Barrett's Esophagus Dysplasia Research Articles

The Aberrant Expression of Biomarkers and Risk Prediction for Neoplastic Changes in Barrett's Esophagus-Dysplasia.

Background: Barrett's esophagus (BE) is a pre-neoplastic condition associated with an increased risk of esophageal adenocarcinoma (EAC). The accurate diagnosis of BE and grading of dysplasia can help to optimize the management of patients with BE. However, BE may be missed and the accurate grading of dysplasia based on a routine histology has a considerable intra- and interobserver variability. Thus, well-defined biomarker testing remains indispensable. The aim of our study was to identify routinely applicable and relatively specific biomarkers for an accurate diagnosis of BE, as well as determining biomarkers to predict the risk of progression in BE-dysplasia. Methods: Retrospectively, we performed immunohistochemistry to test mucin 2(MUC2), trefoil factor 3 (TFF3), p53, p16, cyclin D1, Ki-67, beta-catenin, and minichromosome maintenance (MCM2) in biopsies. Prospectively, to identify chromosomal alterations, we conducted fluorescent in situ hybridization testing on fresh brush samples collected at the time of endoscopy surveillance. Results: We discovered that MUC2 and TFF3 are specific markers for the diagnosis of BE. Aberrant expression, including the loss and strong overexpression of p53, Ki-67, p16, beta-catenin, cyclin D1, and MCM2, was significantly associated with low-grade dysplasia (LGD), high-grade dysplasia (HGD), and EAC histology, with a relatively high risk of neoplastic changes. Furthermore, the aberrant expressions of p53 and p16 in BE-indefinite dysplasia (IND) progressor cohorts predicted the risk of progression. Conclusions: Assessing the biomarkers would be a suitable adjunct to accurate BE histology diagnoses and improve the accuracy of BE-dysplasia grading, thus reducing interobserver variability, particularly of LGD and risk prediction.

Classification of Early Stages of Esophageal Cancer Using Transfer Learning

ObjectivesEsophageal Cancer is the sixth most common cancer with a high fatality rate. Early prognosis of esophageal abnormalities can improve the survival rate of the patients. The sequence of the progress of the esophageal cancer is from esophagitis to non-dysplasia Barrett's esophagus to dysplasia Barrett's esophagus to esophageal adenocarcinoma (EAC). Many studies revealed a 5-fold increase in EAC patients diagnosed with esophagitis, and those diagnosed with Barrett's esophagus have a greater risk of EAC. Material and methodsConvolutional Neural Network (CNN) with efficient feature extractors enable better prognosis of the pre cancerous stage, Barrett's esophagus and esophagitis. The transfer learning techniques with CNN can extract more relevant features for the automated classification of Barrett's esophagus and esophagitis. This paper presents a study on the classification of the esophagitis and Barrett's esophagus (BE) using Deep Convolution Neural Networks (DCNN). ResultsIn the first experiment, the DCNN models perform as a feature extractor, and standard classifiers do the classification. The performance analysis shows that the CNN model ResNet50 with Support Vector Machine (SVM) has an accuracy of 93.5%, recall 93.5%, precision 93.4%, f score 93.5%, AUC 89.8%. In the second experiment, the DCNN classification models perform the classification with Transfer Learning and fine-tuning. The ResNet50 model has improved accuracy of 94.46%, precision 94.46%, f score 94.46%, AUC 96.20%. ConclusionThe ResNet50 model with transfer learning and fine-tuning gives a better performance than the ResNet50 model with SVM classifier. Our experiments show that the DCNN is effective for diagnosing EAC, both as feature extractors and classification models with transfer learning and fine-tuning.

