PMID- 14611676
OWN - NLM
STAT- MEDLINE
DCOM- 20040803
LR  - 20190513
IS  - 1347-9032 (Print)
IS  - 1347-9032 (Linking)
VI  - 94
IP  - 11
DP  - 2003 Nov
TI  - Different expression patterns of KIT, EGFR, and HER-2 (c-erbB-2) oncoproteins 
      between epithelial and mesenchymal components in uterine carcinosarcoma.
PG  - 986-91
AB  - Uterine carcinosarcoma histologically comprises the components of epithelial and 
      mesenchymal malignancies, and is known to be clinically highly aggressive. To 
      reveal the significance of the expression of tyrosine-kinase-receptor-type 
      oncoproteins in this tumor type, the incidence and distribution of the KIT, EGFR, 
      and HER-2 (c-erbB-2) oncoproteins were immunohistochemically examined in 16 
      surgically resected cases. For 6 cases, the EGFR and HER-2 amplifications were 
      also examined by fluorescence in situ hybridization (FISH). In the epithelial 
      component, overexpressions of KIT, EGFR, and HER-2 were detected in 4 (25%), 5 
      (31%), and 9 (56%) cases, respectively, whereas these overexpressions in the 
      mesenchymal component were detected in 6 (38%), 8 (50%), and 1 (6%) cases, 
      respectively. KIT and EGFR were co-overexpressed in the mesenchymal component of 
      4 cases and in the epithelial component of 2 cases. However, HER-2 overexpression 
      was mostly detected in the epithelial component only, and tended to occur 
      independently of KIT and/or EGFR overexpression. By FISH, one of the 4 cases with 
      HER-2 overexpression showed low-level gene amplification. In two cases with EGFR 
      overexpression, the gain of EGFR alleles and/or polyploidization of chromosome 7 
      had occurred. The expression patterns of KIT, EGFR, and HER-2 differed between 
      the epithelial and mesenchymal components, and the regulation of their expression 
      appeared important in the acquisition of mesenchymal metaplasia in uterine 
      carcinosarcoma. Structural and/or numerical alterations of chromosomes might be 
      in part involved in EGFR and/or HER-2 overexpression in this tumor type.
FAU - Sawada, Morio
AU  - Sawada M
AD  - Department of Gynecology, National Cancer Center Hospital, Tokyo, and Department 
      of Pathology II, National Defense Medical College, Tokorozawa.
FAU - Tsuda, Hitoshi
AU  - Tsuda H
FAU - Kimura, Mikihiko
AU  - Kimura M
FAU - Okamoto, Sanshiro
AU  - Okamoto S
FAU - Kita, Tsunekazu
AU  - Kita T
FAU - Kasamatsu, Takahiro
AU  - Kasamatsu T
FAU - Yamada, Takuro
AU  - Yamada T
FAU - Kikuchi, Yoshihiro
AU  - Kikuchi Y
FAU - Honjo, Hideo
AU  - Honjo H
FAU - Matsubara, Osamu
AU  - Matsubara O
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - England
TA  - Cancer Sci
JT  - Cancer science
JID - 101168776
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
RN  - EC 2.7.10.1 (Receptor, ErbB-2)
SB  - IM
MH  - Carcinosarcoma/genetics/*metabolism/surgery
MH  - Chondrosarcoma, Mesenchymal/genetics/*metabolism/surgery
MH  - ErbB Receptors/genetics/*metabolism
MH  - Female
MH  - Gene Amplification
MH  - Humans
MH  - Hysterectomy
MH  - Immunoenzyme Techniques
MH  - In Situ Hybridization, Fluorescence
MH  - Neoplasms, Glandular and Epithelial/genetics/*metabolism/surgery
MH  - Polyploidy
MH  - Proto-Oncogene Proteins c-kit/genetics/*metabolism
MH  - Receptor, ErbB-2/genetics/*metabolism
MH  - Uterine Neoplasms/genetics/*metabolism/surgery
EDAT- 2003/11/13 05:00
MHDA- 2004/08/04 05:00
CRDT- 2003/11/13 05:00
PHST- 2003/11/13 05:00 [pubmed]
PHST- 2004/08/04 05:00 [medline]
PHST- 2003/11/13 05:00 [entrez]
AID - 10.1111/j.1349-7006.2003.tb01389.x [doi]
PST - ppublish
SO  - Cancer Sci. 2003 Nov;94(11):986-91. doi: 10.1111/j.1349-7006.2003.tb01389.x.