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1. Rastogi A, Sharma P: Short-Segment Barrett's Esophagus and Adenocarcinoma. Gastroenterol Hepatol (N Y); 2006 Feb;2(2):134-139

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Short-Segment Barrett's Esophagus and Adenocarcinoma.
  • Barrett's esophagus is a known risk factor for the development of adenocarcinoma of the esophagus and esophagogastric junction.
  • Based on the length of the columnar segment at endoscopy, Barrett's esophagus has been arbitrarily separated into two broad categories: long-segment and short-segment.
  • The rapid rise in the incidence of esophageal adenocarcinoma has generated sustained research interest in this lesion.
  • Studies have shown that although the prevalence of short-segment Barrett's esophagus is higher than that of long-segment Barrett's esophagus, the risk of developing dysplasia and adenocarcinoma may actually be lower in those patients with short segment Barrett's esophagus.
  • Nonetheless, both dysplasia and esophageal adenocarcinoma have been reported in patients with short-segment Barrett's esophagus, making this arbitrary distinction clinically unimportant.
  • The current surveillance guidelines remain the same for both short- and long-segment Barrett's esophagus.
  • Another key issue is differentiating short-segment Barrett's esophagus from intestinal metaplasia of the gastric cardia.
  • The latter is distinct from esophageal intestinal metaplasia (ie, Barrett's esophagus) and probably does not warrant surveillance.

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  • (PMID = 28286441.001).
  • [ISSN] 1554-7914
  • [Journal-full-title] Gastroenterology & hepatology
  • [ISO-abbreviation] Gastroenterol Hepatol (N Y)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Barrett’s esophagus / adenocarcinoma / high-grade dysplasia / long-segment Barrett’s esophagus / low-grade dysplasia / short-segment Barrett’s esophagus
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2. Zhao J, Chang AC, Li C, Shedden KA, Thomas DG, Misek DE, Manoharan AP, Giordano TJ, Beer DG, Lubman DM: Comparative proteomics analysis of Barrett metaplasia and esophageal adenocarcinoma using two-dimensional liquid mass mapping. Mol Cell Proteomics; 2007 Jun;6(6):987-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparative proteomics analysis of Barrett metaplasia and esophageal adenocarcinoma using two-dimensional liquid mass mapping.
  • Esophageal adenocarcinoma, currently the seventh leading cause of cancer-related death, has been associated with the presence of Barrett metaplasia.
  • The malignant potential of Barrett metaplasia is evidenced by ultimate progression of this condition to invasive adenocarcinoma.
  • We utilized liquid phase separation of proteins with chromatofocusing in the first dimension and nonporous reverse phase HPLC in the second dimension followed by ESI-TOF mass spectrometry to identify proteins differentially expressed in six Barrett metaplasia samples as compared with six esophageal adenocarcinoma samples; all six Barrett samples were obtained from the identical six patients from whom we obtained the esophageal adenocarcinoma tissue.
  • Among the proteins that were identified, Rho GDP dissociation inhibitor 2, alpha-enolase, Lamin A/C, and nucleoside-diphosphate kinase A were demonstrated to be up-regulated in both mRNA and protein expression in esophageal adenocarcinomas relative to Barrett metaplasia.
  • The cellular expression patterns were verified in both esophageal adenocarcinomas and in Barrett metaplasia by immunohistochemistry.
  • These differentially expressed proteins may have utility as useful candidate markers of esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Proteomics. Spectrometry, Mass, Electrospray Ionization

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  • (PMID = 16829691.001).
  • [ISSN] 1535-9476
  • [Journal-full-title] Molecular & cellular proteomics : MCP
  • [ISO-abbreviation] Mol. Cell Proteomics
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA71606; United States / NCI NIH HHS / CA / R01CA10010; United States / NCI NIH HHS / CA / R01CA90503; United States / NIGMS NIH HHS / GM / R01GM49500
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger
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3. Helm J, Enkemann SA, Coppola D, Barthel JS, Kelley ST, Yeatman TJ: Dedifferentiation precedes invasion in the progression from Barrett's metaplasia to esophageal adenocarcinoma. Clin Cancer Res; 2005 Apr 1;11(7):2478-85
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  • [Title] Dedifferentiation precedes invasion in the progression from Barrett's metaplasia to esophageal adenocarcinoma.
  • PURPOSE: Adenocarcinoma arises in Barrett's esophagus by progression from metaplasia to cancer through grades of dysplasia.
  • EXPERIMENTAL DESIGN: Microarray analysis was used to obtain individual gene expression profiles from endoscopic biopsies of nine esophageal adenocarcinomas and the Barrett's epithelia from which three of the cancers had arisen.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Gene Expression Profiling
  • [MeSH-minor] Cell Differentiation / genetics. Cluster Analysis. Disease Progression. Epithelium / metabolism. Epithelium / pathology. Gene Expression Regulation, Neoplastic / genetics. Humans. Metaplasia / genetics. Models, Biological. Neoplasm Invasiveness / genetics. Oligonucleotide Array Sequence Analysis. Prognosis

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  • (PMID = 15814623.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24-CA85429-04; United States / NCI NIH HHS / CA / R01-CA098522-01; United States / NCI NIH HHS / CA / RZ1-CA101355-01-A1; United States / NCI NIH HHS / CA / U01-CA85052-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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4. Berndt U, Philipsen L, Bartsch S, Hu Y, Röcken C, Bertram W, Hämmerle M, Rösch T, Sturm A: Comparative Multi-Epitope-Ligand-Cartography reveals essential immunological alterations in Barrett's metaplasia and esophageal adenocarcinoma. Mol Cancer; 2010;9:177
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  • [Title] Comparative Multi-Epitope-Ligand-Cartography reveals essential immunological alterations in Barrett's metaplasia and esophageal adenocarcinoma.
  • BACKGROUND: Barrett's esophagus (BE) is caused by gastroesophageal reflux with consecutive mucosal inflammation, predisposing patients to the development of esophageal adenocarcinoma (EAC).
  • CONCLUSION: Proteomic analysis showed for the first time that proteins, which are critically involved in the mucosal immune system of the esophagus, are distinctly expressed in BE and EAC, whereas others are comparably altered in both diseases, suggesting that many pathogenic events might be shared by both diseases.
  • [MeSH-major] Adenocarcinoma / immunology. Barrett Esophagus / immunology. Epitopes / analysis. Esophageal Neoplasms / immunology

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  • (PMID = 20604962.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Epitopes; 0 / Ligands
  • [Other-IDs] NLM/ PMC2909181
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5. Wang XW, Gao HJ, Fang DC: Advances in gene chip technique in Barrett's metaplasia and adenocarcinoma. J Dig Dis; 2008 May;9(2):68-71
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  • [Title] Advances in gene chip technique in Barrett's metaplasia and adenocarcinoma.
  • Many studies have applied this technology for Barrett's metaplasia and adenocarcinoma, and identified a number of candidate genes useful as biomarkers in cancer staging, prediction of recurrence, prognosis and treatment selection.
  • This review described the gene expression profile and molecular changes related to Barrett's metaplasia and adenocarcinoma of the esophagus, with emphasis on its prognostic value and possibilities for targeted therapy in a clinical setting.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Oligonucleotide Array Sequence Analysis / trends
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Metaplasia / diagnosis. Metaplasia / genetics. Metaplasia / pathology

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  • (PMID = 18419638.001).
  • [ISSN] 1751-2972
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 18
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6. de Faria PC Jr, Andreollo NA, Trevisan MA, Lopes LR: [Relationship of the sialomucins (Tn and Stn antigens) with adenocarcinoma in Barrett's esophagus]. Rev Assoc Med Bras (1992); 2007 Jul-Aug;53(4):360-4
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  • [Title] [Relationship of the sialomucins (Tn and Stn antigens) with adenocarcinoma in Barrett's esophagus].
  • [Transliterated title] A inter-relação das sialomucinas (antígenos Tn e Stn) com o adenocarcinoma no esôfago de Barrett.
  • OBJECTIVE: Barrett's esophagus (BE) is a consequence of chronic gastroesophageal reflux and is considered a risk factor for adenocarcinoma.
  • The study of the mucus, especially acid mucins, such as the sialomucins in the goblet cells which characterize BE, showed that in intestinal metaplasia, frequent in the digestive tract, the organ's original epithelium could express Tn and Stn antigens.
  • This research aimed to analyze these antigens in patients with BE and in adenocarcinoma associated with BE.
  • METHODS: Utilizing immunohistochemistry tests, Tn and Stn antigens were studied in the endoscopic biopsies of 29 patients with BE and seven with adenocarcinoma in BE, as well as eight individuals with normal esophageal epithelium at upper digestive endoscopy.
  • However, in adenocarcinoma in BE, both antigens were 100% positive.
  • CONCLUSION: It is probable that the BE group in which the Tn antigens in the goblet cells are positive, similarly to the same antigen in the adenocarcinoma group, might indicate a higher susceptibility for potential occurrence of cancer.
  • In the future, trials with sialomucins could be used routinely, thereby contributing as a prognostic factor of adenocarcinoma in BE.
  • [MeSH-major] Adenocarcinoma / immunology. Barrett Esophagus / immunology. Esophageal Neoplasms / immunology. Sialomucins / analysis
  • [MeSH-minor] Adult. Aged. Antigens, Tumor-Associated, Carbohydrate / analysis. Biomarkers, Tumor / analysis. Biopsy. Case-Control Studies. Endoscopy, Gastrointestinal. Esophagus / immunology. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 17823742.001).
  • [ISSN] 0104-4230
  • [Journal-full-title] Revista da Associação Médica Brasileira (1992)
  • [ISO-abbreviation] Rev Assoc Med Bras (1992)
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Biomarkers, Tumor; 0 / Sialomucins; 0 / Tn antigen; 0 / sialosyl-Tn antigen
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7. Li Y, Woodall C, Wo JM, Zheng H, Ng CK, Ray MB, Martin RC: The use of dynamic positron emission tomography imaging for evaluating the carcinogenic progression of intestinal metaplasia to esophageal adenocarcinoma. Cancer Invest; 2008 Apr-May;26(3):278-85
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  • [Title] The use of dynamic positron emission tomography imaging for evaluating the carcinogenic progression of intestinal metaplasia to esophageal adenocarcinoma.
  • BACKGROUND: In this study, we investigate the use of PET scanning in the carcinogenic progression of reflux esophagitis to Barrett's esophagus to high grade dysplasia to esophageal adenocarcinoma, and correlate the uptake levels of 18F-FDG related to histological changes, and the rates of proliferation and apoptosis.
  • The higher level of 18F-FDG uptake within esophageal epithelium was identified in intestinal metaplastic transformation and esophagoduodenal adenocarcinoma by histological examination.
  • CONCLUSIONS: Dynamic PET scanning represents a powerful tool in analyzing morphological carcinogenic transformation non-invasively in the esophagus.
  • 18F- FDG accumulation was a sensitive marker in reflux esophageal injury carcinogenic progression from intestinal metaplasia to EAC.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cell Transformation, Neoplastic / pathology. Esophageal Neoplasms / pathology. Positron-Emission Tomography. Precancerous Conditions / pathology
  • [MeSH-minor] Animals. Disease Progression. Fluorodeoxyglucose F18. Immunohistochemistry. Metaplasia / pathology. Proliferating Cell Nuclear Antigen / biosynthesis. Rats. Rats, Sprague-Dawley

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  • (PMID = 18317969.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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8. Jethwa P, Naqvi M, Hardy RG, Hotchin NA, Roberts S, Spychal R, Tselepis C: Overexpression of Slug is associated with malignant progression of esophageal adenocarcinoma. World J Gastroenterol; 2008 Feb 21;14(7):1044-52
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  • [Title] Overexpression of Slug is associated with malignant progression of esophageal adenocarcinoma.
  • AIM: To characterise expression of known E-cadherin repressors; Snail, Slug and Twist in the development of esophageal adenocarcinoma.
  • METHODS: E-cadherin, Slug, Snail and Twist mRNA expression in Barrett's metaplasia and esophageal adenocarcinoma specimens was examined by real-time reverse transcription-polymerase chain reaction (RT-PCR).
  • The effect of Slug on epithelial mesenchymal transition (EMT) markers was examined by transfection of Slug into an adenocarcinoma line OE33.
  • RESULTS: Cellular localisation of Slug in Barrett's metaplasia was largely cytoplasmic whilst in adenocarcinoma it was nuclear.
  • Semi-quantitative analysis indicated that Slug was more abundant in adenocarcinoma compared to matched Barrett's metaplastic specimens.
  • Snail and Twist were expressed in adenocarcinoma but were cytoplasmic in location and not induced compared to Barrett's mucosa.
  • These observations were supported by mRNA studies where only Slug mRNA was shown to be over-expressed in adenocarcinoma and inversely correlated to E-cadherin expression.
  • CONCLUSION: Progression to adenocarcinoma is associated with increased Slug expression and this may represent a mechanism of E-cadherin silencing.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Transcription Factors / genetics
  • [MeSH-minor] Barrett Esophagus / complications. Barrett Esophagus / genetics. Barrett Esophagus / metabolism. Base Sequence. Cadherins / genetics. Cadherins / metabolism. Cell Line, Tumor. DNA Primers / genetics. Gene Expression. Humans. Immunohistochemistry. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Phenotype. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Twist Transcription Factor / genetics. Twist Transcription Factor / metabolism

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  • (PMID = 18286686.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cadherins; 0 / DNA Primers; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TWIST1 protein, human; 0 / Transcription Factors; 0 / Twist Transcription Factor; 0 / snail family transcription factors
  • [Other-IDs] NLM/ PMC2689407
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9. Gibson CJ, Parry NM, Jakowski RM, Cooper J: Adenomatous polyp with intestinal metaplasia of the esophagus (Barrett esophagus) in a dog. Vet Pathol; 2010 Jan;47(1):116-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenomatous polyp with intestinal metaplasia of the esophagus (Barrett esophagus) in a dog.
  • Multiple endoscopic biopsy specimens of esophageal mucosa were received from a 13-year-old castrated male standard Poodle.
  • Endoscopically, the distal aspect of the esophagus was inflamed with a polypoid mass that protruded into the esophageal lumen.
  • Histologically, the stratified squamous epithelium overlying the mass and lining the adjacent esophageal mucosa was replaced by papillary projections covered by columnar epithelium with goblet cells supported by a fibrous stroma.
  • This article reports a case of spontaneous esophageal adenomatous polyp with intestinal metaplasia (Barrett esophagus) and reviews the pathogenesis of esophageal metaplasia and adenocarcinoma.
  • [MeSH-major] Adenomatous Polyps / veterinary. Barrett Esophagus / veterinary. Dog Diseases / pathology. Esophageal Neoplasms / veterinary. Intestines / pathology
  • [MeSH-minor] Animals. Dogs. Esophagus / pathology. Goblet Cells / pathology. Male. Metaplasia / pathology. Metaplasia / veterinary

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  • (PMID = 20080491.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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10. Woodall CE, Li Y, Liu QH, Wo J, Martin RC: Chemoprevention of metaplasia initiation and carcinogenic progression to esophageal adenocarcinoma by resveratrol supplementation. Anticancer Drugs; 2009 Jul;20(6):437-43
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  • [Title] Chemoprevention of metaplasia initiation and carcinogenic progression to esophageal adenocarcinoma by resveratrol supplementation.
  • The effects of resveratrol on the initiation of Barrett's metaplasia and the carcinogenic progression to esophageal adenocarcinoma have not been evaluated.
  • The aim of this study was to evaluate the effects of resveratrol on the transition from reflux esophagitis to Barrett's metaplasia to dysplasia to esophageal adenocarcinoma in an established rat model.
  • The distal esophagus was preserved for blinded histopathological examination at the time of harvest.
  • Thirty-one animals in the 5-month resveratrol group showed a decreased severity of esophagitis (P<0.0001), incidence of intestinal metaplasia (P = 0.3567), and incidence of carcinoma (P = 0.4590) as compared with both the saline and nonoperated control groups.
  • In conclusion, morphological characteristics consistent with decreased esophagitis and incidences of metaplasia and esophageal adenocarcinoma were seen on histopathology in the resveratrol group.
  • Resveratrol resulted in a small diminution of the carcinogenic effects and progression to metaplasia, and further human studies are designed to explore the potential anticarcinogenic mechanism.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Esophageal Neoplasms / prevention & control. Esophagus / drug effects. Stilbenes / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Catalase / metabolism. Disease Models, Animal. Disease Progression. Glutathione / metabolism. Immunohistochemistry. In Situ Nick-End Labeling. Male. Metaplasia. Oxidative Stress / drug effects. Rats. Rats, Sprague-Dawley. Superoxide Dismutase / metabolism. Thiobarbituric Acid Reactive Substances / metabolism

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  • (PMID = 19398904.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Stilbenes; 0 / Thiobarbituric Acid Reactive Substances; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione; Q369O8926L / resveratrol
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11. Bobryshev YV, Tran D, Killingsworth MC, Buckland M, Lord RV: Dendritic cells in Barrett's esophagus and esophageal adenocarcinoma. J Gastrointest Surg; 2009 Jan;13(1):44-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dendritic cells in Barrett's esophagus and esophageal adenocarcinoma.
  • BACKGROUND: Like other premalignant conditions that develop in the presence of chronic inflammation, the development and progression of Barrett's esophagus is associated with the development of an immune response, but how this immune response is regulated is poorly understood.
  • A comprehensive literature search failed to find any report of the presence of dendritic cells in Barrett's intestinal metaplasia and esophageal adenocarcinoma and this prompted our study.
  • MATERIAL AND METHODS: We used immunohistochemical staining and electron microscopy to examine whether dendritic cells are present in Barrett's esophagus and esophageal adenocarcinoma.
  • Immunohistochemical staining with CD83, a specific marker for dendritic cells, was performed on paraffin-embedded sections of Barrett's intestinal metaplasia (IM, n = 12), dysplasia (n = 11) and adenocarcinoma (n = 14).
  • Double immunostaining with CD83, CD20, and CD3, and electron microscopy demonstrated that dendritic cells are present in Barrett's esophagus and form clusters with T cells and B cells directly within the lamina propria.
  • CONCLUSIONS: These findings demonstrate that dendritic cells are present in Barrett's tissues, with a significant increase in density in adenocarcinoma compared to benign Barrett's esophagus.
  • Dendritic cells may have a role in the pathogenesis and immunotherapy treatment of Barrett's esophagus and adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Dendritic Cells / ultrastructure. Esophageal Neoplasms / pathology

