathology, School of Medicine, University of Yamanashi, Japan.
FAU - Suzuki, Shioto
AU  - Suzuki S
FAU - Dobashi, Yoh
AU  - Dobashi Y
FAU - Yamane, Tetsu
AU  - Yamane T
FAU - Kono, Koji
AU  - Kono K
FAU - Enomoto, Nobuyuki
AU  - Enomoto N
FAU - Ooi, Akishi
AU  - Ooi A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 9007-49-2 (DNA)
RN  - EC 2.7.10.1 (ErbB Receptors)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Base Sequence
MH  - Carcinoma, Squamous Cell/*genetics/*metabolism/pathology
MH  - DNA/genetics
MH  - ErbB Receptors/genetics/*metabolism
MH  - Esophageal Neoplasms/*genetics/*metabolism/pathology
MH  - Gene Amplification/*genetics
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Middle Aged
MH  - Neoplasm Invasiveness/pathology
EDAT- 2005/09/15 09:00
MHDA- 2006/03/03 09:00
CRDT- 2005/09/15 09:00
PHST- 2005/09/15 09:00 [pubmed]
PHST- 2006/03/03 09:00 [medline]
PHST- 2005/09/15 09:00 [entrez]
AID - 10.1002/ijc.21454 [doi]
PST - ppublish
SO  - Int J Cancer. 2006 Mar 1;118(5):1173-80. doi: 10.1002/ijc.21454.