Literature DB >> 28265829

A Multicenter Study of a Fluorescence In Situ Hybridization Probe Set for Diagnosing High-Grade Dysplasia and Adenocarcinoma in Barrett's Esophagus.

John M Poneros1, Adam S Faye2, Emily G Barr Fritcher3, Ananda Sen4,5, Sharmila Anandasabapathy6, Robert S Bresalier7, Norman Marcon8,9, D Kim Turgeon10,11, Henry Appelman12, Daniel Normolle13, Larry E Morrison14,15, Dean E Brenner10,16, Kevin C Halling3.   

Abstract

BACKGROUND AND AIMS: Preliminary single-institution data suggest that fluorescence in situ hybridization (FISH) may be useful for detecting high-grade dysplasia (HGD) and esophageal adenocarcinoma (EA) in patients with Barrett's esophagus (BE). This multicenter study aims to validate the measurement of polysomy (gain of at least two loci) by FISH as a way to discriminate degrees of dysplasia in BE specimens.
METHODS: Tissue specimens were collected from four different hospitals and read by both the local pathology department ("Site diagnosis") and a single central pathologist ("Review diagnosis") at a separate institution. The specimens then underwent FISH analysis using probes 8q24 (MYC), 9p21 (CDKN2A), 17q12 (ERBB2), and 20q13 (ZNF217) for comparison. A total of 46 non-BE, 42 non-dysplastic specialized intestinal metaplasia (SIM), 23 indefinite-grade dysplasia (IGD), 10 low-grade dysplasia (LGD), 29 HGD, and 42 EA specimens were analyzed.
RESULTS: We found that polysomy, as detected by FISH, was the predominant chromosomal abnormality present as dysplasia increased. Polysomy was also the best predictor for the presence of dysplasia or EA when comparing its area under the curve to that of other FISH abnormalities. We observed that if at least 10% of cells had polysomy within a specimen, the FISH probe was able to differentiate between EA/HGD and the remaining pathologies with a sensitivity of 80% and a specificity of 88%.
CONCLUSIONS: This study demonstrates that using FISH to determine the percentage of cells with polysomy can accurately and objectively aid in the diagnosis of HGD/EA in BE specimens.

Entities:  

Keywords:  Barrett’s esophagus; Dysplasia; Endoscopy; FISH; Histopathology; Polysomy

Mesh:

Year:  2017        PMID: 28265829      PMCID: PMC6052443          DOI: 10.1007/s10620-017-4517-y

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  22 in total

1.  Endoscopic biopsy can detect high-grade dysplasia or early adenocarcinoma in Barrett's esophagus without grossly recognizable neoplastic lesions.

Authors:  B J Reid; W M Weinstein; K J Lewin; R C Haggitt; G VanDeventer; L DenBesten; C E Rubin
Journal:  Gastroenterology       Date:  1988-01       Impact factor: 22.682

2.  The development of a fluorescence in situ hybridization assay for the detection of dysplasia and adenocarcinoma in Barrett's esophagus.

Authors:  Shannon M Brankley; Kenneth K Wang; Aaron R Harwood; Dylan V Miller; Mona S Legator; Lori S Lutzke; Benjamin R Kipp; Larry E Morrison; Kevin C Halling
Journal:  J Mol Diagn       Date:  2006-05       Impact factor: 5.568

3.  The role of overdiagnosis and reclassification in the marked increase of esophageal adenocarcinoma incidence.

Authors:  Heiko Pohl; H Gilbert Welch
Journal:  J Natl Cancer Inst       Date:  2005-01-19       Impact factor: 13.506

Review 4.  Dysplasia in Barrett's esophagus: limitations of current management strategies.

Authors:  Stuart Jon Spechler
Journal:  Am J Gastroenterol       Date:  2005-04       Impact factor: 10.864

5.  Reproducibility of the diagnosis of dysplasia in Barrett esophagus: a reaffirmation.

Authors:  E Montgomery; M P Bronner; J R Goldblum; J K Greenson; M M Haber; J Hart; L W Lamps; G Y Lauwers; A J Lazenby; D N Lewin; M E Robert; A Y Toledano; Y Shyr; K Washington
Journal:  Hum Pathol       Date:  2001-04       Impact factor: 3.466

6.  Clonal expansion and loss of heterozygosity at chromosomes 9p and 17p in premalignant esophageal (Barrett's) tissue.

Authors:  P C Galipeau; L J Prevo; C A Sanchez; G M Longton; B J Reid
Journal:  J Natl Cancer Inst       Date:  1999-12-15       Impact factor: 13.506

7.  TOPOIIalpha and HER-2/neu overexpression/amplification in Barrett's oesophagus, dysplasia and adenocarcinoma.

Authors:  Elisa Rossi; Vincenzo Villanacci; Gabrio Bassotti; Francesco Donato; Andrea Festa; Gianpaolo Cengia; Salvatore Grisanti; Renzo Cestari
Journal:  Histopathology       Date:  2010-06-16       Impact factor: 5.087

8.  A comparison of conventional cytology, DNA ploidy analysis, and fluorescence in situ hybridization for the detection of dysplasia and adenocarcinoma in patients with Barrett's esophagus.

Authors:  Emily G Barr Fritcher; Shannon M Brankley; Benjamin R Kipp; Jesse S Voss; Michael B Campion; Larry E Morrison; Mona S Legator; Lori S Lutzke; Kenneth K Wang; Thomas J Sebo; Kevin C Halling
Journal:  Hum Pathol       Date:  2008-07-07       Impact factor: 3.466

Review 9.  Epidemiology of esophageal cancer.

Authors:  Yuwei Zhang
Journal:  World J Gastroenterol       Date:  2013-09-14       Impact factor: 5.742

10.  HER-2 overexpression/amplification in Barrett's oesophagus predicts early transition from dysplasia to adenocarcinoma: a clinico-pathologic study.

Authors:  Elisa Rossi; Salvatore Grisanti; Vincenzo Villanacci; Domenico Della Casa; Paolo Cengia; Guido Missale; Luigi Minelli; Michela Buglione; Renzo Cestari; Gabrio Bassotti
Journal:  J Cell Mol Med       Date:  2008-10-06       Impact factor: 5.310

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  1 in total

Review 1.  Utility of ancillary studies in the diagnosis and risk assessment of Barrett's esophagus and dysplasia.

Authors:  Won-Tak Choi; Gregory Y Lauwers; Elizabeth A Montgomery
Journal:  Mod Pathol       Date:  2022-03-08       Impact factor: 8.209

  1 in total

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