The Incidence of Adenocarcinoma and Dysplasia in Barrett's Esophagus: Report on The Cleveland Clinic Barrett's Esophagus Registry

O’Connor, J. Barry; Falk, Gary W.; Richter, Joel E.

doi:10.1111/j.1572-0241.1999.01275.x

Cited by 178 publications

(116 citation statements)

References 15 publications

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“…The median length of BE at the initial endoscopy, with interquartile range (IQR), was 3 (2-12) cm in the fundoplication group, compared with 3 (2-7) cm in the group without fundoplication (P = NS). Median follow-up was 15 (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24) months in the fundoplication group and 12.5 (12)(13)(14)(15)(16)(17) months in the group without fundoplication (P = NS).…”

Section: Resultsmentioning

confidence: 85%

Effects of Nissen fundoplication on endoscopic endoluminal radiofrequency ablation of Barrett’s esophagus

O’Connell

Velanovich

2010

Surg Endosc

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Patients who had fundoplication in conjunction with endoluminal radiofrequency ablation were more likely to achieve durable ablation compared with patients who were treated with proton pump inhibitor therapy. It appears that patients with long-segment Barrett's esophagus are at higher risk for persistent or recurrent Barrett's metaplasia. Consideration should be given for an antireflux operation in patients with long-segment Barrett's esophagus and planned endoluminal radiofrequency ablation.

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Section: Resultsmentioning

confidence: 85%

Effects of Nissen fundoplication on endoscopic endoluminal radiofrequency ablation of Barrett’s esophagus

O’Connell

Velanovich

2010

Surg Endosc

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“…However, the natural history of LGD is not well characterized, with rates of progression to HGD or EAC ranging from 10 to 30%, as well as frequent regression to BE (Hameeteman et al, 1989;Weston et al, 1997;O'Connor et al, 1999;Weston et al, 1999Weston et al, , 2001Skacel et al, 2000;Conio et al, 2003). Moreover, histological classification of dysplasia, especially LGD, has high interobserver variability (Alikhan et al, 1999;Montgomery et al, 2001a, b).…”

Section: Discussionmentioning

confidence: 99%

Inactivation of p16, RUNX3, and HPP1 occurs early in Barrett's-associated neoplastic progression and predicts progression risk

et al. 2005

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Patients with Barrett's esophagus (BE) are at increased risk of developing esophageal adenocarcinoma (EAC). Clinical neoplastic progression risk factors, such as age and the length of the esophageal BE segment, have been identified. However, improved molecular biomarkers predicting increased progression risk are needed for improved risk assessment and stratification. Using realtime quantitative methylation-specific PCR, we screened 10 genes (HPP1, RUNX3, RIZ1, CRBP1, 3-OST-2, APC, TIMP3, p16, MGMT, p14) for promoter hypermethylation in 77 EAC, 93 BE, and 64 normal esophagus (NE) specimens. A subset of genes manifesting significant differences in methylation frequencies between BE and EAC was then analysed in 20 dysplastic specimens. All 10 genes except p14 were frequently methylated in EACs, with RUNX3, HPP1, CRBP1, RIZ1, and OST-2 representing novel methylation targets in EAC and/or BE. p16, RUNX3, and HPP1 displayed increasing methylation frequencies in BE vs EAC. Furthermore, these increases in methylation occurred early, at the interface between BE and low-grade dysplasia (LGD). To demonstrate the silencing effect of hypermethylation, we selected the EAC cells BIC1, in which the HPP1 promoter is natively methylated, and subjected them to 5-aza-2 0 -deoxycytidine (Aza-C) treatment. Real-time RT-PCR indicated increased HPP1 mRNA levels after 3 days of Aza-C treatment, as well as decreased levels of methylated HPP1 DNA. Hypermethylation of a subset of six genes (APC, TIMP3, CRBP1, p16, RUNX3, and HPP1) was then tested in a retrospective longitudinal study of 99 BE and nine LGD specimens obtained from 53 BE patients undergoing surveillance endoscopy. Only highgrade dysplasia (HGD) or EAC were defined as progression end points. Two patient groups were compared: eight progressors (P) and 45 nonprogressors (NP), using Cox proportional hazards models to determine the relative progression risks of age, BE segment length, and methylation events. Multivariate analyses revealed that only hypermethylation of p16 (odds ratio (OR) 1.74, 95% confidence interval (CI) 1.33-2.20), RUNX3 (OR 1.80, 95% CI 1.08-2.81), and HPP1 (OR 1.77, 95% CI 1.06-2.81) were independently associated with an increased risk of progression, whereas age, BE segment length, and hypermethylation of TIMP3, APC, or CRBP1 were not independent risk factors. In combined analyses, risk was detectable up to, but not earlier than, 2 years preceding neoplastic progression. Hypermethylation of p16, RUNX3, and HPP1 in BE or LGD may represent independent risk factors for the progression of BE to HGD or EAC. These findings have implications regarding risk stratification, early EAC detection, and the appropriate endoscopic surveillance interval for patients with BE.

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“…This reflux-related condition develops over time and confers an increased risk for the development of esophageal adenocarcinoma, estimated to be 0.1-0.5% per year [5][6][7][8]. The 5-year carcinoma risk exceeds 30% for patients with high-grade dysplasia (HGD).…”

mentioning

confidence: 99%

Treatment of ultralong-segment Barrett’s using focal and balloon-based radiofrequency ablation

et al. 2009

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The Incidence of Adenocarcinoma and Dysplasia in Barrett's Esophagus: Report on The Cleveland Clinic Barrett's Esophagus Registry

Cited by 178 publications

References 15 publications

Effects of Nissen fundoplication on endoscopic endoluminal radiofrequency ablation of Barrett’s esophagus

Effects of Nissen fundoplication on endoscopic endoluminal radiofrequency ablation of Barrett’s esophagus

Inactivation of p16, RUNX3, and HPP1 occurs early in Barrett's-associated neoplastic progression and predicts progression risk

Treatment of ultralong-segment Barrett’s using focal and balloon-based radiofrequency ablation

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