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  • (PMID = 18685901.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD83 antigen; 0 / Immunoglobulins; 0 / Membrane Glycoproteins
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12. Zhang T, Zhang F, Han Y, Gu Z, Zhou Y, Cheng Q, Zhu Y, Zhang C, Wang Y: A rat surgical model of esophageal metaplasia and adenocarcinoma-induced by mixed reflux of gastric acid and duodenal contents. Dig Dis Sci; 2007 Nov;52(11):3202-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A rat surgical model of esophageal metaplasia and adenocarcinoma-induced by mixed reflux of gastric acid and duodenal contents.
  • Herein we report a novel rat surgical model in which esophageal metaplasia and adenocarcinoma develop as complications of MR.
  • Severe inflammatory and proliferative changes, high prevalence of esophageal metaplasia (78%), and adenocarcinoma (50%) were observed in the lower part of the esophagus of rats 20 weeks after surgery.
  • The resulting esophageal lesions resembled those described in humans and supported a progression from intestinal metaplasia to dysplasia and, ultimately, esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / surgery. Duodenostomy / methods. Esophageal Neoplasms / surgery. Esophagostomy / methods. Esophagus / pathology. Gastroesophageal Reflux / complications. Jejunostomy / methods
  • [MeSH-minor] Animals. Disease Models, Animal. Disease Progression. Duodenum / secretion. Gastric Acid / secretion. Male. Metaplasia / etiology. Metaplasia / pathology. Metaplasia / surgery. Models, Anatomic. Rats. Rats, Sprague-Dawley

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  • (PMID = 17393326.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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13. Botelho NK, Schneiders FI, Lord SJ, Freeman AK, Tyagi S, Nancarrow DJ, Hayward NK, Whiteman DC, Lord RV: Gene expression alterations in formalin-fixed, paraffin-embedded Barrett esophagus and esophageal adenocarcinoma tissues. Cancer Biol Ther; 2010 Jul 15;10(2):172-9
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  • [Title] Gene expression alterations in formalin-fixed, paraffin-embedded Barrett esophagus and esophageal adenocarcinoma tissues.
  • BACKGROUND AND AIM: Widespread applicability of tissue-based mRNA expression screening for Barrett esophagus (BE) is likely to require (1) accurate methods for assaying archival formalin-fixed, paraffin-embedded (FFPE) histopathology specimens taken at endoscopy, and (2) validation studies of promising biomarkers in different patient cohorts.
  • METHODS: mRNA was isolated from 54 FFPE small endoscopic biopsies from patients with Barrett intestinal metaplasia (BE), esophageal adenocarcinoma (EAC), or control patients with a normal squamous-lined esophagus.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Gene Expression Profiling / methods. Polymerase Chain Reaction / methods

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  • (PMID = 20543560.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 1HG84L3525 / Formaldehyde
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14. Abdo-Francis JM, Sobrino-Cossío S, Bernal-Sahagún F, Hernández-Guerrero A: [Prevalence of intestinal metaplasia of the gastric cardia and its relation with Helicobacter pylori strains cagA and vacA]. Cir Cir; 2010 Jul-Aug;78(4):315-21
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  • [Title] [Prevalence of intestinal metaplasia of the gastric cardia and its relation with Helicobacter pylori strains cagA and vacA].
  • [Transliterated title] Prevalencia de metaplasia intestinal en el cardias gástrico y su relación con cepas virulentas de Helicobacter pylori cagA y vacA.
  • BACKGROUND: Esophageal metaplasia progression is a consequence of chronic gastroesophageal reflux (CGR).
  • In addition, they present an increased risk for the development of gastric adenocarcinoma.
  • We undertook this study to establish a relationship between the presence of pathogenic Helicobacter pylori strains and the presence of metaplasia progression in patients with CGR.
  • Cardiac intestinal metaplasia was observed in 35% of the patients.
  • A marked tendency was observed to develop cardiac intestinal metaplasia in those patients diagnosed with high-pathogenicity strains infected in both anatomic areas.
  • CONCLUSIONS: These results suggest that infection with Helicobacter pylori can be considered a risk factor for developing gastric cardiac intestinal metaplasia.
  • [MeSH-major] Antigens, Bacterial / genetics. Bacterial Proteins / genetics. Barrett Esophagus / epidemiology. Cardia / pathology. Gastritis, Atrophic / pathology. Helicobacter Infections / pathology. Helicobacter pylori / pathogenicity
  • [MeSH-minor] Adult. Aged. Biopsy. Cross-Sectional Studies. Female. Gastroesophageal Reflux / complications. Gastroscopy. Humans. Male. Metaplasia / epidemiology. Metaplasia / etiology. Middle Aged. Neutrophils / pathology. Precancerous Conditions / epidemiology. Precancerous Conditions / etiology. Precancerous Conditions / microbiology. Precancerous Conditions / pathology. Prospective Studies. Species Specificity. Virulence. Young Adult

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  • (PMID = 21167097.001).
  • [ISSN] 0009-7411
  • [Journal-full-title] Cirugía y cirujanos
  • [ISO-abbreviation] Cir Cir
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / VacA protein, Helicobacter pylori; 0 / cagA protein, Helicobacter pylori
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15. Schmidt MK, Meurer L, Volkweis BS, Edelweiss MI, Schirmer CC, Kruel CD, Gurski RR: c-Myc overexpression is strongly associated with metaplasia-dysplasia-adenocarcinoma sequence in the esophagus. Dis Esophagus; 2007;20(3):212-6
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  • [Title] c-Myc overexpression is strongly associated with metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.
  • We aim to determine the expression of the proto-oncogene c-Myc in patients with Barrett's esophagus (BE) and esophageal adenocarcinoma, and to evaluate the prevalence of such expression in relation to the metaplasia-dysplasia-adenocarcinoma sequence.
  • BE develops as a result of a severe esophageal mucosa injury from gastroesophageal reflux.
  • BE is a premalignant lesion and plays an important role in the development of esophageal adenocarcinoma.
  • The c-Myc protein expression was determined by immunohistochemical analysis in four different groups: 31 patients with normal tissue, 43 patients with BE without dysplasia, 11 patients with dysplasia in BE and 37 patients with esophageal adenocarcinoma.
  • The material was obtained from esophageal biopsies or the dissection of patient esophagectomy specimens.
  • Demographic and endoscopic data (sex, age, race and intestinal metaplasia extension), and morphologic and histopathologic tumor characteristics (deep tumor invasion, lymph node status, and tumor differentiation) were analyzed.
  • Overexpression of c-Myc was found in only 9.6% of normal tissue specimens, 37.2% of Barrett's esophagus, 45.5% of BE patients with dysplasia and 73% of adenocarcinoma samples, with significant statistical difference among these groups.
  • However, linear correlation of c-Myc overexpression along the metaplasia-dysplasia-adenocarcinoma sequence was observed.
  • This study demonstrates a significant increase in the expression of c-Myc in Barrett's esophagus, dysplasia and adenocarcinoma in relation to the control group, as well as a linear progression of this gene expression in this sequence.
  • These results point out the importance of this marker in the development of esophageal adenocarcinoma from BE.

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  • (PMID = 17509117.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc
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16. Tadiparthi R, Bansal A, Sharma P: What's new in columnar lined esophagus (Barrett's metaplasia)? Curr Opin Gastroenterol; 2008 Jul;24(4):516-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] What's new in columnar lined esophagus (Barrett's metaplasia)?
  • PURPOSE OF REVIEW: The rising incidence of esophageal adenocarcinoma in the Western world has led to continued interest in its precursor lesion, Barrett's esophagus.
  • This review endeavors to summarize the recent advances in our understanding of Barrett's esophagus with an emphasis on novel imaging techniques and endoscopic therapies.
  • RECENT FINDINGS: There are indications that ethnic minorities such as blacks and Hispanics are at considerably lower risk for Barrett's esophagus (<2%) compared with whites.
  • Central obesity rather than BMI could be a more important determinant of Barrett's metaplasia and neoplasia.
  • Novel imaging techniques, in feasibility trials, have shown high accuracy for the detection of metaplasia and dysplasia.
  • SUMMARY: A better appreciation of risk factors that lead to Barrett's esophagus and its neoplastic progression may help in formulating early intervention strategies.
  • The emergence of novel imaging modalities for early and accurate detection of dysplasia, combined with new therapies, may have a substantial impact in improving outcomes among Barrett's esophagus patients.
  • [MeSH-major] Barrett Esophagus / pathology. Barrett Esophagus / therapy. Population Surveillance
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Adenocarcinoma / prevention & control. Esophageal Neoplasms / etiology. Esophageal Neoplasms / pathology. Esophageal Neoplasms / prevention & control. Humans. Metaplasia / pathology. Risk Factors

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  • (PMID = 18622169.001).
  • [ISSN] 1531-7056
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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17. Boult J, Roberts K, Brookes MJ, Hughes S, Bury JP, Cross SS, Anderson GJ, Spychal R, Iqbal T, Tselepis C: Overexpression of cellular iron import proteins is associated with malignant progression of esophageal adenocarcinoma. Clin Cancer Res; 2008 Jan 15;14(2):379-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of cellular iron import proteins is associated with malignant progression of esophageal adenocarcinoma.
  • PURPOSE: There is growing evidence that iron is important in esophageal adenocarcinoma, a cancer whose incidence is rising faster than any other in the Western world.
  • In this study, we investigated the expression of iron transport proteins involved in cellular iron import, export, and storage in the premalignant lesion Barrett's metaplasia and esophageal adenocarcinoma.
  • EXPERIMENTAL DESIGN: Perls' staining was used to examine iron deposition in tissue. mRNA expression in samples of Barrett's metaplasia matched with esophageal adenocarcinoma and samples of Barrett's metaplasia without evidence of adenocarcinoma were examined by real-time PCR.
  • The effect of iron loading on cellular proliferation and iron transporter expression was determined in esophageal cell lines OE33 and SEG-1 using a bromodeoxyuridine assay and real-time PCR, respectively.
  • RESULTS: In the progression of Barrett's metaplasia to adenocarcinoma, there was overexpression of divalent metal transporter 1 (DMT1), transferrin receptor 1, duodenal cytochrome b, ferroportin, and H-ferritin, and these changes were associated with increased iron deposition.
  • Overexpression of DMT1 was further associated with metastatic adenocarcinoma.
  • CONCLUSIONS: Progression to adenocarcinoma is associated with increased expression of iron import proteins.
  • This may represent a novel mechanism of esophageal carcinogenesis.
  • [MeSH-major] Adenocarcinoma / physiopathology. Barrett Esophagus / physiopathology. Cation Transport Proteins / metabolism. Esophageal Neoplasms / physiopathology. Iron / metabolism

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  • (PMID = 18223212.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD71 antigen; 0 / Cation Transport Proteins; 0 / Cytochrome b Group; 0 / Receptors, Transferrin; 0 / metal transporting protein 1; 0 / solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2; 9013-31-4 / Apoferritins; E1UOL152H7 / Iron; EC 1.- / Oxidoreductases; EC 1.6.99.- / CYBRD1 protein, human
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18. Chaves P, Cruz C, Dias Pereira A, Suspiro A, de Almeida JC, Leitão CN, Soares J: Gastric and intestinal differentiation in Barrett's metaplasia and associated adenocarcinoma. Dis Esophagus; 2005;18(6):383-7
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  • [Title] Gastric and intestinal differentiation in Barrett's metaplasia and associated adenocarcinoma.
  • Intestinal metaplasia is a prerequisite criterion for the diagnosis of Barrett's metaplasia and the sole columnar esophageal lining associated with malignancy.
  • The cellular heterogeneity of Barrett's metaplasia is well documented but the relationship between the distinct cell subtypes and neoplasia is unclear.
  • We studied 46 columnar-lined esophageal segments, 15 with associated adenocarcinoma.
  • In metaplasia there were no differences in MUC5AC and MUC6 immunoreactivity, between cases with and without associated neoplasia, except for goblet elements producing MUC6 that were exclusive of metaplasia adjacent to adenocarcinoma (P < 0.05).
  • In metaplasia it was restricted to Barrett's cases and was more frequent in areas with intestinal metaplasia.
  • Columnar-lined esophagus without intestinal metaplasia did not express MUC2.

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  • (PMID = 16336609.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Gastric Mucins; 0 / MUC6 protein, human; 0 / Mucin-6; 0 / Mucins; 0 / apomucin
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19. Grassi A, Giannarelli D, Iacopini F, Paoluzi P, Iannetti A, Giovannelli L, Efrati C, Barberani F, Giovannone M, Tosoni M: Prevalence of intestinal metaplasia in the distal esophagus in patients endoscopically suspected for short Barrett's esophagus. J Exp Clin Cancer Res; 2006 Sep;25(3):297-302
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of intestinal metaplasia in the distal esophagus in patients endoscopically suspected for short Barrett's esophagus.
  • The clinical importance of Barrett's esophagus is related to its correlation to adenocarcinoma.
  • The diagnosis is based on histologic demonstration of specialized intestinal metaplasia in the distal esophagus.
  • The aim of this study was to assess the prevalence of intestinal metaplasia of the distal esophagus in a population submitted to gastroscopy not selected for reflux disease, and with columnar lined distal esophagus between 0.5 and 2 cm.
  • Four biopsies in the distal esophagus were done in 224 patients undergoing routine gastroscopy.
  • In four Centers 224 patients received endoscopy with biopsies demonstrating specialized intestinal metaplasia in 21% of cases.
  • A significant association was present in over 70 (females), as well as with the presence of antral intestinal metaplasia demonstrated in 45 patients by gastric biopsies.
  • Biopsy samplings can diagnose the presence of intestinal metaplasia during endoscopy in patients endoscopically suspected for Barrett's esophagus: at present there is not clear evidence to promote this screening to achieve mortality reduction of esophageal adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal. Esophagus / pathology. Intestinal Mucosa / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Male. Metaplasia / epidemiology. Middle Aged. Prevalence

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  • (PMID = 17167967.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Italy
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20. Colleypriest BJ, Ward SG, Tosh D: How does inflammation cause Barrett's metaplasia? Curr Opin Pharmacol; 2009 Dec;9(6):721-6
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  • [Title] How does inflammation cause Barrett's metaplasia?
  • Oesophageal adenocarcinoma conveys a poor prognosis and has a rapidly increasing incidence.
  • Similarly, Barrett's metaplasia (a precursor lesion for oesophageal adenocarcinoma) has an increasing incidence.
  • Both oesophageal adenocarcinoma and Barrett's metaplasia are more common in the context of inflammation as a result of acid and bile reflux.
  • The cytokine profile of Barrett's metaplasia is predominantly a T-helper 2 response that contrasts with the T-helper 1 response in normal and inflamed oesophagus and normal intestine.
  • A key transcription factor in the development of Barrett's metaplasia, CDX2, has recently been shown to be induced in response to inflammatory mediators.
  • Understanding the role of oesophageal inflammation will provide important insight into the development of Barrett's metaplasia and oesophageal cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / etiology. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Esophagitis / complications
  • [MeSH-minor] Animals. Cyclooxygenase 2 / metabolism. Cytokines / metabolism. Humans. Metaplasia / metabolism. Metaplasia / pathology. Models, Immunological. NF-kappa B / metabolism. Precancerous Conditions / metabolism. Precancerous Conditions / pathology

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  • (PMID = 19828375.001).
  • [ISSN] 1471-4973
  • [Journal-full-title] Current opinion in pharmacology
  • [ISO-abbreviation] Curr Opin Pharmacol
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300415
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / NF-kappa B; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 53
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21. Martin RC, Liu Q, Wo JM, Ray MB, Li Y: Chemoprevention of carcinogenic progression to esophageal adenocarcinoma by the manganese superoxide dismutase supplementation. Clin Cancer Res; 2007 Sep 1;13(17):5176-82
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  • [Title] Chemoprevention of carcinogenic progression to esophageal adenocarcinoma by the manganese superoxide dismutase supplementation.
  • PURPOSE: Oxidative stress is related to the carcinogenic pathway of reflux esophagitis to Barrett's metaplasia to esophageal adenocarcinoma (EAC).
  • Recent studies have shown that a decreased manganese superoxide dismutase (MnSOD) level is associated with the increased incidences of Barrett's esophagus (BE) and EAC.
  • RESULTS: Severe esophagitis was seen in 100% of the EDA rats, and morphologic transformation within the esophageal epithelium was observed with intestinal metaplasia (40% of animals) and cancer (40% of animals) identified after 3 months.
  • CONCLUSION: MnTBAP protected rat esophageal epithelium from oxidative injury induced by EDA, and it could prevent the transformation of esophageal epithelial cell to BE to EAC by preservation of antioxidants.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anticarcinogenic Agents / administration & dosage. Antioxidants / therapeutic use. Esophageal Neoplasms / prevention & control. Metalloporphyrins / therapeutic use. Superoxide Dismutase / administration & dosage
  • [MeSH-minor] Animals. Apoptosis. Cell Proliferation. Deoxyguanosine / analogs & derivatives. Deoxyguanosine / analysis. Esophagus / pathology. Rats. Rats, Sprague-Dawley