Validation and optimization of enhanced volumetric laser endomicroscopy scoring systems for Barrett's esophagus dysplasia

BackgroundVolumetric laser endomicroscopy (VLE) is an advanced imaging modality used in Barrett's esophagus (BE) surveillance. VLE interpretation relies on identification of specific features associated with BE dysplasia and can be enhanced by intelligent real-time image segmentation (IRIS). The diagnostic performance of established VLE interpretation systems has not been validated. This study uses a dataset of histology-matched regions of interest (ROI) to determine the diagnostic performance of VLE with and without IRIS enhancement. MethodsVLE scans with ROIs laser-marked for targeted biopsy and matching histopathology were performed in patients undergoing BE surveillance. ROIs were rated independently for BE dysplasia by 3 blinded VLE experts using established VLE interpretation systems. Following a washout period, ROIs were rated using IRIS adapted to the VLE interpretation systems. Inter-rater agreement, diagnostic performance, and optimal diagnostic thresholds were calculated for each scoring system. ResultsA total of 71 laser-marked ROIs from 44 patients (mean age: 68 years) and BE length of 5 cm were included. About 45.1% of ROIs contained dysplasia. Inter-rater agreement was uniformly very good or excellent and only the surface intensity scoring agreement was enhanced by IRIS. The scoring systems’ AUC ranged from 0.59 to 0.74 and 0.60 to 0.75 for VLE with and without IRIS, respectively. When diagnostic thresholds of the existing scoring systems were optimized, the adjusted AUC ranged from 0.70 to 0.78. ConclusionsThis is the first study to validate and optimize the diagnostic performance of established VLE interpretation systems for BE dysplasia. IRIS image enhancement adapted to these interpretation systems demonstrated similar diagnostic performance.

Current management of Barrett esophagus and esophageal adenocarcinoma.

Barrett esophagus is found in 5% to 15% of patients with gastroesophageal reflux disease and is a precursor of esophageal adenocarcinoma, yet the condition often goes undiagnosed. Patients with reflux disease who are male, over age 50, or white, and who smoke or have central obesity or a family history of Barrett esophagus or esophageal adenocarcinoma, should undergo initial screening endoscopy and, if no dysplasia is noted, surveillance endoscopy every 3 to 5 years. Dysplasia is treated with endoscopic eradication by ablation, resection, or both. Chemoprotective agents are being studied to prevent progression to dysplasia in Barrett esophagus. The authors discuss current recommendations for screening and management.

Su1999 - Barrett's Esophagus Dysplasia Burden Measured by Volumetric Laser Endomicroscopy Predicts Clinical Outcomes of Endoscopic Therapy

Su1999 - Barrett's Esophagus Dysplasia Burden Measured by Volumetric Laser Endomicroscopy Predicts Clinical Outcomes of Endoscopic Therapy

Substantial Interobserver Agreement in the Diagnosis of Dysplasia in Barrett Esophagus Upon Review of a Patient's Entire Set of Biopsies.

The pathologic diagnosis of dysplasia in Barrett esophagus (BE) suffers from interobserver disagreement. Many of the studies demonstrating disagreement in the diagnosis of dysplasia have pathologists review individual biopsy slides in isolation. To more closely mimic daily practice, 3 pathologists reviewed hematoxylin and eosin slides made from 549 individual biopsy jars obtained from 129 unique patients with a diagnosis of BE. Each pathologist reviewed the entirety of a given patient's biopsy material. The grade of dysplasia present in each biopsy jar was given as well as an overall highest grade of dysplasia from the patient's entire set of biopsies. The interobserver agreement in the diagnosis of dysplasia per biopsy jar and per patient's set of biopsies was measured by Fleiss κ statistic for multiple raters. The κ values for each diagnosis was higher in the per patient analysis compared with the per biopsy jar analysis indicating that pathologists are more likely to agree on the overall grade of dysplasia compared with the grade in an individual biopsy jar. In the per patient analysis, the interobserver agreement in the diagnosis of nondysplastic BE and high-grade dysplasia were substantial (κ=0.66; 95% confidence interval [CI], 0.56-0.76 and κ=0.76; 95% CI, 0.66-0.86, respectively). The interobserver agreement in the diagnosis of low-grade dysplasia (LGD) was fair (κ=0.31; 95% CI, 0.21-0.42). When LGD and high-grade dysplasia were collapsed into 1 category of positive for dysplasia, the interobserver agreement in the per patient analysis remained substantial (κ=0.70; 95% CI, 0.60-0.80), suggesting that much of the disagreement in LGD is not due to lack of recognition of dysplastic Barrett's mucosa, but rather the degree of dysplasia. These results indicate that pathologists can reliably distinguish between nondysplastic BE and dysplastic BE when a patient's entire set of biopsies is reviewed as a group. When second opinions are obtained, all available slides from that endoscopic procedure should be sent for review.

