title: Detection of kinase amplifications in gastric adenocarcinomas.
abstract: OBJECTIVE
  To determine the incidences of copy number aberrations of receptor kinases and their relations in Turkish patients with gastric adenocarcinoma.
  
  
  METHODS
  The prevalence of genomic copy number aberrations of epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2)/topoisomerase IIa (TOP2A), centrosome-associated kinase aurora A (AURK A), centrosome-associated kinase aurora B (AURK B), and mesenchymal-epithelial transition factor (MET) genes and polysomies of related chromosomes were analyzed by fluorescent in situ hybridization (FISH) in tumor samples from 35 patients with gastric cancer.
  
  
  RESULTS
  There were 28.6%, 65.7%, 20.0%, 17.1%, 60.0%, and 45.7% cases considered FISH-positive for EGFR, MET, HER2, TOP2A, AURK A, and AURK B genes, respectively. Statistically significant associations were determined in detection of amplifications of 1) EGFR gene with chromosome 7 polysomy, 2) MET gene in nonpolysomic chromosome 7 nuclei, 3) HER2/TOP2A genes in nonpolysomic chromosome 17 nuclei, 4) coamplification of HER2/TOP2A in poorly differentiated carcinomas, and 5) AURK A gene in nonpolysomic chromosome 20 nuclei. Most of the aberrations were predominantly seen in poorly differentiated tumors, but a high rate of the amplified MET gene was also detected in moderately differentiated carcinomas.
  
  
  CONCLUSIONS
  Chromosome 7 polysomy may be responsible for EGFR gene amplifications, and we concluded that MET and AURK A genes amplifications were commonly seen aberrations in gastric adenocarcinomas and may offer information about disease progression and administration of individualized treatment for gastric cancer patients.
authors.affiliation: Department of Medical Genetics, Eskişehir Osmangazi University, Eskişehir, Turkey. mozdemir@ogu.edu.tr
authors.forename: Muhsin
authors.initials: M
authors.lastname: Özdemiri
authors.forename: Murat
authors.initials: M
authors.lastname: Öznur
authors.forename: Evrim
authors.initials: E
authors.lastname: Çiftçi
authors.forename: Beyhan
authors.initials: B
authors.lastname: Durak Aras
authors.forename: Hüseyin
authors.initials: H
authors.lastname: Aslan
authors.forename: Hande
authors.initials: H
authors.lastname: Saygili
authors.forename: Kevser Setenay
authors.initials: KS
authors.lastname: Öner
authors.forename: Serdar Mustafa
authors.initials: SM
authors.lastname: Erkasap
authors.forename: Ayşegiil
authors.initials: A
authors.lastname: Özakyol
authors.forename: Özgiil
authors.initials: Ö
authors.lastname: Paşaoğlu
authors.forename: Oğuz
authors.initials: O
authors.lastname: Çilingir
authors.forename: Sevilhan
authors.initials: S
authors.lastname: Artan
mesh_terms: D000230:Adenocarcinoma / Q000201:enzymology* / Q000235:genetics*; D000328:Adult; D000368:Aged; D056915:DNA Copy Number Variations; D005260:Female; D005784:Gene Amplification; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008297:Male; D008875:Middle Aged; D020794:Receptor Protein-Tyrosine Kinases / Q000737:chemistry / Q000235:genetics*; D013274:Stomach Neoplasms / Q000201:enzymology* / Q000235:genetics*
chemical_list: D020794:Receptor Protein-Tyrosine Kinases