title: Abnormal expression of biomarkers in incompletely ablated Barrett's esophagus.
abstract: OBJECTIVE
  The aim of this study was to evaluate expression of cancer risk-associated biomarkers in columnar epithelium at squamocolumnar junctions produced by an ablation procedure and proton pump inhibitors in incompletely ablated Barrett's esophagus (BE) patients that were nondysplastic prior to ablation.
  
  
  BACKGROUND
  Ablation of BE to squamous epithelium is achievable by combining a re-injury method with acid suppression. We previously reported that, when there is complete ablation, the neo-squamous epithelium is normal histologically and in biomarker expression. However, squamous islands observed after prolonged use of PPIs were associated with abnormalities in p53 expression and Ki-67 labeling.
  
  
  METHODS
  Twenty-one nondysplastic BE cases with incomplete ablation were evaluated for the expression of Ki-67 (proliferation), cyclooxygenase-2 (COX-2), and p53 by immunohistochemistry.
  
  
  RESULTS
  Pre-ablation biopsies showed the normal staining patterns in columnar epithelium, ie, normal Ki-67 labeling, rare positive COX-2 staining of interstitial cells, and negative or mild staining for p53 in the majority of patients' biopsies. However, post-ablation biopsies demonstrated abnormal staining patterns in the glandular area at the new squamocolumnar junctions. In 13 of 21 post-ablation cases (62%), increased Ki-67 staining was seen in BE glands. In 8 of 21 patients (38%), increased COX-2 expression was seen in columnar epithelium. Similarly, in 8 of 21 post-ablation junctions (38%), there was increased p53 staining.
  
  
  CONCLUSIONS
  Our findings of increased expression of cancer-associated biomarkers in incompletely ablated BE patients raise a cautionary note regarding this procedure. We hypothesize that newly formed junctions contain cells undergoing replication, differentiation, etc, and are thus more susceptible to genomic damage.
authors.affiliation: Department of Cell Biology and Anatomy, College of Medicine, University of Arizona, Tucson, AZ, USA.
authors.forename: Katerina
authors.initials: K
authors.lastname: Dvorak
authors.forename: Lois
authors.initials: L
authors.lastname: Ramsey
authors.forename: Claire M
authors.initials: CM
authors.lastname: Payne
authors.forename: Richard
authors.initials: R
authors.lastname: Sampliner
authors.forename: Ronnie
authors.initials: R
authors.lastname: Fass
authors.forename: Harris
authors.initials: H
authors.lastname: Bernstein
authors.forename: Anil
authors.initials: A
authors.lastname: Prasad
authors.forename: Harinder
authors.initials: H
authors.lastname: Garewal
mesh_terms: D000328:Adult; D000368:Aged; D001471:Barrett Esophagus / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D004564:Electrocoagulation; D004848:Epithelium / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D054328:Proton Pump Inhibitors; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D019394:Ki-67 Antigen; D054328:Proton Pump Inhibitors; D016159:Tumor Suppressor Protein p53; D051546:Cyclooxygenase 2