PMID- 20518902
OWN - NLM
STAT- MEDLINE
DCOM- 20100902
LR  - 20181201
IS  - 1440-1827 (Electronic)
IS  - 1320-5463 (Linking)
VI  - 60
IP  - 6
DP  - 2010 Jun
TI  - Gene amplification of ERBB2 and EGFR in adenocarcinoma in situ and intramucosal 
      adenocarcinoma of Barrett's esophagus.
PG  - 466-71
LID - 10.1111/j.1440-1827.2010.02545.x [doi]
AB  - We examined 11 cases of carcinoma arising from Barrett's esophagus consisting of 
      two adenocarcinomas in situ (ACIS), two intramucosal adenocarcinomas, and seven 
      overt invasive adenocarcinomas. Overexpression of p53 (implying a mutation of the 
      p53 gene), ERBB2, and EGFR was measured by immunohistochemistry, and gene 
      amplification of ERBB2 and EGFR was measured by fluorescence in situ 
      hybridization (FISH). In all cases of ACIS and the intramucosal adenocarcinomas, 
      almost all cancer cells overexpressed p53, however the populations overexpressing 
      ERBB2 and EGFR varied in different cases: in one ACIS, ERBB2 was coexpressed in 
      all the cancer cells, in the other ACIS and one intramucosal adenocarcinoma, 
      ERBB2 was overexpressed in about 50% and only 10% of the p53-positive cells 
      respectively. EGFR was co-expressed in 20% in the other intramucosal 
      adenocarcinoma. Protein overexpression of ERBB2 or EGFR corresponded to the 
      amplification of their respective genes on a cell by cell basis. These gene 
      amplifications, however, were not found in the seven invasive adenocarcinomas. 
      Thus we speculate that the gene amplification occurred late in the 
      dysplasia-carcinoma sequence probably after the mutation of p53. Furthermore, new 
      clonal expansion accompanied by tumor invasion might have extinguished the 
      originally amplified genes in these tumors.
FAU - Ooi, Akishi
AU  - Ooi A
AD  - Department of Molecular and Cellular Pathology, Kanazawa University Graduate 
      School of Medical Science, Kanazawa, Ishikawa, Japan. aooi@med.kanazawa-u.ac.jp
FAU - Zen, Yoh
AU  - Zen Y
FAU - Ninomiya, Itasu
AU  - Ninomiya I
FAU - Tajiri, Ryousuke
AU  - Tajiri R
FAU - Suzuki, Shioto
AU  - Suzuki S
FAU - Kobayashi, Hideaki
AU  - Kobayashi H
FAU - Imoto, Issei
AU  - Imoto I
FAU - Dobashi, Yoh
AU  - Dobashi Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Australia
TA  - Pathol Int
JT  - Pathology international
JID - 9431380
RN  - 0 (Tumor Suppressor Protein p53)
RN  - EC 2.7.10.1 (EGFR protein, human)
RN  - EC 2.7.10.1 (ERBB2 protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
SB  - IM
MH  - Adenocarcinoma/*genetics/metabolism/pathology
MH  - Barrett Esophagus/*genetics/metabolism/pathology
MH  - Carcinoma in Situ/*genetics/metabolism/pathology
MH  - ErbB Receptors/*genetics/metabolism
MH  - Esophagus/metabolism/pathology
MH  - *Gene Amplification
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence
MH  - Mucous Membrane/metabolism/pathology
MH  - Neoplasm Invasiveness/genetics
MH  - Receptor, ErbB-2/*genetics/metabolism
MH  - Tumor Suppressor Protein p53/genetics/metabolism
EDAT- 2010/06/04 06:00
MHDA- 2010/09/03 06:00
CRDT- 2010/06/04 06:00
PHST- 2010/06/04 06:00 [entrez]
PHST- 2010/06/04 06:00 [pubmed]
PHST- 2010/09/03 06:00 [medline]
AID - PIN2545 [pii]
AID - 10.1111/j.1440-1827.2010.02545.x [doi]
PST - ppublish
SO  - Pathol Int. 2010 Jun;60(6):466-71. doi: 10.1111/j.1440-1827.2010.02545.x.