title: Correlation of KIT and EGFR overexpression with invasive ductal breast carcinoma of the solid-tubular subtype, nuclear grade 3, and mesenchymal or myoepithelial differentiation.
abstract: Although KIT and EGFR overexpressions are reported to occur in breast cancer, their pathological significance is still unclear. We examined KIT, EGFR, and c-erbB-2 overexpressions immunohistochemically in 150 cases of surgically resected breast cancer and their correlation with the histological type and grade and mesenchymal and/or myoepithelial immunophenotype of primary tumors. To facilitate the analysis, we constructed a tissue microarray comprising 2-mm diameter tissues cored from the representative tissue block of each tumor. KIT, EGFR, and c-erbB-2 overexpressions were detected in 15 (10%), 12 (8%), and 23 (15%), respectively. The KIT was more frequent in the group comprising comedo-type ductal carcinoma in situ and invasive ductal carcinomas (IDCs) of the solid-tubular subtype than in the group of other histological types (P=0.027), and the EGFR was more frequent in IDCs of solid-tubular type than in other histological types (P <0.05). KIT and EGFR overexpressions were correlated with nuclear grade 3 (P=0.0095 and 0.0005) and tended to be concurrent (P=0.005). KIT overexpression was correlated with vimentin and S-100 expression (P=0.003 and P=0.005), and EGFR overexpression was correlated with S100 expression (P=0.0001). These correlations with grade and mesenchymal/myoepithelial markers were not observed for c-erbB-2 overexpression. KIT and EGFR appeared to be indicators of high-grade breast carcinoma groups that often contain the carcinomas with mesenchymal and/or myoepithelial differentiation, which are distinct from the group with c-erbB-2 overexpression.
authors.affiliation: Department of Pathology II, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513. htsuda@cc.ndmc.ac.jp
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Tsuda
authors.forename: Daisaku
authors.initials: D
authors.lastname: Morita
authors.forename: Mikihiko
authors.initials: M
authors.lastname: Kimura
authors.forename: Eiji
authors.initials: E
authors.lastname: Shinto
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Ohtsuka
authors.forename: Osamu
authors.initials: O
authors.lastname: Matsubara
authors.forename: Johji
authors.initials: J
authors.lastname: Inazawa
authors.forename: Kuniyoshi
authors.initials: K
authors.lastname: Tamaki
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Mochizuki
authors.forename: Seiichi
authors.initials: S
authors.lastname: Tamai
authors.forename: Hoshio
authors.initials: H
authors.lastname: Hiraide
mesh_terms: D014408:Biomarkers, Tumor / Q000032:analysis*; D001943:Breast Neoplasms / Q000378:metabolism / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000378:metabolism / Q000473:pathology*; D066246:ErbB Receptors / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D019009:Proto-Oncogene Proteins c-kit / Q000378:metabolism*; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D009418:S100 Proteins / Q000378:metabolism; D015854:Up-Regulation; D014746:Vimentin / Q000378:metabolism
chemical_list: D014408:Biomarkers, Tumor; D066246:ErbB Receptors; D019009:Proto-Oncogene Proteins c-kit; D018719:Erb-b2 Receptor Tyrosine Kinases; D009418:S100 Proteins; D014746:Vimentin