title: c-myc amplification is frequent in esophageal adenocarcinoma and correlated with the upregulation of VEGF-A expression.
abstract: BACKGROUND
  Deregulation of c-myc plays a major role in the carcinogenesis of human malignancies. We investigated the amplification of the c-myc gene in a surgical series of Barrett cancers.
  
  
  METHODS
  Primary resected esophageal (Barrett) adenocarcinomas (n = 84) were investigated for c-myc amplification using chromogene in situ hybridization. Tumor samples were assembled in a tissue microarray. c-myc gene dosage was correlated with clinicopathologic parameters, including the survival and gene expression of cyclooxygenases (COX-1 and COX-2) and proangiogenic growth factors (VEGF-A and VEGF-C).
  
  
  RESULTS
  The majority (70 of 84; 83.3%) exhibited amplification of the c-myc gene. There were low-level amplifications in 63 (75.0%) cases and high-level amplifications in 7 (8.3%) cases. No amplification was found in 14 (16.7%) cases. Tumors without c-myc amplification had lower VEGF-A, VEGF-C, and COX-2 expression levels than tumors with low-level and high-level c-myc amplification (statistically significant for VEGF-A; P = .0348). c-myc amplification was not correlated with clinicopathological parameters or survival. Only diffuse and mixed-type tumors, according to Lauren classification, exhibited c-myc amplifications more frequently (P = .0466).
  
  
  CONCLUSIONS
  Amplifications of the c-myc gene are frequent in Barrett cancer. c-myc may be involved in the regulation of angiogenesis.
authors.affiliation: Department of Surgery, Paracelsus Medical University Salzburg, Salzburg, Austria. vrahden@nt1.chir.med.tu-muenchen.de
authors.forename: Burkhard H A
authors.initials: BH
authors.lastname: von Rahden
authors.forename: Hubert J
authors.initials: HJ
authors.lastname: Stein
authors.forename: Franziska
authors.initials: F
authors.lastname: Pühringer-Oppermann
authors.forename: Mario
authors.initials: M
authors.lastname: Sarbia
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000378:metabolism*; D000368:Aged; D004938:Esophageal Neoplasms / Q000378:metabolism*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D017403:In Situ Hybridization; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism*; D016896:Treatment Outcome; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis*
chemical_list: D016271:Proto-Oncogene Proteins c-myc; D042461:Vascular Endothelial Growth Factor A; D011451:Prostaglandin-Endoperoxide Synthases