633P - Endoscopic resection for Barrett's esophagus: Uzbekistan experience

Background: In the treatment of esophageal dysplasia, particularly Barrett's esophagus, radical endoscopic resection (SRER) has shown its effectiveness. The purpose of this study was to evaluate the long-term results of treatment of Barrett's esophagus dysplasia after a successful SRER. Methods: Patients who received SRER for BE ≤ 5 cm with high-grade dysplasia (HGD) or early cancer (EC) achieved complete elimination of intestinal metaplasia (CE-IM) and neoplasia (CE-neo). Primary outcomes: relapse of neoplasia (HGD/EC), recurrence of dysplasia (including indefinite dysplasia) and recurrence of endoscopically visible BE. METHODS: Patients who received SRER for BE ≤ 5 cm with high-grade dysplasia (HGD) or early cancer (EC) achieved complete elimination of intestinal metaplasia (CE-IM) and neoplasia (CE-neo). Primary outcomes: relapse of neoplasia (HGD/EC), recurrence of dysplasia (including indefinite dysplasia) and recurrence of endoscopically visible BE. Results: Hidden Barrett's glands, IM in biopsy specimens obtained distal to the normal emerging neo-squamocolumnar compound, the need for re-treatment, and sustained by CE-IM and CE-neo at the last follow-up endoscopy. RESULTS: 76 patients were included (65 men, mean age 66 years, median BE C2M3). The median follow-up was 76 months. A repetition of neoplasia was observed in 1 patient (T1bN0M0) after 130 months of observation and was treated with medical surgery (annual frequency 0.22% per year of the patient's observation). Four patients had recurrent dysplasia (0.87% per patient-year of follow-up). Twelve patients had recurrent endoscopically visible BE after median follow-up for 22 months (2.6% for each subsequent patient-year of observation), mostly small islands or languages. Five patients were found to have one Barrett burial gland finding (1.1% per year of the patient's observation), and 27 patients (5.9% per year of the patient's observation) showed MI in biopsies only distal to the neo-squamocolumnar junction was not reproduced in 56%. Repeated treatment was performed in 9 patients. CE-IM and CE-neo (excluding IM in the neon-squamolecular compound) in the last endoscopic endoscopy were seen in 95% and 97% of patients, respectively. Conclusions: This study presents the longest published data on SRER to date. 6-year results show that a successful SRER is a long-term therapy for BE ≤ 5 cm with HGD/EC. Legal entity responsible for the study: Tashkent Medical Academy Funding: None Disclosure: All authors have declared no conflicts of interest.

Endoscopic treatment for Barrett's oesophagus dysplasia and early cancer

Endoscopic treatment of early Barrett's oesophagus neoplasia is now proven to be a safe and effective alternative to oesophagectomy. An ideal candidate for endoscopic treatment should have dysplasia or carcinoma limited to the mucosa or superficial submucosa without lymphovascular invasion or poor differentiation. Two main types of endoscopic therapies are used: (1) endoscopic resection, which comprises of endoscopic mucosal resection or endoscopic submucosal dissection for removal of visible lesions en bloc and (2) endoscopic ablation utilising argon plasma coagulation, radiofrequency ablation or, more recently, cryotherapy. Although endoscopic resection is the cornerstone for Barrett's endotherapy, ablative techniques are complementary in achieving complete eradication of the columnar epithelium and dysplasia.