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  • (PMID = 17785574.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Metalloporphyrins; 0 / manganese(III)-tetrakis(4-benzoic acid)porphyrin; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; EC 1.15.1.1 / Superoxide Dismutase; G9481N71RO / Deoxyguanosine
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22. Goda K, Tajiri H, Ikegami M, Urashima M, Nakayoshi T, Kaise M: Usefulness of magnifying endoscopy with narrow band imaging for the detection of specialized intestinal metaplasia in columnar-lined esophagus and Barrett's adenocarcinoma. Gastrointest Endosc; 2007 Jan;65(1):36-46
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  • [Title] Usefulness of magnifying endoscopy with narrow band imaging for the detection of specialized intestinal metaplasia in columnar-lined esophagus and Barrett's adenocarcinoma.
  • BACKGROUND: Barrett's esophagus with specialized intestinal metaplasia (SIM) from columnar-lined esophagus is difficult to distinguish with routine endoscopy.
  • OBJECTIVE: To examine the values of fine mucosal patterns and the capillary patterns observed by magnifying endoscopy with narrow band imaging (MENBI) for the detection of SIM in columnar-lined esophagus and superficial Barrett's adenocarcinoma.
  • DESIGN: To compare the findings of MENBI, at 217 sites of columnar-lined esophagus, with histologic findings.
  • PATIENTS: Fifty-eight patients, including 4 with superficial Barrett's adenocarcinoma.
  • RESULTS: Upon observation, all 6 adenocarcinoma sites were classified as irregular patterns in both the fine mucosal patterns and capillary patterns.
  • The addition of capillary patterns to fine mucosal patterns appeared to improve the diagnostic value for detecting SIM and superficial Barrett's adenocarcinoma upon observation by MENBI.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal / methods. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Intestinal Mucosa / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Capillaries / pathology. Female. Humans. Image Processing, Computer-Assisted. Male. Metaplasia. Microscopy, Confocal. Middle Aged. Prospective Studies. Sensitivity and Specificity

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  • [CommentIn] Gastrointest Endosc. 2007 Jan;65(1):47-9 [17185079.001]
  • (PMID = 17185078.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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23. Dietz J, Chaves-E-Silva S, Meurer L, Sekine S, de Souza AR, Meine GC: Short segment Barrett's esophagus and distal gastric intestinal metaplasia. Arq Gastroenterol; 2006 Apr-Jun;43(2):117-20
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  • [Title] Short segment Barrett's esophagus and distal gastric intestinal metaplasia.
  • BACKGROUND: Short segment Barrett's esophagus is defined by the presence of <3 cm of columnar-appearing mucosa in the distal esophagus with intestinal metaplasia on histophatological examination.
  • Barrett's esophagus is a risk factor to develop adenocarcinoma of the esophagus.
  • While Barrett's esophagus develops as a result of chronic gastroesophageal reflux disease, intestinal metaplasia in the gastric cardia is a consequence of chronic Helicobacter pylori infection and is associated with distal gastric intestinal metaplasia.
  • It can be difficult to determine whether short-segment columnar epithelium with intestinal metaplasia are lining the esophagus (a condition called short segment Barrett's esophagus) or the proximal stomach (a condition called intestinal metaplasia of the gastric cardia).
  • AIMS: To study the association of short segment Barrett's esophagus (length <3 cm) with gastric intestinal metaplasia (antrum or body) and infection by H. pylori.
  • PATIENTS AND METHODS: Eight-nine patients with short segment columnar-appearing mucosa in the esophagus, length <3 cm, were studied.
  • Biopsies were obtained immediately below the squamous-columnar lining, from gastric antrum and gastric corpus for investigation of intestinal metaplasia and H. pylori.
  • RESULTS: Forty-two from 89 (47.2%) patients were diagnosed with esophageal intestinal metaplasia by histopathology.
  • The mean-age was significantly higher in the group with esophageal intestinal metaplasia.
  • Gastric intestinal metaplasia (antrum or body) was diagnosed in 21 from 42 (50.0%) patients in the group with esophageal intestinal metaplasia and 7 from 47 (14.9%) patients in the group with esophageal columnar appearing mucosa but without intestinal metaplasia.
  • CONCLUSION: Intestinal metaplasia is a frequent finding in patients with <3 cm of columnar-appearing mucosa in the distal esophagus.
  • In the present study, short segment intestinal metaplasia in the esophagus is associated with distal gastric intestinal metaplasia.
  • [MeSH-major] Barrett Esophagus / pathology. Gastroesophageal Reflux / pathology. Helicobacter Infections / pathology. Intestines / pathology. Stomach / pathology
  • [MeSH-minor] Biopsy. Cardia / pathology. Esophagoscopy. Female. Gastritis / microbiology. Gastritis / pathology. Humans. Male. Metaplasia / pathology. Middle Aged

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  • (PMID = 17119666.001).
  • [ISSN] 0004-2803
  • [Journal-full-title] Arquivos de gastroenterologia
  • [ISO-abbreviation] Arq Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
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24. O'Riordan JM, Abdel-latif MM, Ravi N, McNamara D, Byrne PJ, McDonald GS, Keeling PW, Kelleher D, Reynolds JV: Proinflammatory cytokine and nuclear factor kappa-B expression along the inflammation-metaplasia-dysplasia-adenocarcinoma sequence in the esophagus. Am J Gastroenterol; 2005 Jun;100(6):1257-64
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  • [Title] Proinflammatory cytokine and nuclear factor kappa-B expression along the inflammation-metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.
  • BACKGROUND: The incidence of esophageal adenocarcinoma has increased significantly in the western world over the last 20 yr.
  • Most cases arise in a background of chronic gastroesophageal reflux, and specialized intestinal metaplasia in Barrett's esophagus is frequently an antecedent phenotype or evident in association with adenocarcinoma.
  • The molecular events that characterize the pathway from inflammation to metaplasia to dysplasia and adenocarcinoma are poorly understood.
  • AIMS: To examine the expression of the proinflammatory cytokines IL-8 and IL-1beta along the esophagitis, metaplasia, dysplasia, and adenocarcinoma pathway, and to correlate this with histological changes and expression of the transcription factor NF-kappaB.
  • PATIENTS AND METHODS: Fresh biopsy specimens were collected from patients with reflux esophagitis (n=15), Barrett's esophagus (n=35), Barrett's adjacent to adenocarcinoma (n=8), and esophageal adenocarcinoma (n=35).
  • RESULTS: Elevated expression of NF-kappaB was found in 2 (13%) out of 15 patients with reflux esophagitis, 21 (60%) out of 35 patients with Barrett's esophagus, and 28 (80%) out of 35 patients with esophageal adenocarcinoma.
  • All 5 patients with Barrett's esophagus and high-grade dysplasia showed elevated expression of NF-kappaB.
  • IL-8 and IL-1beta were significantly increased in esophagitis, Barrett's, and adenocarcinoma compared with squamous epithelium, and in adenocarcinoma compared with all other groups.
  • There was a stepwise increase in the expression of IL-8, IL-1beta, and NF-kappaB from normal through Barrett's epithelium to adenocarcinoma in eight cases of esophageal adenocarcinoma.
  • The levels of both IL-8 and IL-1beta in adenocarcinoma patients correlated with stage of disease.
  • Patients with adenocarcinoma who were NF-kappaB positive had significantly higher levels of both IL-8 (p=0.04) and IL-1beta (p=0.03) compared to adenocarcinoma patients who were NF-kappaB negative.
  • CONCLUSIONS: The proinflammatory cytokines IL-8 and IL-1beta are elevated in esophagitis and Barrett's epithelium, and markedly elevated in adenocarcinoma.
  • NF-kappaB activation is infrequent in esophagitis, but is increased in Barrett's epithelium and adenocarcinoma.
  • The association of NF-kappaB activation with cytokine upregulation was only evident in patients with adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Esophageal Neoplasms / metabolism. Esophagitis / metabolism. Interleukin-1 / biosynthesis. Interleukin-8 / biosynthesis. NF-kappa B / biosynthesis
  • [MeSH-minor] Barrett Esophagus / metabolism. Barrett Esophagus / pathology. Biomarkers / metabolism. Biopsy. Electrophoresis. Endoscopy, Digestive System. Enzyme-Linked Immunosorbent Assay. Female. Gastroesophageal Reflux / metabolism. Gastroesophageal Reflux / pathology. Humans. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Metaplasia / metabolism. Metaplasia / pathology. Middle Aged. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Prospective Studies

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  • (PMID = 15929754.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Interleukin-1; 0 / Interleukin-8; 0 / NF-kappa B
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25. Kimchi ET, Posner MC, Park JO, Darga TE, Kocherginsky M, Karrison T, Hart J, Smith KD, Mezhir JJ, Weichselbaum RR, Khodarev NN: Progression of Barrett's metaplasia to adenocarcinoma is associated with the suppression of the transcriptional programs of epidermal differentiation. Cancer Res; 2005 Apr 15;65(8):3146-54
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  • [Title] Progression of Barrett's metaplasia to adenocarcinoma is associated with the suppression of the transcriptional programs of epidermal differentiation.
  • We did expressional profiling on 24 paired samples of normal esophageal epithelium, Barrett's metaplasia, and esophageal adenocarcinomas.
  • Matching tissue samples representing the three different histologic types were obtained from each patient undergoing esophagectomy for adenocarcinoma.
  • Our analysis compared the molecular changes accompanying the transformation of normal squamous epithelium with Barrett's esophagus and adenocarcinoma in individual patients rather than in a random cohort.
  • We tested the hypothesis that expressional profiling may reveal gene sets that can be used as molecular markers of progression from normal esophageal epithelium to Barrett's esophagus and adenocarcinoma.
  • The final selection of 214 genes permitted the discrimination of differential gene expression of normal esophageal squamous epithelium, Barrett's esophagus, and adenocarcinoma using two-dimensional hierarchical clustering of selected genes.
  • These data indicate that transformation of Barrett's esophagus to adenocarcinoma is associated with suppression of the genes involved in epidermal differentiation, including genes in 1q21 loci and corresponding to the epidermal differentiation complex.
  • Correlation analysis of genes concordantly expressed in Barrett's esophagus and adenocarcinoma revealed 21 genes that represent potential genetic markers of disease progression and pharmacologic targets for treatment intervention.
  • PCR analysis of genes selected based on DNA array experiments revealed that estimation of the ratios of GATA6 to SPRR3 allows discrimination among normal esophageal epithelium, Barrett's dysplasia, and adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Cell Transformation, Neoplastic / genetics. Esophageal Neoplasms / genetics

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  • (PMID = 15833844.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 71933
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cornified Envelope Proline-Rich Proteins; 0 / DNA-Binding Proteins; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Proteins; 0 / SPRR3 protein, human; 0 / Transcription Factors
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26. Yang L, Lu X, Nossa CW, Francois F, Peek RM, Pei Z: Inflammation and intestinal metaplasia of the distal esophagus are associated with alterations in the microbiome. Gastroenterology; 2009 Aug;137(2):588-97
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  • [Title] Inflammation and intestinal metaplasia of the distal esophagus are associated with alterations in the microbiome.
  • BACKGROUND & AIMS: Gastroesophageal reflux causes inflammation and intestinal metaplasia and its downstream sequelum adenocarcinoma in the distal esophagus.
  • The incidence of esophageal adenocarcinoma has increased approximately 6-fold in the United States since the 1970s, accompanied with a significant increase in the prevalence of gastroesophageal reflux disease (GERD).
  • Microbes are among the environmental factors that may contribute to the etiology of GERD, but very little research has been done on the esophageal microbiome, particularly in its relation to GERD.
  • This is the first comprehensive reported correlation between a change in the esophageal microbiome and esophageal diseases.
  • METHODS: Biopsy samples of the distal esophagus were collected from 34 patients.
  • Host phenotypes were histologically defined as normal, esophagitis, or Barrett's esophagus (intestinal metaplasia).
  • RESULTS: Esophageal microbiomes can be classified into 2 types.
  • The type I microbiome was dominated by the genus Streptococcus and concentrated in the phenotypically normal esophagus.
  • Conversely, the type II microbiome contained a greater proportion of gram-negative anaerobes/microaerophiles and primarily correlated with esophagitis (odds ratio, 15.4) and Barrett's esophagus (odds ratio, 16.5).
  • CONCLUSIONS: In the human distal esophagus, inflammation and intestinal metaplasia are associated with global alteration of the microbiome.

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  • (PMID = 19394334.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI063477-05; United States / NCI NIH HHS / CA / R01 CA097946; United States / NCI NIH HHS / CA / UH2CA140233; United States / NCI NIH HHS / CA / CA140233-01; United States / NCI NIH HHS / CA / R01 CA097946-04; United States / NCI NIH HHS / CA / R01CA97946; United States / NIAID NIH HHS / AI / R01AI063477; United States / NIAID NIH HHS / AI / AI063477-05; United States / NCI NIH HHS / CA / UH2 CA140233-01; United States / NCI NIH HHS / CA / UH2 CA140233; United States / NCI NIH HHS / CA / CA097946-04; United States / NIAID NIH HHS / AI / R01 AI063477
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS135974; NLM/ PMC2963147
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27. Anderson LA, Johnston BT, Watson RG, Murphy SJ, Ferguson HR, Comber H, McGuigan J, Reynolds JV, Murray LJ: Nonsteroidal anti-inflammatory drugs and the esophageal inflammation-metaplasia-adenocarcinoma sequence. Cancer Res; 2006 May 1;66(9):4975-82
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  • [Title] Nonsteroidal anti-inflammatory drugs and the esophageal inflammation-metaplasia-adenocarcinoma sequence.
  • Observational studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of esophageal adenocarcinoma, but it is not known at what stage they may act in the esophageal inflammation-metaplasia-adenocarcinoma sequence.
  • In an all-Ireland case-control study, we investigated the relationship between the use of NSAIDs and risk of reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma.
  • Patients with esophageal adenocarcinoma, long-segment Barrett's esophagus and population controls were recruited from throughout Ireland.
  • Data were collected on known and potential risk factors for esophageal adenocarcinoma and on the use of NSAIDs, including aspirin, at least 1 year before interview.
  • Associations between use of NSAIDs and the stages of the esophageal inflammation-metaplasia-adenocarcinoma sequence were estimated by multiple logistic regression.
  • In total, 230 reflux esophagitis, 224 Barrett's esophagus, and 227 esophageal adenocarcinoma and 260 population controls were recruited.
  • Use of aspirin and NSAIDs was associated with a reduced risk of Barrett's esophagus [odds ratio [OR; 95% confidence interval (95% CI)], 0.53 (0.31-0.90) and 0.40 (0.19-0.81), respectively] and esophageal adenocarcinoma [OR (95% CI), 0.57 (0.36-0.93) and 0.58 (0.31-1.08), respectively].
  • Barrett's esophagus and esophageal adenocarcinoma patients were less likely than controls to have used NSAIDs.
  • Selection or recall bias may explain these results and the results of previous observational studies indicating a protective effect of NSAIDs against esophageal adenocarcinoma.
  • If NSAIDs have a true protective effect on the esophageal inflammation-metaplasia-adenocarcinoma sequence, they may act early in the sequence.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Barrett Esophagus / prevention & control. Esophageal Neoplasms / prevention & control. Esophagitis, Peptic / prevention & control
  • [MeSH-minor] Acetaminophen / administration & dosage. Aged. Aged, 80 and over. Aspirin / administration & dosage. Case-Control Studies. Esophagus / drug effects. Esophagus / pathology. Female. Humans. Male. Metaplasia. Middle Aged


28. Pera M, Grande L, Iglesias M, Ramón JM, Conio M: [New advances in the diagnosis and treatment of early onset dysplasia and adenocarcinoma in Barrett's oesophagus]. Cir Esp; 2009 Jun;85(6):331-40
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  • [Title] [New advances in the diagnosis and treatment of early onset dysplasia and adenocarcinoma in Barrett's oesophagus].
  • [Transliterated title] Nuevos avances en el diagnóstico y el tratamiento de la displasia y el adenocarcinoma precoz en el esófago de Barrett.
  • Periodic endoscopic follow-up is recommended after the diagnosis of Barrett's oesophagus, particularly in patients with dysplasia.
  • The new endoscopic techniques show promising results in identifying areas suspected of housing high grade dysplasia and adenocarcinoma.
  • Likewise, this technique may be the therapeutic option in patients with high grade dysplasia and adenocarcinoma, although its application must be complemented with ablation techniques such as radiofrequency to eliminate the residual Barrett's metaplasia.
  • Oesophagectomy associated with lymphadenectomy is the option of choice in patients with submucosal adenocarcinoma.
  • The diagnosis and treatment of patients with early onset high grade dysplasia and adenocarcinoma must be carried out with multidisciplinary teams who can evaluate each case individually.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / surgery. Esophagus / pathology

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  • (PMID = 19463990.001).
  • [ISSN] 0009-739X
  • [Journal-full-title] Cirugía española
  • [ISO-abbreviation] Cir Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Number-of-references] 71
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29. Villanacci V, Bellone G, Battaglia E, Rossi E, Carbone A, Prati A, Verna C, Niola P, Morelli A, Grassini M, Bassotti G: Ski/SnoN expression in the sequence metaplasia-dysplasia-adenocarcinoma of Barrett's esophagus. Hum Pathol; 2008 Mar;39(3):403-9
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  • [Title] Ski/SnoN expression in the sequence metaplasia-dysplasia-adenocarcinoma of Barrett's esophagus.
  • Barrett's esophagus (BE) is a precancerous condition.
  • Biopsy samples from 37 patients (26 men, aged 60 +/- 8 years) with histologically proven BE were evaluated; 10 patients had concomitant low-grade dysplasia, 7 high-grade dysplasia (HGD), and 6 HGD associated with adenocarcinoma.
  • Neither Ski nor SnoN was expressed in normal esophageal epithelium, but both were strongly expressed in BE tissue, with intense cytoplasmic positivity.
  • Expression of these proteins decreased markedly in dysplastic areas in patients with low-grade dysplasia and was absent in those with HGD or HGD/adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. DNA-Binding Proteins / biosynthesis. Esophageal Neoplasms / metabolism. Precancerous Conditions / metabolism. Proto-Oncogene Proteins / biosynthesis
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Humans. Immunohistochemistry. Intracellular Signaling Peptides and Proteins. Male. Metaplasia. Middle Aged. Transforming Growth Factor beta / metabolism

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  • (PMID = 18261624.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins; 0 / SKIL protein, human; 0 / Transforming Growth Factor beta; 126648-96-2 / SKI protein, human
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30. Segat D, Cassaro M, Dazzo E, Cavallini L, Romualdi C, Salvador R, Vitale MP, Vitiello L, Fassan M, Rugge M, Zaninotto G, Ancona E, Baroni MD: Pericentriolar material analyses in normal esophageal mucosa, Barrett's metaplasia and adenocarcinoma. Histol Histopathol; 2010 05;25(5):551-60
MedlinePlus Health Information. consumer health - Esophageal Cancer.

