Surveillance and survival in Barrett's adenocarcinomas: A population-based study

Corley, Douglas A.; Levin, Theodore R.; Habel, Laurel A.; Weiss, Noel S.; Buffler, Patricia A.

doi:10.1053/gast.2002.31879

Cited by 457 publications

(274 citation statements)

References 36 publications

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“…Patients with BE have a 30-125-fold increased risk of developing EAC relative to the general population (Hameeteman et al, 1989). Therefore, regular endoscopic surveillance has been recommended for patients with BE (Sampliner, 2002;Spechler, 2002), and it has been shown that cancers detected in surveillance programs occur at an earlier stage and have a better prognosis (Streitz et al, 1993;Peters et al, 1994;Schnell et al, 2001;Corley et al, 2002). However, endoscopic surveillance has several drawbacks, including its high cost, low yield, and procedure-related risks.…”

Section: Introductionmentioning

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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Section: Introductionmentioning

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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“…In order for the number of QALYs to be the same whether the natural history model was based on progression through dysplasia, or through the biomarker, the prevalence of the biomarker condition among patients with Barrett's oesophagus must be 33%. No dysplasia to HGD 0.01 37,39,40,42,48 No dysplasia to cancer 0.005 45 LGD to HGD 0.05 37,42,45,47 LGD LGD to no dysplasia 0.63 39,42 HGD to no dysplasia 0.1 42,49 HGD to LGD 0.07 40,42,49 Biomarker + to biomarker ) 0 * Cancer treatment probabilities Resectablity: without surveillance 0.5 5,28,54 Resectablity: with surveillance 0.95 5,28,33 Surgical mortality: without surveillance 0.05 [54][55][56][57] In the best-case scenario, the biomarker-guided oesophagectomy strategy (ME) prevented 76% of cancers, and 93% of cancer deaths compared with OBS. Patients in ME experienced an average 16.707 QALYs at a cost of $2,291 per patient.…”

Section: Natural Historymentioning

confidence: 99%

The cost‐effectiveness of biomarkers for predicting the development of oesophageal adenocarcinoma

Rubenstein

Vakil²,

Inadomi

2005

Aliment Pharmacol Ther

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SUMMARYBackground: The recommended surveillance strategy for oesophageal adenocarcinoma may prevent as few as 50% of cancer deaths. Tissue biomarkers have been proposed to identify high-risk patients. Aim: To determine performance characteristics of an ideal biomarker, or panel of biomarkers, that would make its use more cost-effective than the current surveillance strategy. Methods: We created a Markov model using data from published literature, and performed a cost-utility analysis. The population consisted of 50-year-old Caucasian men with gastro-oesophageal reflux, who were monitored until age 80. We examined strategies of observation only, current practice (dysplasiaguided surveillance), surveillance every 3 months

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“…Surgical retrospective analyses indicate that the patients from the observation arm are significantly better in terms of the stage of cancer and recovery in comparison to patients studied when the symptoms occur (26)(27)(28)(29)(30)(31)(32)(33)(34)(35).…”

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confidence: 99%

How should we describe, diagnose and observe the Barrett's esophagus?

Akın¹,

Aydın²

2017

Turk J Gastroenterol

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A universal consensus on the definition Barrett's esophagus (BE) has not been achieved yet. Different definitions were made in the British Society of Gastroenterology (BSG) 2013 and American Gastroenterological Association (AGA) 2011 guidelines (1,2). With reference to the former, while the presence of any columnar epithelium between the gastroesophageal junction and squamocolumnar junction (fundic, cardiac, or specialized intestinal metaplasia (SIM)) is sufficient for the diagnosis of BE. The presence of SIM is required for the diagnosis, according to AGA 2011.There are some retrospective studies showing that cardiac-or fundic-type columnar epithelium is precancerous at the same rate with SIM (3,4). In addition, it was put forward in published histochemical and genetic studies that SIM and the other two columnar epithelia showed similar DNA abnormalities and the other columnar epithelia showed intestinal differentiation like SIM. A conclusion was made that the other columnar epithelia were a precursor lesion for SIM (5,6). However, population-based cohort studies with large numbers of patients have revealed that SIM-positive patients carry a much greater risk than SIM-negative patients in terms of the development of LGD, HGD, and esophagus adenocarcinoma (EAC) (7-9). While the annual progression rate to the EAC of SIM-positive patients was 0.24% in the analyses performed in this study, this rate was found to be 0.04% in SIM-negative patients. These results indicate that the presence of SIM is necessary for the diagnosis of BE.On the other hand, the definition of BE should be disassociated from the concept of irregular Z-lines. An ir- S26 ABSTRACT Barrett's esophagus (BE) is one of the major complications of gastroesophageal reflux disease (GERD) commonly encountered in gastroenterology clinics. A consensus has not been achieved yet with respect to the definition of BE in published guidelines. It is advised to use the Prague classification and not to use the definition of short and long segments for the endoscopic standardization of BE. Undertaking biopsies with white-light endoscopy from each of the 4 quadrants at 2-cm intervals is the standard method for the diagnosis of BE. Because of the ability to perform targeted biopsies, the available data indicate that advanced endoscopic techniques may reduce the number of biopsies needed for diagnoses. In the presence of severe esophagitis along with BE, the biopsies should be taken after 8 weeks of PPI therapy. The evidence values of the suggestions about the surveillance requirements and surveillance frequencies are low because the available data mostly rely on retrospective studies. We suggest that all the patients with BE should be referred to specialized centers for surveillance in Turkey. Considering the additional risk factors of the patient, endoscopy surveillance intervals of the patients with BE without dysplasia should be in a range of 3-5 years and annual surveillance should be made in BE with low-grade dysplasia. In the presence of BE with high-grade dysp...

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Surveillance and survival in Barrett's adenocarcinomas: A population-based study

Cited by 457 publications

References 36 publications

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

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

The cost‐effectiveness of biomarkers for predicting the development of oesophageal adenocarcinoma

How should we describe, diagnose and observe the Barrett's esophagus?

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