IMP3 Immunoreactivity is More Sensitive Than AMACR in Detecting Dysplastic Epithelium and Early Adenocarcinoma in Barrett Esophagus.

α-methylacyl coenzyme A racemase (AMACR) and insulin-like growth factor-II mRNA-binding protein 3 (IMP3) are 2 markers helpful in detecting difficult cases of dysplasia in Barrett esophagus (BE). However, no comparison studies have been performed to assess their performance in the same patient population. The aim of our study was to compare the immunohistochemical expression of IMP3 and AMACR in dysplastic lesions and early adenocarcinoma (EAC) arising in BE and evaluate their sensitivity and specificity. A total of 98 cases [BE negative for dysplasia, n=24; indefinite for dysplasia (BE-IND), n=18; low-grade dysplasia (LGD), n=24; high-grade dysplasia (HGD), n=16; and EAC, n=16] were immunostained for AMACR and IMP3 and evaluated for the degree, the extent, and the intensity of staining. No immunoreactivity for AMACR or IMP3 was observed in all 24 cases of BE negative for dyplasia. One of 18 (5.5%) cases of BE-IND was positive for IMP3, but all were negative for AMACR. AMACR and IMP3 were positive in 16.7% versus 41.7 % of the cases with BE-LGD, 25% versus 62.5% of BE-HGD, and 62.5% versus 93.7% of EAC, respectively. The sensitivity of AMACR and IMP3 for the detection of dysplasia in BE is 16.7% and 41.7% for LGD, 25% and 62.5% for HGD, and 62.5% and 93.7% in EAC, respectively. The specificity is 100% for both markers. In addition, a comparison of the intensity of reactivity shows a better result with IMP3 (36/98, 36.7%) than with AMACR (18/98, 18.4%) (P<0.001). IMP3 has a similar specificity, but a better sensitivity, intensity, and extent of reactivity in comparison with AMACR, and may be used as an alternative to AMACR, in support of the diagnosis of BE-dysplasia and EAC.

Diagnosis and risk stratification of Barrett’s dysplasia by flow cytometric DNA analysis of paraffin-embedded tissue

ObjectiveThe diagnosis of dysplasia in Barrett’s oesophagus (BO) can be challenging, and reliable ancillary techniques are not available. This study examines if DNA content abnormality detected by flow cytometry can...

Sa1106 Topography of Intestinal Metaplasia and Dysplasia in Barrett's Esophagus

Sa1106 Topography of Intestinal Metaplasia and Dysplasia in Barrett's Esophagus

OC-053 Lectin-Based Near infra-red Molecular Imaging for Dysplasia Detection in Barrett’s Oesophagus: An ex-vivo Study on Human Tissue