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  • [Title] Pericentriolar material analyses in normal esophageal mucosa, Barrett's metaplasia and adenocarcinoma.
  • Barrett's esophagus metaplasia is a pre-cancerous condition caused by chronic esophagitis.
  • Chromosomal instability (CIN) is common in Barrett's cells: therefore, we investigated the possible presence of centrosomal aberrations (a main cause of CIN) by centrosomal protein immunostaining in paraffined esophageal samples of patients who developed a Barrett's adenocarcinoma.
  • In most (55%) patients, alterations of the pericentriolar material (PCM) signals were evident and consistently marked the transition between normal epithelium to metaplasia.
  • The alterations could even be found in adjacent native squamous epithelium, Barrett's mucosa and submucosal gland cells, as well as in the basal/epibasal layers of the mucosa and submucosal gland duct, which are the regions hosting esophageal stem and progenitor cells.
  • These findings strongly support the hypothesis that the three esophageal histotypes (one being pathological) can have a common progenitor.
  • Importantly, PCM altered signals in Barrett's mucosa and their apparent evolution in successive histopathological steps were correlated to adenocarcinoma aggressiveness, suggesting PCM as a possible prognostic marker for tumor relapse.
  • Extending our observations in a prospective study might help in the development of new prevention protocols for adenocarcinoma patients.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Centrosome / metabolism. Esophageal Neoplasms / metabolism. Esophagus / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens / metabolism. Chromosomal Instability. Female. Humans. Immunohistochemistry. Male. Metaplasia. Middle Aged. Models, Biological. Mucous Membrane / anatomy & histology. Mucous Membrane / metabolism. Mucous Membrane / pathology. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Prognosis. Tubulin / metabolism

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  • (PMID = 20238294.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antigens; 0 / Tubulin; 0 / pericentrin
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31. Maru DM, Singh RR, Hannah C, Albarracin CT, Li YX, Abraham R, Romans AM, Yao H, Luthra MG, Anandasabapathy S, Swisher SG, Hofstetter WL, Rashid A, Luthra R: MicroRNA-196a is a potential marker of progression during Barrett's metaplasia-dysplasia-invasive adenocarcinoma sequence in esophagus. Am J Pathol; 2009 May;174(5):1940-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA-196a is a potential marker of progression during Barrett's metaplasia-dysplasia-invasive adenocarcinoma sequence in esophagus.
  • Barrett's esophagus (BE)/Barrett's metaplasia (BM) is a recognized precursor of esophageal adenocarcinoma (EA) with an intermediary stage of dysplasia.
  • The low yield and high cost of endoscopic screening of patients with BE underscores the need for novel biomarkers, such as microRNA (miRNA), which have emerged as important players in neoplastic progression for risk assessment of developing dysplasia/adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Esophagus / pathology. MicroRNAs / genetics
  • [MeSH-minor] Adult. Aged. Calgranulin B / genetics. Calgranulin B / metabolism. Cornified Envelope Proline-Rich Proteins / genetics. Cornified Envelope Proline-Rich Proteins / metabolism. DNA Primers / chemistry. Disease Progression. Female. Humans. Keratin-5 / genetics. Keratin-5 / metabolism. Male. Metaplasia. Middle Aged. Neoplasm Invasiveness. RNA, Messenger / genetics. RNA, Messenger / metabolism. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19342367.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calgranulin B; 0 / Cornified Envelope Proline-Rich Proteins; 0 / DNA Primers; 0 / KRT5 protein, human; 0 / Keratin-5; 0 / MIRN196 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / SPRR2C protein, human
  • [Other-IDs] NLM/ PMC2671281
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32. Chennat J, Waxman I: Endoscopic treatment of Barrett's esophagus: From metaplasia to intramucosal carcinoma. World J Gastroenterol; 2010 Aug 14;16(30):3780-5
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  • [Title] Endoscopic treatment of Barrett's esophagus: From metaplasia to intramucosal carcinoma.
  • The annual incidence of adenocarcinoma arising from Barrett's esophagus (BE) is approximately 0.5%.
  • Through a process of gradual transformation from low-grade dysplasia to high-grade dysplasia (HGD), adenocarcinoma can develop in the setting of BE.
  • The clinical importance of appropriate identification and treatment of BE in its various stages, from intestinal metaplasia to intramucosal carcinoma (IMC) hinges on the dramatically different prognostic status between early neoplasia and more advanced stages.
  • Once a patient has symptoms of adenocarcinoma, there is usually locally advanced disease with an approximate 5-year survival rate of about 20%.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophagoscopy. Esophagus / surgery. Precancerous Conditions / surgery
  • [MeSH-minor] Catheter Ablation. Cryosurgery. Disease Progression. Humans. Metaplasia. Mucous Membrane / pathology. Mucous Membrane / surgery. Photochemotherapy. Treatment Outcome

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  • (PMID = 20698040.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2921089
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33. Zhang HY, Spechler SJ, Souza RF: Esophageal adenocarcinoma arising in Barrett esophagus. Cancer Lett; 2009 Mar 18;275(2):170-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Esophageal adenocarcinoma arising in Barrett esophagus.
  • The major risk factors for esophageal adenocarcinoma are gastroesophageal reflux disease (GERD) and Barrett esophagus, a squamous-to-columnar cell metaplasia that predisposes to malignancy.
  • Adenocarcinomas in Barrett esophagus are thought to arise through a sequence of growth-promoting, genetic alterations that accumulate until the cells have acquired the physiologic hallmarks of cancer proposed by Hanahan and Weinberg.
  • Moreover, GERD and Barrett esophagus are associated with chronic esophagitis, and inflammation is a well known risk factor for cancer formation.
  • The cell that gives rise to Barrett metaplasia is not known.
  • It has been proposed that the metaplasia may arise from a change in the differentiation pattern of stem cells that either reside in the esophagus or are recruited to the esophagus from the bone marrow.
  • Alternatively, it is possible that Barrett metaplasia develops through the conversion of one differentiated cell type into another.
  • Regardless of the cell of origin, Barrett metaplasia ultimately must be sustained by stem cells, which might be identified by intestinal stem cell markers.
  • If Barrett cancers develop from Barrett stem cells, then a therapy targeted at those stem cells might prevent esophageal adenocarcinoma.
  • This report reviews the risk factors for Barrett esophagus and esophageal adenocarcinoma, the mechanisms by which genetic alterations might contribute to carcinogenesis in Barrett esophagus, and the role of stem cells in the development of Barrett metaplasia and adenocarcinoma.

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  • (PMID = 18703277.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK063621-06A2; United States / NIDDK NIH HHS / DK / R01 DK063621; United States / NIDDK NIH HHS / DK / DK 63621; United States / NIDDK NIH HHS / DK / R01 DK063621-06A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Ireland
  • [Number-of-references] 71
  • [Other-IDs] NLM/ NIHMS98405; NLM/ PMC2673195
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34. Tantau M, Mosteanu O, Pop T, Tantau A, Mester G: Endoscopic therapy of Barrett's esophagus and esophageal adenocarcinoma. J Gastrointestin Liver Dis; 2010 Jun;19(2):213-7
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic therapy of Barrett's esophagus and esophageal adenocarcinoma.
  • The normal squamous esophageal epithelium reacts as a chronic inflammation to the severe gastro-esophageal reflux.
  • Esophagitis will progress to Barrett metaplasia in 10% of patients who would be of minor clinical interest if it then did not advance to low, high grade dysplasia and invasive carcinoma.
  • The rise of esophageal adenocarcinoma (EAC) incidence surpasses any other cancer, including melanoma, lymphoma and small cell lung cancer.
  • A multimodal approach of Barrett's esophagus with high grade dysplasia is required, including endoscopic mucosal resection, photodynamic therapy and thermal ablation.
  • The correction of the malignant esophageal obstruction improves the symptomatology and life quality, but not survival.
  • [MeSH-major] Adenocarcinoma / therapy. Barrett Esophagus / therapy. Esophageal Neoplasms / therapy. Esophagoscopy

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  • (PMID = 20593060.001).
  • [ISSN] 1841-8724
  • [Journal-full-title] Journal of gastrointestinal and liver diseases : JGLD
  • [ISO-abbreviation] J Gastrointestin Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Romania
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35. Bu X, Ma Y, Der R, Demeester T, Bernstein L, Chandrasoma PT: Body mass index is associated with Barrett esophagus and cardiac mucosal metaplasia. Dig Dis Sci; 2006 Sep;51(9):1589-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Body mass index is associated with Barrett esophagus and cardiac mucosal metaplasia.
  • A positive association between body mass index (BMI) and risk of esophageal adenocarcinoma has been reported.
  • Barrett esophagus (BE) is a precursor lesion for esophageal adenocarcinoma.
  • Cardiac mucosa (CM) and BE are both reflux-induced metaplastic columnar epithelia in the esophagus.
  • Linear regression analysis was employed to examine the relationship between length of columnar lined esophagus (CLE) and BMI.
  • In conclusion, BMI is associated with BE and CM and appears to act early in the sequence of events leading from gastroesophageal reflux disease to metaplasia (CM and BE) to dysplasia and finally to adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / etiology. Body Mass Index. Cardia / pathology. Gastric Mucosa / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Esophagoscopy. Female. Humans. Male. Metaplasia. Middle Aged. Risk Factors

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  • (PMID = 16927134.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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36. Griffiths EA, Pritchard SA, McGrath SM, Valentine HR, Price PM, Welch IM, West CM: Increasing expression of hypoxia-inducible proteins in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence. Br J Cancer; 2007 May 7;96(9):1377-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increasing expression of hypoxia-inducible proteins in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
  • Our aim was to assess the immunohistochemical expression of hypoxia-inducible factor (HIF)-1alpha, HIF-2alpha, erythropoietin (Epo), Epo receptor (Epo-R), Glut-1 and vascular endothelial growth factor (VEGF) along with Ki67/MIB-1 in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
  • Endoscopic biopsies of normal squamous epithelium (NSE) (n=20), columnar-lined oesophagus (CLO) (n=15), CLO with intestinal metaplasia (n=20), dysplasia (n=17) and Barrett's type adenocarcinoma (n=20) were obtained.
  • Significant increases in the expression of HIF-2alpha (P=0.014), VEGF (P<0.0001), Epo-R (P<0.0001) and Ki67 (P<0.0001) were found as tissue progressed from NSE to adenocarcinoma.
  • HIF-2alpha was expressed late in the sequence and was only seen in dysplasia and adenocarcinoma.
  • High HIF-2alpha expression was seen in 12 out of 20 Barrett's type adenocarcinoma.
  • The late expression of HIF-2alpha in the Barrett's carcinogenesis sequence and its high expression in adenocarcinoma suggest that it is worth further investigation as a marker of disease progression and therapeutic target.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Basic Helix-Loop-Helix Transcription Factors / metabolism. Esophageal Neoplasms / pathology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • [MeSH-minor] Biopsy. Disease Progression. Epithelial Cells / cytology. Epithelial Cells / pathology. Esophageal Diseases / pathology. Esophagus / cytology. Esophagus / pathology. Immunohistochemistry. Ki-67 Antigen / metabolism. Metaplasia. Receptors, Erythropoietin / metabolism. Reference Values. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 17437013.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / Receptors, Erythropoietin; 0 / Vascular Endothelial Growth Factor A; 0 / endothelial PAS domain-containing protein 1
  • [Other-IDs] NLM/ PMC2360174
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37. Sharma P, Wani S, Bansal A: The quest for intestinal metaplasia--is it worth the effort? Am J Gastroenterol; 2007 Jun;102(6):1162-5
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  • [Title] The quest for intestinal metaplasia--is it worth the effort?
  • The columnar-lined esophagus (CLE) has remained an enigma for several decades.
  • Starting with the basics, the definition and diagnosis of Barrett's esophagus (BE) continues to be a point of major debate globally leading to definitions that have been restrictive (requiring histologically confirmed intestinal metaplasia) or all-encompassing (simply the presence of CLE at endoscopy).
  • The interest in intestinal metaplasia stems from studies that have consistently demonstrated intestinal metaplasia and dysplasia both adjacent to and remote from esophageal adenocarcinoma.
  • The proponents of not requiring histology suggest that if a sufficient number of biopsies is obtained over an adequate period of time, intestinal metaplasia can usually be demonstrated in such cases and that the true neoplastic potential of the cardiac and fundic-type mucosa detected in the CLE has not been delineated.
  • The optimal number of biopsies required to detect intestinal metaplasia is largely unknown, and in this issue of The American Journal of Gastroenterology, Harrison et al. add to the limited data on this subject.
  • There is ample evidence that once a diagnosis of BE is made, it has significant implications on the financial, psychosocial, and insurance status of the patients.
  • We feel that an optimal, practical definition of BE requires clear, accepted, reproducible, and clinically relevant criteria with evidence of an increased risk of cancer--the most crucial consequence of the lesion--and discuss the pros and cons of the need for documenting intestinal metaplasia in the CLE.
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Biopsy. Diagnostic Imaging. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology. Gastric Mucosa / pathology. Humans. Metaplasia. Precancerous Conditions / pathology

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  • [CommentOn] Am J Gastroenterol. 2007 Jun;102(6):1154-61 [17433019.001]
  • (PMID = 17531009.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
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38. Colleypriest BJ, Farrant JM, Slack JM, Tosh D: The role of Cdx2 in Barrett's metaplasia. Biochem Soc Trans; 2010 Apr;38(2):364-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of Cdx2 in Barrett's metaplasia.
  • Metaplasia (or transdifferentiation) is defined as the transformation of one tissue type to another.
  • Clues to the molecular mechanisms that control the development of metaplasia are implied from knowledge of the transcription factors that specify tissue identity during normal embryonic development.
  • Barrett's metaplasia describes the development of a columnar/intestinal phenotype in the squamous oesophageal epithelium and is the major risk factor for oesophageal adenocarcinoma.
  • The homoeotic transcription factor Cdx2 (Caudal-type homeobox 2) has been implicated as a master switch gene for intestine and therefore for Barrett's metaplasia.
  • In addition, Cdx2 is sufficient to provoke intestinal metaplasia in the stomach.
  • In the present paper, we review the evidence for the role of Cdx2 in the development of Barrett's metaplasia.

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  • (PMID = 20298184.001).
  • [ISSN] 1470-8752
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / G0300415; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins
  • [Number-of-references] 72
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39. Shi XY, Bhagwandeen B, Leong AS: CDX2 and villin are useful markers of intestinal metaplasia in the diagnosis of Barrett esophagus. Am J Clin Pathol; 2008 Apr;129(4):571-7
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  • [Title] CDX2 and villin are useful markers of intestinal metaplasia in the diagnosis of Barrett esophagus.
  • The identification of intestinal metaplasia (IM) in the esophagus is necessary for the selection of patients with Barrett esophagus (BE) for surveillance.
  • We studied 108 esophageal biopsy and resection specimens, clinically diagnosed as BE, and stained them for CDX2, villin, HepPar-1, and cytokeratin (CK) 7 to investigate sensitivity for identifying IM.
  • CDX2 and villin are sensitive markers for early-stage IM and can supplement the histologic identification of this premalignant condition in the esophagus.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / metabolism. Biomarkers, Tumor / metabolism. Homeodomain Proteins / metabolism. Microfilament Proteins / metabolism. Precancerous Conditions / diagnosis. Precancerous Conditions / metabolism
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Adenocarcinoma / surgery. Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / surgery. Female. Humans. Keratin-7 / metabolism. Male. Metaplasia. Middle Aged. Mucous Membrane / metabolism. Mucous Membrane / pathology

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  • (PMID = 18343784.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-7; 0 / Microfilament Proteins; 0 / villin
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40. Chandrasoma P, Wickramasinghe K, Ma Y, DeMeester T: Is intestinal metaplasia a necessary precursor lesion for adenocarcinomas of the distal esophagus, gastroesophageal junction and gastric cardia? Dis Esophagus; 2007;20(1):36-41
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  • [Title] Is intestinal metaplasia a necessary precursor lesion for adenocarcinomas of the distal esophagus, gastroesophageal junction and gastric cardia?
  • Adenocarcinoma of the distal esophagus and gastroesophageal junction are believed to arise in Barrett's esophagus with intestinal metaplasia.
  • Whether adenocarcinoma can arise in columnar lined esophagus without intestinal metaplasia is in doubt.
  • Whether adenocarcinoma of the gastric cardia arises in intestinal metaplasia of the gastric cardia is also in doubt.
  • We aim to evaluate the relationship of size and stage of adenocarcinoma of the distal esophagus, gastroesophageal junction and gastric cardia to intestinal metaplasia and other types of columnar epithelium.
  • Seventy-four patients who had esophagogastrectomy for adenocarcinomas in this region were examined histologically to assess the frequency of residual intestinal metaplasia in the surrounding epithelium.
  • Tumors without residual intestinal metaplasia were evaluated for the presence of other columnar epithelia and correlated with tumor size and stage.
  • Residual intestinal metaplasia was present in 48 (65%) tumors, including 33/38 (87%) distal esophageal, 10/25 (45%) junctional and 5/11 (45%) gastric cardia tumors.
  • The prevalence of intestinal metaplasia was 100% in all tumors that were less than 1 cm in maximum diameter and all intramucosal tumors.
  • The prevalence of residual intestinal metaplasia decreased with increasing tumor size and stage.
  • The absence of residual intestinal metaplasia in larger tumors is the result of tumor overgrowing the intestinal metaplasia from which it arose.

