Abnormal expression of biomarkers in incompletely ablated Barrett's esophagus

Katerina Dvorak, Lois Ramsey, Claire M. Payne, Richard Sampliner, Ronnie Fass, Harris Bernstein, Anil P Rama Rao, Harinder Garewal

Research output: Contribution to journalArticle

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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. SUMMARY BACKGROUND DATA: 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.

Original languageEnglish (US)
Pages (from-to)1031-1036
Number of pages6
JournalAnnals of Surgery
Volume244
Issue number6
DOIs
StatePublished - Dec 2006
Externally publishedYes

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Barrett Esophagus
Biomarkers
Staining and Labeling
Epithelium
Cyclooxygenase 2
Biopsy
Intercellular Junctions
Proton Pump Inhibitors
Tumor Biomarkers
Islands
Immunohistochemistry
Acids
Wounds and Injuries
Neoplasms

ASJC Scopus subject areas

  • Surgery

Cite this

Dvorak, K., Ramsey, L., Payne, C. M., Sampliner, R., Fass, R., Bernstein, H., ... Garewal, H. (2006). Abnormal expression of biomarkers in incompletely ablated Barrett's esophagus. Annals of Surgery, 244(6), 1031-1036. https://doi.org/10.1097/01.sla.0000224913.19922.7e

Abnormal expression of biomarkers in incompletely ablated Barrett's esophagus. / Dvorak, Katerina; Ramsey, Lois; Payne, Claire M.; Sampliner, Richard; Fass, Ronnie; Bernstein, Harris; Rama Rao, Anil P; Garewal, Harinder.

In: Annals of Surgery, Vol. 244, No. 6, 12.2006, p. 1031-1036.

Research output: Contribution to journalArticle

Dvorak, K, Ramsey, L, Payne, CM, Sampliner, R, Fass, R, Bernstein, H, Rama Rao, AP & Garewal, H 2006, 'Abnormal expression of biomarkers in incompletely ablated Barrett's esophagus', Annals of Surgery, vol. 244, no. 6, pp. 1031-1036. https://doi.org/10.1097/01.sla.0000224913.19922.7e
Dvorak K, Ramsey L, Payne CM, Sampliner R, Fass R, Bernstein H et al. Abnormal expression of biomarkers in incompletely ablated Barrett's esophagus. Annals of Surgery. 2006 Dec;244(6):1031-1036. https://doi.org/10.1097/01.sla.0000224913.19922.7e
Dvorak, Katerina ; Ramsey, Lois ; Payne, Claire M. ; Sampliner, Richard ; Fass, Ronnie ; Bernstein, Harris ; Rama Rao, Anil P ; Garewal, Harinder. / Abnormal expression of biomarkers in incompletely ablated Barrett's esophagus. In: Annals of Surgery. 2006 ; Vol. 244, No. 6. pp. 1031-1036.
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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. SUMMARY BACKGROUND DATA: 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.",
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AU - Bernstein, Harris

AU - Rama Rao, Anil P

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AB - 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. SUMMARY BACKGROUND DATA: 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.

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