Predictors of Progression To Cancer in Barrett's Esophagus: Baseline Histology and Flow Cytometry Identify Low- and High-Risk Patient Subsets

Reid, Brian J.; Levine, Douglas S.; Longton, Gary; Blount, Patricia L.; Rabinovitch, Peter S.

doi:10.1111/j.1572-0241.2000.02196.x

Cited by 383 publications

(412 citation statements)

References 54 publications

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“…26,27 Brush cytology may be complementary to endoscopic biopsies, and is recommended by some to be part of the routine endoscopic surveillance of patients with Barrett's esophagus. 28 Cytology has a good sensitivity for the detection of adenocarcinoma and HGD, as well as a good specificity for intestinal metaplasia without dysplasia.…”

Section: Discussionmentioning

confidence: 99%

“…26,27 A variety of gains and losses of specific chromosomes and chromosome regions have also been detected in esophageal adenocarcinoma specimens and adjacent mucosa by both traditional cytogenetics and by comparative genomic hybridization. [34][35][36][37][38][39] The studies consistently show an accumulation of chromosomal abnormalities as the histologic changes progress from intestinal metaplasia to dysplasia and carcinoma.…”

Section: Discussionmentioning

confidence: 99%

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Chromosomal gains and genomic loss of p53 and p16 genes in Barrett's esophagus detected by fluorescence in situ hybridization of cytology specimens

et al. 2004

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Endoscopic brush cytology is a promising surveillance technique for Barrett's esophagus. Ancillary markers are sought to increase the sensitivity of cytology and allow identification of patients at increased risk for disease progression. To determine if there are specific genetic changes in Barrett's esophagus with associated high-grade dysplasia/intramucosal adenocarcinoma compared to those without dysplasia, we performed fluorescence in situ hybridization (FISH) on cytologic specimens using probes to chromosomes and genomic regions previously described as altered in this disease. We studied archival brush cytology slides from 40 Barrett's esophagus patients: 21 with biopsy-proven high-grade dysplasia/carcinoma and 19 with no dysplasia and a minimum 5 years of negative follow-up. Centromeric enumeration probes (CEP) for chromosomes 6, 7, 11, and 12, and locus-specific probes (LSI) for 9p21 (p16 gene), and 17p13.1 (p53 gene) loci along with their corresponding CEP (9 and 17, respectively) were used in this study. A positive FISH result was defined as the presence of cells with 42 CEP signals or with a loss of the LSI signals relative to their corresponding CEP. p53 locus loss and/or aneusomy of chromosomes 6, 7, 11, and 12 abnormalities could be detected by FISH in routinely processed endoscopic brush cytology specimens from 95% of biopsy-positive cases with a specificity of 100%. Interestingly, all five cases with cytologic changes classified as indefinite for dysplasia from patients with a positive biopsy showed changes by FISH. Loss of the p16 locus was seen commonly in patients both with and without dysplasia/carcinoma. Selected biomarkers from this study merit further investigation to determine their potential to detect genetic changes in patients with Barrett's esophagus prior to the development of high-grade dysplasia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chromosomal gains and genomic loss of p53 and p16 genes in Barrett's esophagus detected by fluorescence in situ hybridization of cytology specimens

et al. 2004

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“…49 Based on careful, prospective observation of a well characterized cohort of patients with Barrett esophagus, it was reported recently that individuals who had baseline esophageal biopsies that showed no dysplasia, indefinite dysplasia, or lowgrade dysplasia and no flow cytometric evidence of aneuploidy were at low risk for disease progression and may have endoscopic surveillance at 5-year intervals. 50 By contrast, biomarkers that are predictive of disease progression in high-risk patients (other than patients with high-grade dysplasia) include aneuploidy (DNA content Ͼ 2.7 N; 4-N fraction Ͼ 6%; or Nuclear only 0 1 2 2 3 1 2 3 2 Nuclear and cytoplasmic 4 7 1 3 3 2 1 3 3 Cytoplasmic only 5 7 2 2 3 2 0 2 0 Negative 11 24 10 25 57 22 9 19 12 GERD, gastroesophageal reflux disease-induced esophagitis; EADC, esophageal adenocarcinoma. a Tissue sections were considered positive only if cell nuclear staining was observed.…”

Section: Discussionmentioning

confidence: 99%

Cyclin D1 polymorphism (G870A) and risk for esophageal adenocarcinoma

Casson

Zheng

Evans

et al. 2005

Cancer

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“…For example, among experienced gastrointestinal pathologists, the interobserver discordance for low-grade dysplasia is Ͼ50%; fortunately, disagreement is only Ϸ15% for diagnosis of high-grade dysplasia, and improvements in diagnosis are not necessary (5). Additional markers for dysplasia, such as the presence of aneuploidy on flow cytometry, have been used to help predict patient risk for developing adenocarcinoma (6). However, this laboratory assay is prone to sampling error because dysplasia in Barrett's is usually flat, patchy, and endoscopically invisible (7).…”

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confidence: 99%

Detection of endogenous biomolecules in Barrett's esophagus by Fourier transform infrared spectroscopy

Wang

Triadafilopoulos²,

Crawford

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Fourier transform infrared (FTIR) spectroscopy provides a unique molecular fingerprint of tissue from endogenous sources of light absorption; however, specific molecular components of the overall FTIR signature of precancer have not been characterized. In attenuated total reflectance mode, infrared light penetrates only a few microns of the tissue surface, and the influence of water on the spectra can be minimized, allowing for the analyses of the molecular composition of tissues. Here, spectra were collected from 98 excised specimens of the distal esophagus, including 38 squamous, 38 intestinal metaplasia (Barrett's), and 22 gastric, obtained endoscopically from 32 patients. We show that DNA, protein, glycogen, and glycoprotein comprise the principal sources of infrared absorption in the 950-to 1,800-cm ؊1 regime. The concentrations of these biomolecules can be quantified by using a partial leastsquares fit and used to classify disease states with high sensitivity, specificity, and accuracy. Moreover, use of FTIR to detect premalignant (dysplastic) mucosa results in a sensitivity, specificity, positive predictive value, and total accuracy of 92%, 80%, 92%, and 89%, respectively, and leads to a better interobserver agreement between two gastrointestinal pathologists for dysplasia ( ‫؍‬ 0.72) versus histology alone ( ‫؍‬ 0.52). Here, we demonstrate that the concentration of specific biomolecules can be determined from the FTIR spectra collected in attenuated total reflectance mode and can be used for predicting the underlying histopathology, which will contribute to the early detection and rapid staging of many diseases.dysplasia ͉ pathology ͉ optical biopsy ͉ diagnostics

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Predictors of Progression To Cancer in Barrett's Esophagus: Baseline Histology and Flow Cytometry Identify Low- and High-Risk Patient Subsets

Cited by 383 publications

References 54 publications

Chromosomal gains and genomic loss of p53 and p16 genes in Barrett's esophagus detected by fluorescence in situ hybridization of cytology specimens

Chromosomal gains and genomic loss of p53 and p16 genes in Barrett's esophagus detected by fluorescence in situ hybridization of cytology specimens

Cyclin D1 polymorphism (G870A) and risk for esophageal adenocarcinoma

Detection of endogenous biomolecules in Barrett's esophagus by Fourier transform infrared spectroscopy

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