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  • (PMID = 17227308.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Szachnowicz S, Cecconello I, Iriya K, Marson AG, Takeda FR, Gama-Rodrigues JJ: Origin of adenocarcinoma in Barrett's esophagus: p53 and Ki67 expression and histopathologic background. Clinics (Sao Paulo); 2005 Apr;60(2):103-12
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  • [Title] Origin of adenocarcinoma in Barrett's esophagus: p53 and Ki67 expression and histopathologic background.
  • Barrett's esophagus is the substitution of squamous epithelium of the distal esophagus by columnar epithelium.
  • Intestinal metaplasia in Barrett's esophagus is considered to be the main risk factor for the development of adenocarcinoma.
  • Diffuse adenocarcinoma and Barrett's esophagus without intestinal metaplasia are rare, and reports on the subject are scarce.
  • PURPOSE AND METHOD: To estimate the prevalence of adenocarcinoma in 297 patients with Barrett's esophagus, during the period of 1990 to 2002, and in 13 patients undergoing surgery, to conduct detailed macroscopic and microscopic analysis, with performance of immunohistochemical tests for p53 and Ki67, correlating the type of tumor with its adjacent epithelium.
  • RESULTS: In our patients with Barrett's esophagus, there was a prevalence of 5.7% of adenocarcinoma.
  • The tumors developed only when the Barrett's esophagus segment was long (>3.0 cm).
  • The histological study revealed 2 patients (15.4%) with Barrett's esophagus adjacent to a tumor with gastric metaplasia without the presence of intestinal metaplasia.
  • CONCLUSION: Adenocarcinoma develops from mixed columnar epithelium, either intestinal or gastric, showing both the gastric and the intestinal patterns; thus, tumors can also grow in columnar epithelium without intestinal metaplasia.
  • Barrett's esophagus should be followed up for the possibility of progression to malignancy, especially when the segment is longer than 3 cm.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Ki-67 Antigen / analysis. Tumor Suppressor Protein p53 / analysis
  • [MeSH-minor] Adult. Aged. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Female. Humans. Male. Metaplasia / metabolism. Metaplasia / pathology. Middle Aged. Prevalence

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  • (PMID = 15880245.001).
  • [ISSN] 1807-5932
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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42. Izzo JG, Luthra R, Wu TT, Correa AM, Luthra M, Anandasabapathy S, Chao KS, Hung MC, Aggarwal B, Hittelman WN, Ajani JA: Molecular mechanisms in Barrett's metaplasia and its progression. Semin Oncol; 2007 Apr;34(2 Suppl 1):S2-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular mechanisms in Barrett's metaplasia and its progression.
  • The dramatic increase in the incidence and poor overall survival rates of esophageal/gastroesophageal junction adenocarcinoma underscore the necessity to discover molecular markers that can be used for risk assessment, early diagnosis, and targeted therapeutic intervention.
  • Barrett's esophagus (BE) is proposed to represent a precursor of esophageal/gastroesophageal junction adenocarcinoma.
  • BE progression to invasive cancer is defined by a metaplasia-dysplasia-carcinoma progression characterized by an increasing accumulation of genetic changes associated with alterations in molecular gatekeepers of cell circuitries and tissue homeostasis.
  • [MeSH-major] Barrett Esophagus / pathology. Biomarkers, Tumor / analysis. Esophageal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Cell Transformation, Neoplastic / pathology. Chemoprevention. Cyclin D1 / physiology. Disease Progression. Early Diagnosis. Humans. Metaplasia. NF-kappa B / physiology. Risk Assessment. Signal Transduction / physiology. Treatment Outcome

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  • (PMID = 17449347.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 86390; United States / NIDCR NIH HHS / DE / R01 DE 13157-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NF-kappa B; 136601-57-5 / Cyclin D1
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43. Modena SF, Meirelles LR, Araújo MR, Lopes LR, Andreollo NA: Role of nitrites in the genesis of adenocarcinoma associated with Barrett's esophagus. In Vivo; 2009 Nov-Dec;23(6):919-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of nitrites in the genesis of adenocarcinoma associated with Barrett's esophagus.
  • BACKGROUND: Barrett's esophagus (BE) is one of the complications of gastroesophageal reflux disease (GERD) and a premalignant condition.
  • It consists of a process of replacement of the squamous epithelium of the esophagus by intestinal columnar epithelium containing goblet cells, known as specialized intestinal metaplasia with goblet cells, and several factors have been related to its pathogenesis.
  • The objective of this study was to evaluate an experimental model of duodenogastroesophageal reflux and the effect of ingestion of sodium nitrite solution on the genesis of adenocarcinoma associated with Barrett's esophagus.
  • The Vienna classification for dysplasia and adenocarcinoma was used in the analysis of results.
  • RESULTS: After 42 weeks of observation, Barrett's esophagus was found in 26.3% (5/19) of the animals submitted to surgery that had not ingested nitrites compared to 72.3% (13/18) of the animals in the group submitted to surgery and given nitrites.
  • Six cases of adenocarcinoma (33.3%) were also found in this latter group.
  • Barrett's esophagus was not found in any of the animals that were not submitted to surgery.
  • CONCLUSION: The ingestion of sodium nitrite associated with duodenogastroesophageal reflux plays an important role in the genesis of adenocarcinoma associated with Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / chemically induced. Barrett Esophagus / chemically induced. Food Preservatives / toxicity. Sodium Nitrite / toxicity

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  • (PMID = 20023233.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Food Preservatives; M0KG633D4F / Sodium Nitrite
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44. Mokrowiecka A, Wierzchniewska-Ławska A, Smolarz B, Romanowicz-Makowska H, Malecka-Panas E: [Polymorphism/loss of heterozygosity of APC gene in GERD-Barrett's metaplasia-dysplasia-adenocarcinoma sequence]. Pol Merkur Lekarski; 2009 May;26(155):385-9
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  • [Title] [Polymorphism/loss of heterozygosity of APC gene in GERD-Barrett's metaplasia-dysplasia-adenocarcinoma sequence].
  • The incidence of esophageal adenocarcinoma (ADC) has been increasing rapidly over the past few decades.
  • Gastro-esopageal reflux disease (GERD), Barrett's esophagus (BE) and Barrett-associated dysplasia are a risk factor for esophageal cancer, but endoscopic surveillance have only a limited influence on cancer mortality.
  • There is a great need to find molecular biomarkers predicting increased progression risk in GERD-Barrett's metaplasia-dysplasia-adenocarcinoma sequence to improve risk assessment and stratification of patients to surveillance program.
  • AIM OF THE STUDY: To evaluate the polymorphism and prevalence of loss of heterozygosity (LOH) of APC tumor suppressor gene in mataplasia, dysplasia and adenocarcinoma.
  • MATERIAL AND METHODS: In esophageal mucosal samples of 79 patients with: GERD (n=33), BE (n=27), BE+dysplasia (n=8) and ADC (n=11) we have studied LOH of APC tumor suppressor gene using PCR-restriction fragment length polymorphism (RFLP).
  • CONCLUSIONS: APC gene inactivation concerns minority of patients with esophageal adenocarcinoma, however, its detection indicates higher risk of progression to ADC.
  • [MeSH-major] Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Gastroesophageal Reflux / genetics. Genes, APC. Loss of Heterozygosity / genetics. Polymorphism, Genetic. Precancerous Conditions / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adult. Aged. Biomarkers, Tumor / analysis. Disease Progression. Esophagus / pathology. Female. Gastric Mucosa / pathology. Heterozygote. Humans. Hyperplasia. Male. Metaplasia. Middle Aged

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  • (PMID = 19606680.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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45. Kuester D, El-Rifai W, Peng D, Ruemmele P, Kroeckel I, Peters B, Moskaluk CA, Stolte M, Mönkemüller K, Meyer F, Schulz HU, Hartmann A, Roessner A, Schneider-Stock R: Silencing of MGMT expression by promoter hypermethylation in the metaplasia-dysplasia-carcinoma sequence of Barrett's esophagus. Cancer Lett; 2009 Mar 8;275(1):117-26
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  • [Title] Silencing of MGMT expression by promoter hypermethylation in the metaplasia-dysplasia-carcinoma sequence of Barrett's esophagus.
  • Hypermethylation was detected in 78.9% of esophageal adenocarcinomas, in 100% of Barrett's intraepithelial neoplasia, in 88.9% of Barrett's metaplasia, but only in 21.4% of normal esophageal mucosa samples (P<0.001) and correlated significantly with downregulation of MGMT transcripts (P=0.048) and protein expression (P=0.02).
  • We conclude, that aberrant promoter methylation of MGMT is a frequent and early event during tumorigenesis of Barrett's esophagus.
  • High prevalence of MGMT hypermethylation may represent a candidate marker for improved diagnosis and targeted therapy in Barrett's adenocarcinoma.

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  • (PMID = 19027227.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / R01CA106176
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ NIHMS576423; NLM/ PMC4028828
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46. Thompson OM, Beresford SA, Kirk EA, Bronner MP, Vaughan TL: Serum leptin and adiponectin levels and risk of Barrett's esophagus and intestinal metaplasia of the gastroesophageal junction. Obesity (Silver Spring); 2010 Nov;18(11):2204-11
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  • [Title] Serum leptin and adiponectin levels and risk of Barrett's esophagus and intestinal metaplasia of the gastroesophageal junction.
  • Persons diagnosed with Barrett's esophagus (BE) are at increased risk of developing esophageal adenocarcinoma (EA).
  • The primary purposes of this study were to determine whether circulating levels of leptin and adiponectin, both of which are deregulated in obese states, predict risk of specialized intestinal metaplasia (SIM) occurring in the esophagus (BE) and/or gastroesophageal junction, and evaluate the extent to which they mediate the relationship between obesity and these conditions.

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  • (PMID = 20111023.001).
  • [ISSN] 1930-739X
  • [Journal-full-title] Obesity (Silver Spring, Md.)
  • [ISO-abbreviation] Obesity (Silver Spring)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA072866-04; United States / NCI NIH HHS / CA / R25 CA092408; United States / NCI NIH HHS / CA / K05 CA124911; United States / NCI NIH HHS / CA / R25 CA092408-06; United States / NCI NIH HHS / CA / CA124911-05; United States / NCI NIH HHS / CA / CA072866-04; United States / NCI NIH HHS / CA / 2R25CA092408-06; United States / NCI NIH HHS / CA / R01 CA72866; United States / NCI NIH HHS / CA / CA092408-06; United States / NCI NIH HHS / CA / K05 CA124911-05; United States / NCI NIH HHS / CA / R01 CA072866
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Leptin
  • [Other-IDs] NLM/ NIHMS299614; NLM/ PMC3125020
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47. Harrison R, Perry I, Haddadin W, McDonald S, Bryan R, Abrams K, Sampliner R, Talley NJ, Moayyedi P, Jankowski JA: Detection of intestinal metaplasia in Barrett's esophagus: an observational comparator study suggests the need for a minimum of eight biopsies. Am J Gastroenterol; 2007 Jun;102(6):1154-61
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  • [Title] Detection of intestinal metaplasia in Barrett's esophagus: an observational comparator study suggests the need for a minimum of eight biopsies.
  • OBJECTIVES: Intestinal metaplasia (IM) and dysplasia in Barrett's esophagus are recognized surrogates for esophageal adenocarcinoma risk.
  • While few would argue with the "hunt for dysplasia," there is a divide regarding the usefulness of the histological confirmation of intestinal metaplasia in endoscopically apparent long segment Barrett's esophagus.
  • We aimed to assess the frequency of intestinal metaplasia in 125 consecutive patients with columnar-lined esophagus and to determine the optimal biopsy protocol to detect intestinal metaplasia.
  • METHODS: Two-hundred ninety-six endoscopies were performed over a 4-yr period in Barrett's esophagus segments of mean length 4 cm (range 1-11 cm) at a single center and the resulting biopsies were analyzed retrospectively.
  • RESULTS: Using H&E staining, we found that the optimum number of biopsies to diagnose intestinal metaplasia was 8 per endoscopy, mean 67.9% endoscopies having intestinal metaplasia.
  • In contrast, if only four were taken the yield was 34.7% with intestinal metaplasia.
  • Unless more than 16 biopsies were taken (100% yield of intestinal metaplasia), no additional significant detection was achieved.
  • Using additional alcian blue/periodic-acid Schiff staining only had a marginal benefit, with 5.4% of new cases of intestinal metaplasia being identified.
  • There is a proximal cephalo-caudal gradient of intestinal metaplasia, especially with increased chronological age, but doing repeat endoscopies on patients did not increase the detection of intestinal metaplasia.
  • CONCLUSIONS: The data suggest that at least 8 random biopsies is the minimum to be taken and analyzed with conventional H&E staining to diagnose benign intestinal metaplasia.
  • Taking more biopsies did not statistically increase the diagnosis of intestinal metaplasia except when greater than 16 were taken when 100% yield was obtained.
  • [MeSH-major] Barrett Esophagus / pathology. Biopsy / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Coloring Agents. Endoscopy, Digestive System. Esophagus / pathology. Female. Humans. Male. Metaplasia. Middle Aged. Precancerous Conditions / pathology. Retrospective Studies

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  • [CommentIn] Am J Gastroenterol. 2007 Oct;102(10):2352-3; author reply 2353-4 [17897347.001]
  • [CommentIn] Gastroenterology. 2007 Dec;133(6):2060-2; discussion 2062 [18054580.001]
  • [CommentIn] Nat Clin Pract Gastroenterol Hepatol. 2008 Mar;5(3):140-1 [18212774.001]
  • [CommentIn] Am J Gastroenterol. 2008 Jan;103(1):250-1 [18184138.001]
  • [CommentIn] Am J Gastroenterol. 2007 Jun;102(6):1162-5 [17531009.001]
  • (PMID = 17433019.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents
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48. Cai JC, Liu D, Liu KH, Zhang HP, Zhong S, Xia NS: Microsatellite alterations in phenotypically normal esophageal squamous epithelium and metaplasia-dysplasia-adenocarcinoma sequence. World J Gastroenterol; 2008 Jul 7;14(25):4070-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Microsatellite alterations in phenotypically normal esophageal squamous epithelium and metaplasia-dysplasia-adenocarcinoma sequence.
  • AIM: To investigate the microsatellite alterations in phenotypically normal esophageal squamous epithelium and metaplasia-dysplasia-adenocarcinoma sequence.
  • METHODS: Forty-one specimens were obtained from esophageal cancer (EC) patients.
  • Histopathological assessment identified 23 squamous cell carcinomas (SCC) and 18 adenocarcinomas (ADC), including only 8 ADC with Barrett esophageal columnar epithelium (metaplasia) and dysplasia adjacent to ADC.
  • Paraffin-embedded normal squamous epithelium, Barrett esophageal columnar epithelium (metaplasia), dysplasia and esophageal tumor tissues were dissected from the surrounding tissues under microscopic guidance.
  • The levels of MSI and LOH were high in the metaplasia-dysplasia-adenocarcinoma sequence of diluted DNA.
  • CONCLUSION: The sequence of metaplasia-dysplasia-adenocarcinoma is associated with microsatellite alterations, including MSI and LOH.
  • The MSI and LOH may be the early genetic events during esophageal carcinogenesis, and genetic alterations at the D3S1616, D5S346 and D3S123 loci may play a role in the progress of microsatellite alterations.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Carcinoma, Squamous Cell / genetics. Cell Transformation, Neoplastic / genetics. Esophageal Neoplasms / genetics. Esophagus / pathology. Gene Expression Regulation, Neoplastic. Microsatellite Instability. Precancerous Conditions / genetics
  • [MeSH-minor] Genetic Markers. Genotype. Humans. Loss of Heterozygosity. Metaplasia. Paraffin Embedding. Phenotype. Polymerase Chain Reaction

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  • (PMID = 18609693.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Other-IDs] NLM/ PMC2725348
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49. Wang DH, Clemons NJ, Miyashita T, Dupuy AJ, Zhang W, Szczepny A, Corcoran-Schwartz IM, Wilburn DL, Montgomery EA, Wang JS, Jenkins NA, Copeland NA, Harmon JW, Phillips WA, Watkins DN: Aberrant epithelial-mesenchymal Hedgehog signaling characterizes Barrett's metaplasia. Gastroenterology; 2010 May;138(5):1810-22
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  • [Title] Aberrant epithelial-mesenchymal Hedgehog signaling characterizes Barrett's metaplasia.
  • BACKGROUND & AIMS: The molecular mechanism underlying epithelial metaplasia in Barrett's esophagus remains unknown.
  • Recognizing that Hedgehog signaling is required for early esophageal development, we sought to determine if the Hedgehog pathway is reactivated in Barrett's esophagus, and if genes downstream of the pathway could promote columnar differentiation of esophageal epithelium.
  • METHODS: Immunohistochemistry, immunofluorescence, and quantitative real-time polymerase chain reaction were used to analyze clinical specimens, human esophageal cell lines, and mouse esophagi.
  • Human esophageal squamous epithelial (HET-1A) and adenocarcinoma (OE33) cells were subjected to acid treatment and used in transfection experiments.
  • An in vivo transplant culture system was created using esophageal epithelium from Sonic hedgehog transgenic mice.
  • Finally, transgenic expression of Sonic hedgehog in mouse esophageal epithelium induces expression of stromal Bmp4, epithelial Sox9, and columnar cytokeratins.
  • CONCLUSIONS: Epithelial Hedgehog ligand expression may contribute to the initiation of Barrett's esophagus through induction of stromal BMP4, which triggers reprogramming of esophageal epithelium in favor of a columnar phenotype.