Introduction Detection of early neoplasia in Barrett’s oesophagus (BO) by white-light endoscopy is challenging due to the inconspicuous nature of dysplasia. Molecular imaging using fluorescently labelled wheat-germ agglutinin (WGA) is a promising tool as this topically applied imaging agent shows lower binding to dysplastic versus non-dysplastic BO. 1 However in an endoscopy setting, the detection of fluorescence in the blue/green range is limited by high-levels of tissue autofluorescence. This limitation can be overcome by using near infra-red (NIR) imaging. We aimed to assess in an ex-vivo model the feasibility of WGA-based NIR imaging for detection of dysplasia in BO. Methods we recruited patients with early BO-related neoplasia undergoing endoscopic mucosal resection (EMR). Freshly collected EMR specimens were sprayed with WGA-IR800CW and then imaged with a high-sensitivity NIR camera. Fluorescence images were captured and up to two punch biopsies were collected from each EMR under fluorescence guidance. The EMRs were paraffin embedded, cut every 2 mm and processed for histopathological assessment. Each section was scored by an expert GI pathologist every 1 mm to construct a pathology grid, which was manually co-registered with the fluorescence image. The mean fluorescence intensity (MFI) of cells in dysplastic and non-dysplastic areas was compared by the Wilcoxon matched-pairs signed rank test. Only EMR specimens with at least one dysplastic gland were included in the analysis. In addition, the MFI of punch biopsies taken from dysplastic and non-dysplastic areas was also compared by Mann-Whitney test. Results Ten patients were recruited at a single centre. A total of 18 EMR specimens and 33 punch biopsies were collected, of which 10 were dysplastic. In the whole EMR analysis, we found a significantly lower MFI for dysplastic versus non-dysplastic areas (P = 0.0012), in accordance with the reported reduced binding of WGA to neoplastic BO epithelium. Similarly, we found a nearly 2 fold reduction in the MFI of punch biopsies taken from dysplastic as compared to non-dysplastic (ND) areas (P = 0.0002) (Figure 1). Conclusion WGA-based NIR imaging is an effective method for differentiating dysplastic from non-dysplastic BO mucosa ex vivo , which reduces the effects of tissue autofluorescence. In-vivo studies are now required to test the efficacy of this method for detecting dysplasia during endoscopic surveillance. Reference 1 Bird-Lieberman, et al . Nat Med 2012. Disclosure of Interest None Declared

Combining endoscopic submucosal dissection and endoscopic mucosal resection to treat neoplasia in Barrett's esophagus.

Piecemeal endoscopic mucosal resection (EMR) is the standard treatment of nodular Barrett's esophagus dysplasia and T1a cancer. Piecemeal resection may be incomplete and makes precise histologic assessment difficult. Endoscopic submucosal dissection (ESD) is a technique that enables en-bloc resection but has not gained widespread acceptance due to its technical difficulty, risk and long procedure time. We developed a protocol consisting of a combination of a limited ESD with supplementary EMR in the same session if necessary, designed to increase en-bloc resection of the most worrisome neoplastic area while maximizing the rate of complete resection of dysplasia. Records of consecutive patients referred for treatment during a 2-year period were reviewed. Eleven patients were treated: two with ESD and nine with combined ESD/EMR. Eight patients had mucosal lesions; three patients had submucosally invasive cancer and were referred to surgery. Five of the 8 mucosal lesions were removed en-bloc by ESD with dysplasia-free margins. Two patients with T1a cancer had low-grade dysplasia in the ESD margins and removal of all dysplasia on EMR. One patient with T1a cancer had high-grade dysplasia in the ESD margins and on EMR. He required a second endoscopy to remove residual neoplasia. There were no adverse events. The mean procedure time was 66.4±15.1min. Combining a limited ESD with EMR in the same session enables efficient treatment of visible dysplastic lesions in Barrett's esophagus.

Oral steroid prophylaxis is effective in preventing esophageal strictures after large endoscopic resection.

BackgroundStrictures are frequent complications of large endoscopic mucosal resections (EMR) and endoscopic submucosal dissections of the esophagus. Local or systemic steroid therapy has shown promise in the prevention of secondary stenosis. The aim of this study was to evaluate the safety and efficacy of systemic steroid therapy following endoscopic resection of at least hemi-circumferential esophageal mucosa.MethodsThis was a single-center retrospective study in a tertiary center. We evaluated patients who were treated with oral steroids between July 2013 and September 2015, after undergoing a large EMR for Barrett’s esophagus associated with dysplasia or carcinoma. The steroid protocol used was an initial dose of 30 mg prednisolone, tapered over 8 weeks. Exclusion criteria were a previous attempt at radiofrequency ablation or resection.ResultsThirty-one patients (27 men) were analyzed: 13 with low-grade dysplasia Barrett’s esophagus, 16 with in situ adenocarcinoma, 1 with pT1SM1 adenocarcinoma, and 1 with pT1SM2 adenocarcinoma. Twenty-eight resections (28/31) were completed (R0) in 1-3 sessions (median 2), while 3 resections were R1. The median length of Barrett’s esophagus was C3M5 (range C0M2-C10M11) according to the Prague classification. The median follow up was 10 months (range 4-17), during which 4 patients (13%) developed a secondary stenosis. All stenoses were successfully treated by endoscopic dilation (range 1-4). No complications related to dilation or to the steroid therapy were observed.ConclusionsOur rate of secondary stricture was lower than expected, given the rates of 17-88% in published studies. Systemic oral steroid therapy seems to be effective in reducing potential esophageal stenosis after EMR. Complementary randomized studies are required to confirm whether systemic steroids are an effective primary prophylaxis for esophageal stenosis.

