An endoscopic biopsy protocol can differentiate high-grade dysplasia from early adenocarcinoma in Barrett's esophagus

Levine, Douglas S.; Haggitt, Rodger C.; Blount, Patricia L.; Rabinovitch, Peter S.; Rusch, Valerie W.; Reid, Brian J.

doi:10.1016/0016-5085(93)90008-z

Cited by 563 publications

(286 citation statements)

References 35 publications

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“…An intensive biopsy protocol may be successful at endoscopically differentiating high grade dysplasia from cancer (47). The surgical literature contrasts with this experience.…”

Section: Ajg -July 1998mentioning

confidence: 94%

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Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Sampliner

1998

The American Journal of Gastroenterology

105

110

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“…An intensive biopsy protocol may be successful at endoscopically differentiating high grade dysplasia from cancer (47). The surgical literature contrasts with this experience.…”

Section: Ajg -July 1998mentioning

confidence: 94%

“…However, the published database of the natural history of dysplasia is limited to only four centers that have performed prospective studies (43)(44)(45)(46)(47). A total of 285 patients have been followed for 1-5 yr. Only 5 of 150 patients have been followed from no dysplasia to cancer over a time interval of 3.4 -10 yr.…”

Section: Ajg -July 1998mentioning

confidence: 99%

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Sampliner

1998

The American Journal of Gastroenterology

105

110

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“…[51][52][53] These high grade dysplastic lesions may already have irreversibly progressed; at least 50% have immediately adjacent adenocarcinoma and a variable proportion of the rest may remain static for at least 1 to 3 years regardless of the presence or absence of refluxed gastric or duodenal contents. 53,54 Dysplastic cells may have proliferative controls that are relaxed or uncoupled from the appropriate regulatory cues. In part this may be a result of altered expression of cytokines and growth factors, 40 although the acquisition of genomic alterations of cell cycle-associated genes also occurs.…”

Section: Dysplasia and Aneuploidy: Clonal Expansion By Increased Cellmentioning

confidence: 99%

Molecular Evolution of the Metaplasia-Dysplasia-Adenocarcinoma Sequence in the Esophagus

Jankowski

Wright

Meltzer

et al. 1999

The American Journal of Pathology

365

254

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The incidence of adenocarcinoma of the esophagus has been increasing in developing countries over the last three decades and probably reflects a genuine increase in the incidence of its recognized precursor lesion , Barrett's metaplasia. Despite advances in multimodality therapy , the prognosis for invasive esophageal adenocarcinoma is poor. An improved understanding of the molecular biology of this disease may allow improved diagnosis , therapy , and prognosis. We focus on recent developments in the molecular and cell biology of Barrett's metaplasia , a heterogeneous lesion affecting the transitional zone of the gastro-esophageal junction whose associated molecular alterations may vary both in nature and temporally. Early premalignant clones produce biological and genetic heterogeneity as seen by multiple p53 mutations , p16 mutations , aneuploidy , and abnormal methylation resulting in stepwise changes in differentiation , proliferation , and apoptosis , allowing disease progression under selective pressure. Abnormalities in expression of growth factors of the epidermal growth factor family and cell adhesion molecules, especially cadherin/catenin complexes , may occur early in invasion. Exploitation of these molecular events may lead to a more appropriate diagnosis and understanding of these lesions in the future. (Am J Pathol 1999, 154:965-973)

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“…5 Current guidelines for surveillance of IMC/HGD include 4-quadrant biopsies every 2 cm along the axial length of the Barrett's segment. 6 However, the accuracy of surveillance endoscopy is limited by sampling error. 7-9 Debate continues regarding the optimal surveillance strategy for BE, but many analyses have identified surveillance frequency and the cost of endoscopy as key determinants of cost-effectiveness.…”

mentioning

confidence: 99%

Optical Coherence Tomography to Identify Intramucosal Carcinoma and High-Grade Dysplasia in Barrett’s Esophagus

Evans

Poneros

Bouma

et al. 2006

Clinical Gastroenterology and Hepatology

241

175

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Background & Aims-Optical coherence tomography (OCT) is an optical technique that produces high-resolution images of the esophagus during endoscopy. OCT can distinguish specialized intestinal metaplasia (SIM) from squamous mucosa, but image criteria for differentiating intramucosal carcinoma (IMC) and high-grade dysplasia (HGD) from low-grade dysplasia (LGD), indeterminate-grade dysplasia (IGD), and SIM without dysplasia have not been validated. The purpose of this study was to establish OCT image characteristics of IMC and HGD in Barrett's esophagus.

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An endoscopic biopsy protocol can differentiate high-grade dysplasia from early adenocarcinoma in Barrett's esophagus

Cited by 563 publications

References 35 publications

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Molecular Evolution of the Metaplasia-Dysplasia-Adenocarcinoma Sequence in the Esophagus

Optical Coherence Tomography to Identify Intramucosal Carcinoma and High-Grade Dysplasia in Barrett’s Esophagus

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