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 20138038.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA123945-03; United States / NCI NIH HHS / CA / F32 CA123945-03; United States / NCI NIH HHS / CA / F32 CA123945-02; United States / NCI NIH HHS / CA / F32 CA123945-01; United States / NIDDK NIH HHS / DK / 1K23DK068149; United States / NIDDK NIH HHS / DK / K23 DK068149; United States / NCI NIH HHS / CA / CA123945-01; United States / NCI NIH HHS / CA / F32CA-123945; United States / NCI NIH HHS / CA / F32 CA123945; United States / NCI NIH HHS / CA / CA123945-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bmp4 protein, mouse; 0 / Bone Morphogenetic Protein 4; 0 / DMBT1 protein, human; 0 / Hedgehog Proteins; 0 / Receptors, Cell Surface; 0 / SOX9 Transcription Factor; 0 / SOX9 protein, human; 0 / Shh protein, mouse; 0 / Sox9 protein, mouse; 0 / patched receptors; 68238-35-7 / Keratins
  • [Other-IDs] NLM/ NIHMS176618; NLM/ PMC3422577
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50. Quinlan JM, Colleypriest BJ, Farrant M, Tosh D: Epithelial metaplasia and the development of cancer. Biochim Biophys Acta; 2007 Sep;1776(1):10-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epithelial metaplasia and the development of cancer.
  • Metaplasia means the conversion, in postnatal life, of one cell type to another.
  • Understanding the steps leading to metaplasia is important for two reasons.
  • Secondly, metaplasia predisposes to certain forms of neoplasia.
  • So understanding the molecular and cellular mechanisms underlying metaplasia will provide insights into clinical diagnosis and potential therapies.
  • One of the best-described examples of metaplasia is Barrett's metaplasia or the appearance of intestinal-like columnar tissue in the oesophagus.
  • Barrett's metaplasia develops as a result of gastro-oesophageal reflux and is considered the precursor lesion for oesophageal adenocarcinoma.
  • While we know quite a bit about the molecular events associated with the development of oesophageal adenocarcinoma, our understanding of the initial events leading to Barrett's metaplasia is lacking.
  • In the present review we will focus on examples of metaplasia that lead to neoplasia and discuss some of the underlying molecular and cellular mechanisms.

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  • (PMID = 17618050.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / G0300415; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 137
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51. Wong RK, Altekruse SF: Where are you and how do we find you? The dilemma of identifying Barrett's epithelium before adenocarcinoma of the esophagus. Am J Gastroenterol; 2009 Jun;104(6):1363-5
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  • [Title] Where are you and how do we find you? The dilemma of identifying Barrett's epithelium before adenocarcinoma of the esophagus.
  • The incidence of esophageal adenocarcinoma in white males has been increasing steadily over the past decade.
  • However, attempts to identify the precursor lesion, intestinal metaplasia of the esophagus, or early in-situ cancers have been dismal, with no increase in the diagnosis of early cancers over 9 years of follow-up, as noted in the study by Cooper et al.
  • Important predictors of survival,such as a previous diagnosis of gastroesophageal reflux disease, endoscopy, and the diagnosis of intestinal metaplasia, continue to represent a minority of patients who present with esophageal adenocarcinoma.
  • It may be that most patients are relatively asymptomatic, or have very distal, endoscopically imperceptible intestinal metaplasia.
  • Over time, factors that encourage localized, distal esophageal reflux may be the insidious culprit that leads to intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Intestinal Mucosa / pathology. Precancerous Conditions / pathology. SEER Program

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  • [CommentOn] Am J Gastroenterol. 2009 Jun;104(6):1356-62 [19491849.001]
  • (PMID = 19436281.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
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52. Buskens CJ, Hulscher JB, van Gulik TM, Ten Kate FJ, van Lanschot JJ: Histopathologic evaluation of an animal model for Barrett's esophagus and adenocarcinoma of the distal esophagus. J Surg Res; 2006 Oct;135(2):337-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histopathologic evaluation of an animal model for Barrett's esophagus and adenocarcinoma of the distal esophagus.
  • INTRODUCTION: Barrett's esophagus and adenocarcinoma of the esophagus are related to long-standing duodeno-gastroesophageal reflux.
  • The development of an animal model in which Barrett's esophagus and/or carcinoma is induced by duodeno-(gastro-)esophageal reflux could provide better understanding of the pathogenesis of the metaplasia-dysplasia-carcinoma sequence and would create the possibility of investigating new treatment strategies for this aggressive disease.
  • Sequential morphological changes (i.e., esophagitis, intestinal metaplasia, dysplasia, and carcinoma) were studied after 4, 6, and 12 months.
  • After 1 year, 9 of the 10 animals had developed a glandular metaplastic segment (median length, 10 mm), which was histologically and immunohistologically characteristic for the specialized columnar epithelium of Barrett's esophagus without signs of dysplasia.
  • Finally, in seven animals a mucinous tumor with cytologic characteristics of a well-differentiated mucinous adenocarcinoma was found without infiltrative growth.
  • Although they showed cytological characteristics of malignancy, histopathologic evaluation was more suggestive of a reactive mucous producing lesion fitting the diagnosis "esophagitis cystica profunda."
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Disease Models, Animal. Esophageal Neoplasms / pathology. Gastrointestinal Tract / surgery


53. Avilés A, Reymunde A, Santiago N: Balloon-based electrode for the ablation of non-dysplastic Barrett's esophagus: ablation of intestinal metaplasia (AIM II Trial). Bol Asoc Med P R; 2006 Oct-Dec;98(4):270-5
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  • [Title] Balloon-based electrode for the ablation of non-dysplastic Barrett's esophagus: ablation of intestinal metaplasia (AIM II Trial).
  • INTRODUCTION: Barrett's esophagus (BE) is a condition in which an abnormal intestinal-type epithelium called specialized intestinal metaplasia (SIM) replaces the stratified squamous epithelium that normally lines the distal esophagus.
  • This intestinal metaplasia predisposes patients to esophageal adenocarcinoma, the most rapidly rising tumor incidence over the last 30 years, with an annual incidence of 0.5% in patients with BE and a survival rate less than 10% in 5 years.
  • The objective of the study was to assess the safety and efficacy of circumferential endoscopic ablation of Barrett's esophagus using the HALO360 System.
  • METHODS: Patients with non-dysplastic Barrett's esophagus confirmed within the previous year were treated twice per session with a balloon-based, bipolar radiofrequency ablation device with a pre selected energy of 10 J/ cm2 at 260 W for 10 secs, achieving full thickness ablation of epithelium followed by Omeprazole 40 mg PO BID for 1 month and then, daily.
  • [MeSH-major] Barrett Esophagus / surgery. Catheter Ablation / instrumentation. Catheterization / instrumentation
  • [MeSH-minor] Electrodes. Equipment Design. Esophagus / pathology. Esophagus / surgery. Female. Humans. Male. Metaplasia. Middle Aged. Prospective Studies

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  • (PMID = 19610568.001).
  • [ISSN] 0004-4849
  • [Journal-full-title] Boletín de la Asociación Médica de Puerto Rico
  • [ISO-abbreviation] Bol Asoc Med P R
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Puerto Rico
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54. Burjonrappa SC, Reddimasu S, Nawaz Z, Gao X, Sharma P, Loggie B: Mucin expression profile in Barrett's, dysplasia, adenocarcinoma sequence in the esophagus. Indian J Cancer; 2007 Jan-Mar;44(1):1-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mucin expression profile in Barrett's, dysplasia, adenocarcinoma sequence in the esophagus.
  • BACKGROUND: The molecular events that accompany the progression to adenocarcinoma (ADC) of the esophagus are poorly understood.
  • AIM: The aim of this study was to establish a pattern for mucin (MUC) gene expression in the esophageal mucosa under normal and pathological conditions.
  • MATERIALS AND METHODS: Tissue samples were obtained from the archives of patients with histological evidence of Barrett's esophagus (BE) progressing to ADC.
  • MUC1 expression was upregulated (7/7) in progression to adenocarcinoma (P=0.008).
  • Upregulation of MUC2 reflects intestinal metaplasia in BE.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Esophagus / metabolism. Mucins / metabolism. Precancerous Conditions / metabolism
  • [MeSH-minor] Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Gene Expression Regulation, Neoplastic. Humans. Intestinal Neoplasms / metabolism. Intestinal Neoplasms / pathology. Metaplasia / metabolism. Metaplasia / pathology. Mucin 5AC. Mucin-1. Mucin-2. Mucin-6. Retrospective Studies

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  • (PMID = 17401217.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / MUC1 protein, human; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / MUC6 protein, human; 0 / Muc2 protein, mouse; 0 / Muc5ac protein, mouse; 0 / Muc6 protein, mouse; 0 / Mucin 5AC; 0 / Mucin-1; 0 / Mucin-2; 0 / Mucin-6; 0 / Mucins
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55. Theisen J, Stein HJ, Feith M, Kauer WK, Dittler HJ, Pirchi D, Siewert JR: Preferred location for the development of esophageal adenocarcinoma within a segment of intestinal metaplasia. Surg Endosc; 2006 Feb;20(2):235-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preferred location for the development of esophageal adenocarcinoma within a segment of intestinal metaplasia.
  • BACKGROUND: Barrett's metaplasia is the predominant precursor for the development of esophageal adenocarcinoma.
  • This study aimed to identify preferred locations within a segment of Barrett's mucosa for the development of esophageal adenocarcinoma.
  • METHODS: The study group consisted of 213 patients with histologically proven esophageal adenocarcinoma.
  • The frequency of intestinal metaplasia and the location of the tumor occurrence within the segment of intestinal metaplasia were assessed.
  • RESULTS: Intestinal metaplasia was found in 83% of the early lesions and in 98% of the advanced tumors after neoadjuvant chemotherapy.
  • In 82.2% of the cases, the tumor was located at the distal margin of the intestinal metaplasia in patients with early tumor manifestations.
  • The remaining tumor mass after neoadjuvant therapy also was located predominantly at the distal margin of the segment of intestinal metaplasia (85% of the cases).
  • CONCLUSIONS: The results demonstrate that almost all adenocarcinomas of the esophagus are based on the development of a segment of intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / etiology. Esophageal Neoplasms / etiology. Intestines / pathology. Precancerous Conditions / complications. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Endoscopy, Gastrointestinal. Female. Humans. Intestinal Mucosa / pathology. Male. Metaplasia. Middle Aged. Neoadjuvant Therapy. Neoplasm Invasiveness / pathology

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  • (PMID = 16391958.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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56. Gil J, Błaszak A, Wojtuń S, Wojtkowiak M: [Endoscopic methods of gastro-esophageal reflux disease (GERD) treatment and their complications]. Pol Merkur Lekarski; 2007 May;22(131):429-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Endoscopic methods of gastro-esophageal reflux disease (GERD) treatment and their complications].
  • Tretament in gastro-esophageal reflux disease (GERD) is in constant change.
  • Some of them as endoscopic fundoplication or methods of polimerizing substances injection in the area of lower esophageal sphincer have been abandoned because of low quickly diminishing efficacy Endoscopic sewing that implicate all layers of gaster is still under clinical trials and is considered as interesting.
  • Stertt's procedure that is based on electromagnetic wave application in the area of lower esophageal sphincter is used in clinical practice.
  • It is still common to find esophagus stricture as the first illness manifastation.
  • Chronic character of GERD is associated with intestinal metaplasia and adenocarcinoma of the esophagus in its distal part.
  • The most effective endoscopic methods of the treatment include: endoscopic dilation of the strictures and endoscopic methods of patological epithelium removal in Barrett's esophagus.
  • [MeSH-minor] Animals. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Esophagogastric Junction / pathology. Esophagogastric Junction / surgery. Fundoplication / methods. Humans. Laser Coagulation. Laser Therapy. Metaplasia. Monitoring, Ambulatory. Postoperative Complications. Proton Pump Inhibitors. Proton Pumps / drug effects

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  • (PMID = 17679388.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors; 0 / Proton Pumps
  • [Number-of-references] 25
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57. Quaroni L, Casson AG: Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy. Analyst; 2009 Jun;134(6):1240-6
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  • [Title] Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy.
  • The objective of this exploratory study was to evaluate the feasibility of using Fourier-Transform Infrared (FTIR) spectromicroscopy to characterize formalin-fixed, paraffin-embedded human esophageal tissues.
  • Matched histologically normal esophageal squamous epithelium (NS), premalignant Barrett esophagus (BE), and primary esophageal adenocarcinoma (EADC) tissues, each defined according to strict clinicopathologic criteria, were obtained from patients who underwent esophageal resection.
  • Normal esophageal epithelia were characterized by a few well defined regions, mostly of large size (tens of contiguous pixels), which correlated with tissue histology, specifically the basal cell layer.
  • The technical feasibility of using FTIR to characterize formalin-fixed, paraffin-embedded human esophageal tissues demonstrates the potential of this technique to study archival human BE tissue specimens via automated screening techniques.
  • [MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Spectroscopy, Fourier Transform Infrared / methods
  • [MeSH-minor] Adenocarcinoma / pathology. Cluster Analysis. Goblet Cells / cytology. Goblet Cells / pathology. Humans. Intestines / pathology. Light. Metaplasia / pathology. Microscopy. Synchrotrons

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  • (PMID = 19475154.001).
  • [ISSN] 1364-5528
  • [Journal-full-title] The Analyst
  • [ISO-abbreviation] Analyst
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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58. Chang Y, Liu B: Difference of gene expression profiles between Barrett's esophagus and cardia intestinal metaplasia by gene chip. J Huazhong Univ Sci Technolog Med Sci; 2006;26(3):311-3
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  • [Title] Difference of gene expression profiles between Barrett's esophagus and cardia intestinal metaplasia by gene chip.
  • The difference of gene expression profile changes in Barrett's esophagus (BE) and cardia intestinal metaplasia (CIM) epithelium was studied and the novel associated genes were screened in the early stage by cDNA microarray.
  • 141 genes with the expression more than two time were probably related to the occurrence and development of BE and the promotion or progress in adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / genetics. Cardia / pathology. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis. Upper Gastrointestinal Tract / metabolism
  • [MeSH-minor] Humans. Metaplasia

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  • (PMID = 16961278.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] China
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59. Abraham SC, Krasinskas AM, Correa AM, Hofstetter WL, Ajani JA, Swisher SG, Wu TT: Duplication of the muscularis mucosae in Barrett esophagus: an underrecognized feature and its implication for staging of adenocarcinoma. Am J Surg Pathol; 2007 Nov;31(11):1719-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Duplication of the muscularis mucosae in Barrett esophagus: an underrecognized feature and its implication for staging of adenocarcinoma.
  • Depth of invasion is one of the most important prognostic indicators in esophageal adenocarcinoma.
  • Unlike other regions of the gastrointestinal tract, the esophagus in Barrett metaplasia frequently develops duplication of the muscularis mucosae (MM), but this feature is underrecognized, and its effect on appropriate staging of superficially invasive adenocarcinoma is unclear.
  • We first randomly selected 50 esophageal resections for high-grade dysplasia or T1 adenocarcinoma in Barrett esophagus (BE) to evaluate the sensitivity and specificity of MM duplication for BE and its histologic characteristics, including percentage of the Barrett segment involved by MM duplication, origin of the duplicated muscle layer, and appearance of the tissue between duplicated MM.
  • Twenty esophageal resections for squamous cell carcinoma served as controls.
  • Next, to study the clinical significance of MM duplication, we evaluated 30 resections for BE that had superficial adenocarcinoma confined to regions of duplicated MM.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology

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  • [CommentIn] Am J Surg Pathol. 2008 Dec;32(12):1913; author reply 1913-4 [18824891.001]
  • (PMID = 18059229.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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60. Oh DS, Hagen JA, Chandrasoma PT, Dunst CM, Demeester SR, Alavi M, Bremner CG, Lipham J, Rizzetto C, Cote R, Demeester TR: Clinical biology and surgical therapy of intramucosal adenocarcinoma of the esophagus. J Am Coll Surg; 2006 Aug;203(2):152-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical biology and surgical therapy of intramucosal adenocarcinoma of the esophagus.
  • BACKGROUND: Mucosal ablation and endoscopic mucosal resection have been proposed as alternatives to surgical resection as therapy for intramucosal adenocarcinoma (IMC) of the esophagus.
  • RESULTS: The tumor was located in a visible segment of Barrett's esophagus in 65 (83%) and in cardia intestinal metaplasia in 13 (17%).
  • CONCLUSIONS: IMC occurred in cardia intestinal metaplasia and in Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagectomy / methods