OC-040 First in-vivo study on the use of lectin-based molecular imaging in barrett’s oesophagus

Introduction The current standard for Barrett’s oesophagus (BO) endoscopic surveillance is based on random quadrantic biopsies every 2 cm. This is limited by sampling error due to inconspicuous dysplasia. We have previously found that an edible lectin (wheat germ agglutinin or WGA) has lower affinity for dysplastic compared to non-dysplastic BO and in an ex vivomodel of molecular imaging we showed that WGA-fluorescein in combination with autofluorescence imaging (AFI) can target dysplasia in BO (Bird-Lieberman, Nat Med, 2012). In this study we used a pre-operative setting to investigate in vivoWGA-based molecular imaging Method Inclusion criteria were: i. MDT referral to oesophagectomy for oesophageal adenocarcinoma (OAC) and ii.evidence of endoscopically visible BO associated to OAC on index endoscopy or staging endoscopic ultrasound. In the operating theatre prior to oesophagectomy, the oesophagus was first inspected by white light imaging to locate the tumour and measure the size of the associated BO. Imaging was then switched to AFI to locate AFI positive areas (red-purple colour). Up to two AFI negative areas (green colour) were also selected for control biopsy sampling. 20–30 mL of 5 µg/mL WGA-fluorescein were then sprayed onto the mucosal surface. After 5 min, the mucosa was gently washed with water and the oesophagus was inspected again in AFI mode. On WGA-enhanced AFI, areas of high WGA binding were located (WGA positive, green colour), as well as areas of low binding (WGA negative, red-purple and hence high risk). Targeted biopsies were taken for histopathological correlation. Histological outcome was binarised based on the presence or absence of dysplasia. Chi-squared test was used to compare diagnostic accuracy for dysplasia of AFI alone and WGA-enhanced AFI Results 16 patients were recruited at a single centre, of which 12 completed the protocol. 4 patients were excluded due to absence of visible BO associated with the OAC at the time of resection. Across the 12 patients a total of 41 endoscopic locations were selected for biopsy of which 29 were WGA negative and 12 were WGA positive. The overall sensitivity for dysplasia of AFI alone was 78% and the specificity was 50%. When compared to AFI alone, WGA improved sensitivity from 78% to 88%, with a slight increase in the specificity to 56%. AFI and WGA-enhanced AFI had an equal false positive rate (24%). No toxicity events where recorded. Conclusion WGA-based molecular imaging is safe and feasible in vivo. The use of WGA may improve the sensitivity of AFI for dysplasia, but larger studies in a surveillance population are required Disclosure of interest None Declared.

OC-017 Autofluorescence-targeted Optical Biopsy Accurately Diagnoses Dysplasia In Barrett’s Oesophagus And Can Detect The Field Of Molecular Change

IntroductionProbe-based confocal laser endomicroscopy (pCLE) allows optical biopsies in Barrett’s oesophagus (BO) to predict histological outcome but it is subject to sampling error if performed in a random fashion. We...