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  • [CommentIn] J Am Coll Surg. 2006 Dec;203(6):973 [17116569.001]
  • (PMID = 16864027.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 68238-35-7 / Keratins
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61. Bresalier R: Barrett's Metaplasia: defining the problem. Semin Oncol; 2005 Dec;32(6 Suppl 8):21-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Barrett's Metaplasia: defining the problem.
  • Concern over how best to manage individuals with Barrett's esophagus (BE) has grown because of the consistent rise in the incidence of esophageal adenocarcinoma.
  • Since the 1970s, the rate of increase in incidence of esophageal adenocarcinoma has been greater than that for any other cancer in the US population.
  • Patients with BE have increased risk for esophageal cancer, but the rate of progression and potential risk factors in progression remain poorly understood.
  • Much remains to be learned about BE and its association with adenocarcinoma before effective surveillance or management strategies can be defined and implemented.
  • In this article, the relationship between BE and gastroesophageal reflux disease, risk for adenocarcinoma, and prospects for molecular diagnosis are discussed.
  • [MeSH-major] Barrett Esophagus / pathology
  • [MeSH-minor] Humans. Metaplasia

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  • (PMID = 16360008.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 24
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62. Demura TA, Kogan EA, Sklianskaia OA, Mol' R: [Role of tight junction claudins in the morphogenesis of adenocarcinoma in the presence of Barrett's esophagus]. Arkh Patol; 2008 Sep-Oct;70(5):20-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Role of tight junction claudins in the morphogenesis of adenocarcinoma in the presence of Barrett's esophagus].
  • The purpose of the investigation was to study a role of tight junction (TJ) claudins (CL) in the morphogenesis of adenocarcinoma (AC) in the presence of Barrett's esophagus (BE).
  • 2) GERD-esophagitis with gastric metaplasia (n = 15);.
  • 3) BE with enteric metaplasia (EM) without dysplasia (n = 9);.
  • 4) BE with colonic metaplasia (CM) without dysplasia (n = 9);.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications. Membrane Proteins / metabolism. Tight Junctions / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Membrane / metabolism. Cytoplasm / metabolism. Female. Humans. Male. Metaplasia / metabolism. Middle Aged. Young Adult

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  • (PMID = 19137778.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Membrane Proteins
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63. Mashimo H, Wagh MS, Goyal RK: Surveillance and screening for Barrett esophagus and adenocarcinoma. J Clin Gastroenterol; 2005 Apr;39(4 Suppl 2):S33-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surveillance and screening for Barrett esophagus and adenocarcinoma.
  • Current recommendations for screening and surveillance of Barrett esophagus and related lesions are based on recent guidelines by the Practice Parameters Committee of the American College of Gastroenterology.
  • There is strong rationale for vigorous initial testing to document the baseline status and identify early adenocarcinoma, and for surveillance of high-grade dysplasia.
  • However, recommendations for surveillance of low-grade dysplasia and specialized intestinal metaplasia without dysplasia are largely opinion statements not well supported by objective data.
  • Recommendations for screening and surveillance are not evidence-based and unlikely to alter national mortality from esophageal adenocarcinoma.
  • Current recommendations are limited by inconsistent endoscopic findings and sampling errors, inconsistent histologic diagnoses of Barrett esophagus and dysplasia, and our poor understanding of the natural history of various histologic lesions.
  • Effective screening programs depend on development of simple, inexpensive, and reliable methods to identify the small group of patients truly at high risk for adenocarcinoma for endoscopic screening.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis
  • [MeSH-minor] Biopsy. Esophagoscopy. Esophagus / pathology. Humans. Mass Screening / methods. Population Surveillance. Practice Guidelines as Topic. Risk Factors. Time Factors

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  • (PMID = 15758657.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK031092; United States / NIDDK NIH HHS / DK / DK62867
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 52
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64. Norimura D, Isomoto H, Nakayama T, Hayashi T, Suematsu T, Nakashima Y, Inoue N, Matsushima K, Yamaguchi N, Ohnita K, Mizuta Y, Inoue K, Shikuwa S, Nakao K, Kohno S: Magnifying endoscopic observation with narrow band imaging for specialized intestinal metaplasia in barrett's esophagus with special reference to light blue crests. Dig Endosc; 2010 Apr;22(2):101-6
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  • [Title] Magnifying endoscopic observation with narrow band imaging for specialized intestinal metaplasia in barrett's esophagus with special reference to light blue crests.
  • AIM: Barrett's esophagus (BE) with specialized intestinal metaplasia (SIM) is at high risk of esophageal adenocarcinoma.
  • RESULTS: IM pit pattern with ME-NBI for the diagnosis of IM yielded acceptable sensitivity, specificity and accuracy at 92%, 77% and 83%, respectively.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Endoscopy, Gastrointestinal / methods. Intestinal Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cohort Studies. Female. Humans. Male. Metaplasia. Middle Aged. Predictive Value of Tests. Reproducibility of Results. Retrospective Studies

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  • (PMID = 20447202.001).
  • [ISSN] 1443-1661
  • [Journal-full-title] Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
  • [ISO-abbreviation] Dig Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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65. Bonino JA, Sharma P: Barrett's esophagus. Curr Opin Gastroenterol; 2005 Jul;21(4):461-5
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  • [Title] Barrett's esophagus.
  • PURPOSE OF REVIEW: Significant advances have been made over the past year to identify individuals with Barrett's esophagus, who are at increased risk of malignant transformation.
  • We summarize some of the important advances in that regard including: improved understanding in areas of epidemiology of those with Barrett's esophagus, identification of the pathways responsible for dysplastic and metaplastic development, selection of patient populations who would most benefit from surveillance protocols, and identification of biomarkers signifying progression of metaplastic changes.
  • RECENT FINDINGS: Barrett's esophagus is being better recognized in patients presenting with extra-esophageal symptoms of gastroesophageal reflux such as chronic cough and asthma.
  • Recent reports from some surgical series further suggest the importance of gastric and even duodenal reflux in the etiology of esophageal metaplastic development.
  • There appears to be a select group of individuals with familial predilection for the development of Barrett's esophagus.
  • Retrospective studies continue to show apparent survival benefit in individuals with Barrett's esophagus undergoing surveillance endoscopy.
  • Endoscopic ablative therapy may provide clinicians an attractive alternative to surgical resection in individuals with high-grade esophageal dysplasia and early adenocarcinoma.
  • SUMMARY: The past year has brought many advances in the epidemiology, pathogenesis, surveillance, and treatment of those with Barrett's esophagus.
  • [MeSH-major] Barrett Esophagus. Precancerous Conditions
  • [MeSH-minor] Adenocarcinoma / pathology. Disease Progression. Esophageal Neoplasms / pathology. Humans. Intestinal Mucosa / pathology. Metaplasia / pathology. Prevalence. Risk Factors

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  • (PMID = 15930989.001).
  • [ISSN] 0267-1379
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 25
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66. Ong CA, Lao-Sirieix P, Fitzgerald RC: Biomarkers in Barrett's esophagus and esophageal adenocarcinoma: predictors of progression and prognosis. World J Gastroenterol; 2010 Dec 7;16(45):5669-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biomarkers in Barrett's esophagus and esophageal adenocarcinoma: predictors of progression and prognosis.
  • Barrett's esophagus is a well-known premalignant lesion of the lower esophagus that is characterized by intestinal metaplasia of the squamous epithelium.
  • It is clinically important due to the increased risk (0.5% per annum) of progression to esophageal adenocarcinoma (EA), which has a poor outcome unless diagnosed early.
  • The current clinical management of Barrett's esophagus is hampered by the lack of accurate predictors of progression.
  • Biomarkers have the potential to improve radically the clinical management of patients with Barrett's esophagus and EA but have not yet entered mainstream clinical practice.
  • This review aims to highlight the most promising predictive and prognostic biomarkers in Barrett's esophagus and EA and to discuss what is required to move the field forward towards clinical application.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Biomarkers, Tumor / analysis. Esophageal Neoplasms / diagnosis

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  • (PMID = 21128316.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Genetic Markers
  • [Other-IDs] NLM/ PMC2997982
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67. Bobryshev YV, Freeman AK, Botelho NK, Tran D, Levert-Mignon AJ, Lord RV: Expression of the putative stem cell marker Musashi-1 in Barrett's esophagus and esophageal adenocarcinoma. Dis Esophagus; 2010 Sep;23(7):580-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the putative stem cell marker Musashi-1 in Barrett's esophagus and esophageal adenocarcinoma.
  • Cancer stem cells have been identified in several solid tumors, but stem cells in normal human esophagus or in Barrett's esophagus or adenocarcinoma have not been reported.
  • The present study investigated whether Musashi-1 is expressed in the esophagus and its relation to immune inflammation of the mucosa in Barrett's esophagus and esophageal adenocarcinoma.
  • A total of 41 esophageal tissue specimens from 41 patients were studied.
  • Of these, 15 were esophageal adenocarcinoma, 17 were Barrett's esophagus (10 intestinal metaplasia and 7 dysplasia), and 9 were normal squamous esophagus tissue specimens from patients without esophageal pathology.
  • Immunohistochemistry demonstrated the presence of small numbers of Musashi-1+ cells scattered in the connective tissue stroma and within the epithelium in cardiac-type glands in biopsies from patients without Barrett's esophagus.
  • Musashi-1 expression was present in Barrett's intestinal metaplasia and in dysplastic Barrett's in which the majority of epithelial cells in individual glands expressed this antigen.
  • Expression of Musashi-1 was highest in esophageal adenocarcinoma, where it was most intense in glands that displayed features of early stages of adenocarcinoma formation.
  • In contrast, Musashi-1 staining level was weaker in glands that displayed features of advanced adenocarcinoma.
  • Musashi-1 mRNA expression levels were significantly higher in esophageal adenocarcinoma than in normal esophagus or Barrett's esophagus tissues.
  • Dendritic cell-specific intercellular molecule-3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) mRNA expression levels were significantly increased in both Barrett's tissues and adenocarcinoma tissues.
  • Expression of the putative stem cell marker Musashi-1 is absent in normal squamous epithelium, weak in esophageal cardiac-type glands and Barrett's esophagus, and markedly increased in adenocarcinoma, especially in glands displaying features of early cancer development.
  • Musashi-1 expressing cells may be significant in the etiology of Barrett's esophagus and adenocarcinoma, and perhaps even a cell of origin for this disease.
  • We speculate that immune inflammation occurring in Barrett's esophagus alters the mucosal microenvironment in a manner which is favorable to the activation of dormant stem cells.

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  • [Copyright] © 2010 Copyright the Authors. Journal compilation © 2010, Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus.
  • (PMID = 20459440.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MSI1 protein, human; 0 / Nerve Tissue Proteins; 0 / RNA-Binding Proteins
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68. Trakál E, Guidi A, Butti AL, Trakál JJ, Sambuelli R, Zárate FE: Detection of the risk of adenocarcinoma in Barrett's esophagus by means of tumor markers (p53 and Ki67). Acta Gastroenterol Latinoam; 2010 Sep;40(3):211-5
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  • [Title] Detection of the risk of adenocarcinoma in Barrett's esophagus by means of tumor markers (p53 and Ki67).
  • The rising incidence of adenocarcinoma in Barrett's esophagus has intensified the research into methods of early recognition of cancer risk, detecting cytological and architectural changes (dysplasia) or using biomarkers as predictive tests.
  • The aim of this paper is to evaluate the involvement of two tumor markers: p53 (tumor suppressor gene) and Ki67 (proliferation marker), by means of immunohistochemical analysis with monoclonal antibodies designed for the specific localization of p53 and Ki67 antigens, in esophageal biopsies with columnar metaplasia of patients with and without dysplasia and adenocarcinoma, and to anticipate which ones are liable to suffer it in the future.
  • Both markers were positive in all intestinal metaplasia patients with high-grade dysplasia and adenocarcinoma, and even in some cases with low grade or without dysplasia.
  • In contrast, in those who have gastric metaplasia, tumor markers were negative.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Biomarkers, Tumor / analysis. Esophageal Neoplasms / pathology. Ki-67 Antigen / analysis. Precancerous Conditions / pathology. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 21049770.001).
  • [ISSN] 0300-9033
  • [Journal-full-title] Acta gastroenterologica Latinoamericana
  • [ISO-abbreviation] Acta Gastroenterol. Latinoam.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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69. Ormeci N, Savas B, Coban S, Palabiyikoğlu M, Ensari A, Kuzu I, Kursun N: The usefulness of chromoendoscopy with methylene blue in Barrett's metaplasia and early esophageal carcinoma. Surg Endosc; 2008 Mar;22(3):693-700
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  • [Title] The usefulness of chromoendoscopy with methylene blue in Barrett's metaplasia and early esophageal carcinoma.
  • BACKGROUND: Barrett's esophagus is a condition that is premalignant for adenocarcinoma of the esophagus and the esophagogastric junction.
  • Early detection of Barrett's metaplasia and dysplasia is very important to decrease the mortality and morbidity from esophageal adenocarcinoma cancer.
  • This study aimed to evaluate the effectiveness of methylene blue-targeted biopsies in the differential diagnosis of intestinal metaplasia, dysplasia, and superficial esophageal carcinoma.
  • The esophagus was stained with methylene blue, after which six biopsies were taken from stained and unstained areas.
  • However, there was no statistical difference between the two methods in the diagnosis of esophagitis or esophageal carcinoma (p > 0.05).
  • Stained biopsies were superior to unstained biopsies in terms of sensitivity for Barrett's epithelium and esophageal carcinoma (p < 0.001).
  • CONCLUSION: Chromoendoscopy is useful for delineating Barrett's epithelium and for indicating the correct location for securing biopsies where dysplasia or early esophageal cancer is suspected.
  • [MeSH-major] Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Esophagoscopy / methods. Methylene Blue. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Risk Assessment. Sensitivity and Specificity. Staining and Labeling / methods

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  • (PMID = 17704887.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] T42P99266K / Methylene Blue
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70. Anderson LA, Murphy SJ, Johnston BT, Watson RG, Ferguson HR, Bamford KB, Ghazy A, McCarron P, McGuigan J, Reynolds JV, Comber H, Murray LJ: Relationship between Helicobacter pylori infection and gastric atrophy and the stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence: results from the FINBAR case-control study. Gut; 2008 Jun;57(6):734-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relationship between Helicobacter pylori infection and gastric atrophy and the stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence: results from the FINBAR case-control study.
  • OBJECTIVE: A number of studies have shown an inverse association between infection with Helicobacter pylori and oesophageal adenocarcinoma (OAC).
  • The relationship between all stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence and H pylori infection and gastric atrophy was explored.
  • [MeSH-major] Adenocarcinoma / complications. Esophageal Neoplasms / complications. Gastritis, Atrophic / complications. Helicobacter Infections / complications. Helicobacter pylori / isolation & purification
  • [MeSH-minor] Aged. Antibodies, Bacterial / blood. Antigens, Bacterial / blood. Bacterial Proteins / blood. Barrett Esophagus / complications. Case-Control Studies. Esophagitis, Peptic / complications. Female. Humans. Male. Middle Aged. Precancerous Conditions / complications. Risk Assessment


71. Bobryshev YV, Lu J, Lord RV: Expression of C1q complement component in Barrett's esophagus and esophageal adenocarcinoma. J Gastrointest Surg; 2010 Aug;14(8):1207-13
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  • [Title] Expression of C1q complement component in Barrett's esophagus and esophageal adenocarcinoma.
  • The present study investigated whether C1q is expressed in Barrett's esophagus and esophageal adenocarcinoma and, if so, whether its expression is associated with dendritic cells.
  • MATERIAL AND METHODS: Endoscopic biopsy or operative surgical specimens were obtained from 15 patients with Barrett's esophagus, 13 patients with esophageal adenocarcinoma and 12 patients whose biopsy specimens did not show the presence of specialized intestinal metaplasia or adenocarcinoma.
  • Barrett's esophagus was diagnosed by the presence of a macroscopic area of columnar-lined esophagus as well as microscopic intestinal metaplasia with goblet cells.
  • A computerized quantitative analysis showed that C1q expression was significantly higher in tissue specimens without specialized intestinal-type metaplasia than in Barrett's esophagus specimens and specimens with adenocarcinoma.
  • Double immunostaining revealed that dendritic cells and macrophages expressed C1q in all analyzed esophageal specimens.
  • CONCLUSION: The findings suggest that reduced levels of the expression of C1q by dendritic cells and macrophages in the esophagus may play a role in the formation of immune responses associated with the formation of specialized intestinal metaplasia and the development of adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Complement C1q / genetics. Esophageal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Precancerous Conditions / genetics. RNA, Neoplasm / genetics

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  • (PMID = 20496011.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Neoplasm; 80295-33-6 / Complement C1q
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72. Lord RV, Brabender J, Wickramasinghe K, DeMeester SR, Holscher A, Schneider PM, Danenberg PV, DeMeester TR: Increased CDX2 and decreased PITX1 homeobox gene expression in Barrett's esophagus and Barrett's-associated adenocarcinoma. Surgery; 2005 Nov;138(5):924-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased CDX2 and decreased PITX1 homeobox gene expression in Barrett's esophagus and Barrett's-associated adenocarcinoma.
  • Forced expression of Cdx2 alone in the murine stomach results in gastric intestinal metaplasia (IM).
  • METHODS: CDX2 and PITX1 messenger RNA (mRNA) expression levels, relative to the control gene beta-actin, were measured by reverse transcription-polymerase chain reaction in specimens of Barrett's IM (n = 21), dysplasia (n = 18), adenocarcinoma (n = 20), and matching normal squamous esophagus tissues (n = 39) collected from 19 patients with Barrett's esophagus and 20 patients with esophageal adenocarcinoma.
  • CDX2 protein expression was assessed by immunohistochemistry in specimens of normal squamous esophagus (n = 13), IM (n = 10), dysplasia (n = 8,) and adenocarcinoma (n = 5).
  • RESULTS: The median relative CDX2 mRNA expression was approximately 200 times higher in Barrett's esophagus tissues (0.83) than in matching normal squamous esophagus (0.004) in the patients with Barrett's esophagus (P < .001).
  • The mRNA expression in cancer tissues (0.49) was also higher than in matching normal squamous esophagus specimens (0.009, P < .001).
  • There was no significant difference between the mRNA expression levels in Barrett's esophagus and adenocarcinoma.
  • There was no CDX2 protein expression in normal squamous esophagus, but moderate to strong protein expression was seen in all Barrett's tissues and in a majority of the dysplasia and adenocarcinoma cells.
  • Relative median PITX1 mRNA expression was decreased in Barrett's esophagus (8.02 for all specimens), compared with normal esophagus specimens (47.46 for all specimens, P < .001), and was further reduced in cancer specimens (2.21), compared with either Barrett's esophagus or normal esophagus (both P < .001).
  • CONCLUSIONS: CDX2 mRNA and CDX2 protein expression are upregulated in Barrett's IM tissues, compared with normal squamous esophagus, and remain elevated in dysplasia and adenocarcinoma tissues.
  • In contrast, PITX1 mRNA expression is decreased in Barrett's esophagus, compared with matching normal squamous esophagus specimens, and is further decreased in Barrett's-associated cancer.
  • These descriptive findings suggest a possible role for these genes in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Homeodomain Proteins / genetics. Paired Box Transcription Factors / genetics