Sa1852 Autofluorescence-Targeted Optical Biopsy Accurately Diagnoses Dysplasia in Barrett's Esophagus and Can Detect the Field of Molecular Change

Introduction Probe-based confocal laser endomicroscopy (pCLE) allows optical biopsies in Barrett’s oesophagus (BO) to predict histological outcome but it is subject to sampling error if performed in a random fashion. We used autofluorescence imaging (AFI) to direct pCLE and added molecular biomarkers to the histopathological diagnosis. The aims of this study were to assess the diagnostic accuracy for dysplasia of AFI-targeted optical biopsies and to investigate the correlation between pCLE patterns and field of molecular change. Methods 46 patients with BO (non-dysplastic BE n = 20, indefinite for dysplasia n = 4, low grade dysplasia n = 10, high grade dysplasia (HGD) or intramucosal cancer (IMC) n = 12) were recruited at a single centre. Patients underwent high-resolution endoscopy followed by AFI and then pCLE was performed on AFI positive (AFI+) areas. Targeted biopsies were taken from AFI+ areas, followed by random biopsies as per Seattle protocol. pCLE sequences were graded according to published criteria. Cyclin A and p53 expression were assessed by immunohistochemistry and aneuploidy by flow-cytometry on AFI-targeted biopsies. Statistical analyses were performed using chi-square test. Results AFI-targeted pCLE correctly classified all the HGD/EC patients and had a sensitivity and specificity for any grade of dysplasia of 93 and 83%, respectively. The Seattle protocol had similar sensitivity for HGD/IMC and any grade of dysplasia (83 and 89%, respectively). For the per-location analysis, a total of 155 endoscopic areas were analysed with pCLE and molecular biomarkers. pCLE had a sensitivity and a specificity for HGD/IMC and any grade of dysplasia of 100/64% and 78/75%, respectively. Overall, 40% of pCLE irregular sequences corresponded to non-dysplastic areas (false positive). We found a statistically significant enrichment (p Conclusion AFI-targeted pCLE has a high diagnostic accuracy for dysplasia in BO. Tissue biomarkers are a useful adjunct to characterise the field of molecular abnormality associated with optical dysplasia. These results suggest that the presence of pCLE irregularity, even in the absence of histological dysplasia, relates to molecular changes and may warrant close follow up. Disclosure of Interest None Declared.

162 The Yield of Early Follow-up Endoscopy in Patients With Initial Nondysplastic or Low-Grade Dysplasia Barrett's Esophagus

Current screening guidelines for Barrett's esophagus (BE) recommend patients undergo repeat esophagogastroduodenoscopy (EGD) after the diagnosis of Barrett's to exclude prevalent dysplasia that could potentially alter management and surveillance protocols. The yield of repeat EGD in this setting remains unknown.

The combination of autofluorescence endoscopy and molecular biomarkers is a novel diagnostic tool for dysplasia in Barrett's oesophagus

ObjectiveEndoscopic surveillance for Barrett's oesophagus (BO) is limited by sampling error and the subjectivity of diagnosing dysplasia. We aimed to compare a biomarker panel on minimal biopsies directed by autofluorescence...

Treatment of Dysplasia in Barrett Esophagus

Barrett esophagus is recognized as a risk factor for the development of dysplasia and adenocarcinoma of the esophagus. Cancer is usually diagnosed at an advanced stage with a 5-year survival rate of 15%. Most of these patients present de novo and are not part of a surveillance program. Endoscopic screening with improvement in recognition of early lesions may change this pattern. In the past, patients diagnosed with dysplasia and mucosal cancer were best managed by esophagectomy. Endoscopic techniques such as endoscopic mucosal resection and radiofrequency ablation have resulted in high curative rates and a shift away from esophagectomy. This pathway is supported by the literature review of esophagectomies performed for mucosal disease, as well as pathologists' interpretation of endoscopic mucosal specimens, which document the low risk of lymph node metastasis. The role of endoscopic therapy for superficial submucosal disease continues to be a challenge.