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  • (PMID = 16291394.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Paired Box Transcription Factors; 0 / RNA, Messenger; 0 / homeobox protein PITX1
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73. Gatenby PA, Ramus JR, Caygill CP, Shepherd NA, Watson A: Relevance of the detection of intestinal metaplasia in non-dysplastic columnar-lined oesophagus. Scand J Gastroenterol; 2008;43(5):524-30

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  • [Title] Relevance of the detection of intestinal metaplasia in non-dysplastic columnar-lined oesophagus.
  • OBJECTIVE: In the USA, detection of intestinal metaplasia is a requirement for enrollment in surveillance programmes for dysplasia or adenocarcinoma in columnar-lined oesophagus.
  • In the UK, it is believed that failure to detect intestinal metaplasia at index endoscopy does not imply its absence within the columnarized segment or that the tissue is not at risk of neoplastic transformation.
  • The aim of this study was to investigate the factors predicting the probability of detection of intestinal metaplasia in the columnarized segment.
  • MATERIAL AND METHODS: Demonstration of intestinal metaplasia was analysed in 3568 biopsies of non-dysplastic columnar-lined oesophagus from 1751 patients from 7 centres in the UK.
  • Development of dysplasia and adenocarcinoma was analysed in 322 patients without intestinal metaplasia and compared with that in 612 patients with intestinal metaplasia.
  • RESULTS: Intestinal metaplasia was more commonly detected in males than in females (odds ratio 1.244), longer segment length (10.3% increase per centimetre) and increasing number of biopsies taken (24% increase per unit increase).
  • After 5 years of follow-up, 54.8% of patients without intestinal metaplasia at index endoscopy demonstrated intestinal metaplasia, and 90.8% after 10 years.
  • There was no significant difference in the rate of development of dysplasia or adenocarcinoma between patients with or without intestinal metaplasia detection at index endoscopy.
  • CONCLUSIONS: Detection of intestinal metaplasia is subject to significant sampling error.
  • In the majority of patients, if sufficient biopsies are taken over time, intestinal metaplasia will be demonstrated.
  • The decision to offer surveillance should not be based upon the presence or absence of intestinal metaplasia at index endoscopy as the risk of dysplasia and adenocarcinoma is similar in both groups.
  • [MeSH-major] Barrett Esophagus / pathology. Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Biopsy, Needle. Esophageal Neoplasms / etiology. Esophageal Neoplasms / pathology. Female. Follow-Up Studies. Humans. Male. Metaplasia

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  • (PMID = 18415743.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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74. Downs-Kelly E, Mendelin JE, Bennett AE, Castilla E, Henricks WH, Schoenfield L, Skacel M, Yerian L, Rice TW, Rybicki LA, Bronner MP, Goldblum JR: Poor interobserver agreement in the distinction of high-grade dysplasia and adenocarcinoma in pretreatment Barrett's esophagus biopsies. Am J Gastroenterol; 2008 Sep;103(9):2333-40; quiz 2341
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  • [Title] Poor interobserver agreement in the distinction of high-grade dysplasia and adenocarcinoma in pretreatment Barrett's esophagus biopsies.
  • OBJECTIVE: Grading Barrett's dysplasia at the lower end of the metaplasia-dysplasia spectrum (negative, indefinite, and low-grade dysplasia) suffers from poor interobserver agreement, even among gastrointestinal pathologists.
  • Data evaluating interobserver agreement in Barrett's mucosal biopsies with changes at the upper end of the dysplasia spectrum (high-grade dysplasia, intramucosal, and submucosal adenocarcinoma) have not been published.
  • METHODS: All study pathologists agreed upon the histologic criteria distinguishing four diagnostic categories, including high-grade dysplasia; high-grade dysplasia with marked distortion of glandular architecture, cannot exclude intramucosal adenocarcinoma; intramucosal adenocarcinoma; and submucosally invasive adenocarcinoma.
  • The histologic criteria were used to independently review preresection biopsies from 163 consecutive Barrett's esophagus patients with at least high-grade dysplasia who ultimately underwent esophagectomy.
  • Agreement for high-grade dysplasia was moderate (kappa= 0.47), while agreement for high-grade dysplasia with marked architectural distortion, cannot exclude intramucosal adenocarcinoma and intramucosal adenocarcinoma were only fair (kappa= 0.21 and 0.30, respectively) and agreement for submucosal adenocarcinoma was poor (kappa= 0.14).
  • CONCLUSIONS: The overall poor interobserver reproducibility among gastrointestinal pathologists who see a high volume of Barrett's cases calls into question treatment regimens based on the assumption that high-grade dysplasia, intramucosal adenocarcinoma, and submucosal adenocarcinoma can reliably be distinguished in biopsy specimens.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Precancerous Conditions / pathology


75. Sampliner RE, Camargo E, Prasad AR: Association of ablation of Barrett's esophagus with high grade dysplasia and adenocarcinoma of the gastric cardia. Dis Esophagus; 2006;19(4):277-9
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  • [Title] Association of ablation of Barrett's esophagus with high grade dysplasia and adenocarcinoma of the gastric cardia.
  • There has been increasing application of endoscopic ablation therapy for patients with high-grade dysplasia (HGD) and Barrett's esophagus (BE).
  • Three cases are reported in which the patient developed adenocarcinoma of the gastric cardia after thermal ablation of HGD.
  • A definition of BE including endoscopic abnormality and intestinal metaplasia by biopsy was used.
  • Biopsies documented adenocarcinoma of the gastric cardia.
  • The development of adenocarcinoma of the cardia is unexpected.

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  • (PMID = 16866860.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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76. Gatenby PA, Ramus JR, Caygill CP, Charlett A, Winslet MC, Watson A: Treatment modality and risk of development of dysplasia and adenocarcinoma in columnar-lined esophagus. Dis Esophagus; 2009;22(2):133-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment modality and risk of development of dysplasia and adenocarcinoma in columnar-lined esophagus.
  • Columnar metaplasia is the precursor lesion for esophageal adenocarcinoma, resulting from prolonged gastroesophageal reflux.
  • The influence of the efficacy of reflux control on the development of neoplastic change in columnar-lined esophagus is not established.
  • This study compares the rate of development of dysplasia and adenocarcinoma in patients with columnar metaplasia of the esophagus between patients treated pharmacologically and those treated with antireflux surgery.
  • No patient in the surgical group developed high-grade dysplasia (HGD) or adenocarcinoma.
  • Twenty patients treated medically developed adenocarcinoma and 10 developed HGD.
  • Hazards ratio comparing pharmacological to surgical therapy for development of all grades of dysplasia and adenocarcinoma 1.77 (P = 0.272).
  • Log rank test comparing antireflux surgery to pharmacological therapy for development of HGD or adenocarcinoma P = 0.1287 and for adenocarcinoma P = 0.2125.
  • Although there was a trend towards greater efficacy of antireflux surgery over pharmacological therapy in reducing the development of dysplasia and adenocarcinoma, this did not reach statistical significance.

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  • (PMID = 19018855.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors
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77. Ling FC, Khochfar J, Baldus SE, Brabender J, Drebber U, Bollschweiler E, Hoelscher AH, Schneider PM: HIF-1alpha protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasia. Dis Esophagus; 2009;22(8):694-9

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  • [Title] HIF-1alpha protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasia.
  • Squamous epithelium (SE), metaplastic, low- and high-grade dysplastic lesions, and tumor tissue of 57 resection specimens from patients with Barrett's adenocarcinoma were immunohistochemically analyzed.
  • HIF-1alpha protein expression increased significantly from SE to Barrett's metaplasia (BM) (P < 0.0001).
  • From metaplasia through low- and high-grade dysplasia to cancer, no further increase could be detected.
  • All were significantly increased in metaplasia compared to SE without further change in tumor development.

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  • (PMID = 19302222.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
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78. Dickman R, Levi Z, Vilkin A, Zvidi I, Niv Y: Predictors of specialized intestinal metaplasia in patients with an incidental irregular Z line. Eur J Gastroenterol Hepatol; 2010 Feb;22(2):135-8
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  • [Title] Predictors of specialized intestinal metaplasia in patients with an incidental irregular Z line.
  • INTRODUCTION: Barrett's esophagus is a well-known complication of gastroesophageal reflux disease (GERD) and is associated with dysplasia and esophageal adenocarcinoma.
  • Data on the prevalence of specialized intestinal metaplasia (SIM) in biopsy taken from an incidental irregular Z line are scarce.
  • Specialized intestinal metaplasia was found in 43.5% of all cases.
  • [MeSH-major] Barrett Esophagus / pathology. Esophagoscopy. Esophagus / pathology. Gastroesophageal Reflux / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Female. Hernia, Hiatal / complications. Humans. Israel / epidemiology. Logistic Models. Male. Metaplasia. Middle Aged. Prevalence. Retrospective Studies. Risk Assessment. Risk Factors. Sex Factors. Young Adult

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  • [CommentIn] Eur J Gastroenterol Hepatol. 2010 Aug;22(8):1022 [20631542.001]
  • (PMID = 19907339.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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79. Baczewska-Mazurkiewicz D, Rydzewska G, Milewski J, Durlik M, Lao M, Rydzewski A: Magnification chromoendoscopy in comparison to standard chromoendoscopy for detection of intestinal metaplasia in renal transplant recipients. Adv Med Sci; 2006;51:115-8
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  • [Title] Magnification chromoendoscopy in comparison to standard chromoendoscopy for detection of intestinal metaplasia in renal transplant recipients.
  • Intestinal metaplasia is a feature of atrophic gastritis whereas the diagnosis of Barrett's esophagus is based on histological demonstration of specialized metaplasia.
  • Both conditions are associated with increased risk of adenocarcinoma.
  • The aim of the present study was to assess whether magnification endoscopy improves the diagnostic accuracy of intestinal metaplasia in stomach and in esophagus.
  • MATERIAL AND METHODS: In this non-randomized, feasibility study thirty one (12 women and 19 men) renal transplant recipients, with a mean age of 44.0 years were evaluated for the presence of intestinal metaplasia.
  • The presence of gastritis and intestinal metaplasia was classified according to modified updated Sydney classification.
  • RESULTS: Of 31 patients, 16 patients had endoscopic and histopathological evidence of gastric intestinal metaplasia, and standard endoscopy with methylene blue staining was sufficient for diagnosis (15 from 16).
  • Magnification endoscopy allowed identification of 6 patients with specialized intestinal metaplasia in Barrett's esophagus, which would be otherwise missed.
  • CONCLUSIONS: In this study diagnostic accuracy of standard endoscopy for identification of intestinal metaplasia in the stomach was not improved by the use of magnification endoscopy, but the latter was an accurate method of predicting specialized intestinal metaplasia in Barrett's esophagus.
  • [MeSH-major] Endoscopy, Gastrointestinal / methods. Intestinal Diseases / diagnosis. Intestines / pathology. Kidney Transplantation
  • [MeSH-minor] Adult. Barrett Esophagus / pathology. Feasibility Studies. Female. Humans. Intestinal Neoplasms / diagnosis. Male. Metaplasia / diagnosis. Middle Aged. Reproducibility of Results. Sensitivity and Specificity

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  • (PMID = 17357289.001).
  • [ISSN] 1896-1126
  • [Journal-full-title] Advances in medical sciences
  • [ISO-abbreviation] Adv Med Sci
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Poland
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80. Fujita M, Fujimori T, Chiba T: [The definition of Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1325-32
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  • [Title] [The definition of Barrett's esophagus].
  • Recently, according to increasing gastroesophageal reflux disease (GERD), the patients with Barrett's esophagus (BE) are increasing.
  • Since Barrett have reported cases of esophageal ulcers surrounding by columnar epithelium, the various criteria of the BE have been proposed.
  • They proposed that BE was a chance in the esophageal epithelium of any length that can be recognized at endoscopy, and confirmed to have intestinal metaplasia by biopsy of the tubular esophagus and excludes intestinal metaplasia of the cardia.
  • Endoscopically, BE is determined, when 'gastric-appearing mucosa' or apparent 'columnar lined esophagus' is evident proximal to the esophagogastric junction.
  • Especially SCE is distinctive features of BE, available for diagnosis.
  • On the other hand, BE is premalignant condition for the adenocarcinoma of the esophagus, therefore the features of the BE are researched to prevent and find out earlier development of adenocarcinoma.
  • [MeSH-major] Barrett Esophagus
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control. Esophagoscopy. Gastroesophageal Reflux / complications. Humans

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  • (PMID = 16101217.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 21
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81. Fléjou JF: Barrett's oesophagus: from metaplasia to dysplasia and cancer. Gut; 2005 Mar;54 Suppl 1:i6-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Barrett's oesophagus: from metaplasia to dysplasia and cancer.
  • Barrett's oesophagus is a premalignant condition that predisposes to the development of oesophageal adenocarcinoma.
  • It is detected on endoscopy and confirmed histologically by the presence in the lower oesophagus of a metaplastic mucosa, the so-called specialised epithelium, which resembles incomplete intestinal metaplasia in the stomach.
  • These similarities with incomplete intestinal metaplasia are present on histology, mucin histochemistry, and immunohistochemistry with various differentiation markers (cytokeratins and MUC antigens).
  • [MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Aneuploidy. Cell Transformation, Neoplastic / pathology. DNA, Neoplasm / analysis. Esophagus / pathology. Genes, p53 / genetics. Humans. Immunohistochemistry / methods. Mucins / analysis. Mucous Membrane / pathology. Neoplasms, Glandular and Epithelial / classification. Neoplasms, Glandular and Epithelial / pathology. Risk Factors

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  • (PMID = 15711008.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Mucins
  • [Number-of-references] 66
  • [Other-IDs] NLM/ PMC1867794
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82. Dvorak K, Watts GS, Ramsey L, Holubec H, Payne CM, Bernstein C, Jenkins GJ, Sampliner RE, Prasad A, Garewal HS, Bernstein H: Expression of bile acid transporting proteins in Barrett's esophagus and esophageal adenocarcinoma. Am J Gastroenterol; 2009 Feb;104(2):302-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of bile acid transporting proteins in Barrett's esophagus and esophageal adenocarcinoma.
  • OBJECTIVES: Barrett's esophagus (BE) is a metaplastic lesion characterized by replacement of the normal squamous epithelium by columnar intestinal epithelium containing goblet cells.
  • We hypothesized that one of the possible functions of newly arising metaplastic epithelium, in the esophagus, is to transport bile acids.
  • Our major goal was to evaluate the expression of bile acid transporters in normal squamous epithelium, BE with different grades of dysplasia, and esophageal adenocarcinoma (EAC).

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  • (PMID = 19174784.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA023074; United States / NIEHS NIH HHS / ES / P30 ES006694; United States / NCI NIH HHS / CA / P50 CA095060
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Membrane Glycoproteins; 0 / Multidrug Resistance-Associated Proteins; 0 / Organic Anion Transporters, Sodium-Dependent; 0 / RNA, Messenger; 0 / Symporters; 0 / bile acid binding proteins; 0 / multidrug resistance-associated protein 3; 145420-23-1 / sodium-bile acid cotransporter
  • [Other-IDs] NLM/ NIHMS693533; NLM/ PMC4450811
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83. Popnikolov NK, Gatalica Z, Adegboyega PA, Norris BA, Pasricha PJ: Downregulation of TNF-related apoptosis-inducing ligand (TRAIL)/Apo2L in Barrett's esophagus with dysplasia and adenocarcinoma. Appl Immunohistochem Mol Morphol; 2006 Jun;14(2):161-5
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  • [Title] Downregulation of TNF-related apoptosis-inducing ligand (TRAIL)/Apo2L in Barrett's esophagus with dysplasia and adenocarcinoma.
  • Therefore, they hypothesized that similar changes may occur during the malignant transformation of Barrett's esophagus.
  • The aim of this study was to compare TRAIL/Apo2L expression in normal gastroesophageal (GE) junction, Barrett's esophagus with and without dysplasia, and associated adenocarcinoma.
  • Immunohistochemical evaluation of TRAIL expression was performed on formalin-fixed paraffin-embedded sections from 29 GE junction/esophageal biopsies, 20 gastric biopsies, 6 esophagectomies, 2 small bowel resection specimens, and 5 colon biopsies.
  • TRAIL was always detected in Barrett's metaplasia (21/21, 100%), and the overall expression was similar to that of the columnar portion of the normal GE junction (8/8, 100%).
  • TRAIL was rarely and weakly (1+) expressed in Barrett's esophagus with dysplasia (3/18, 16.7%) and adenocarcinoma (1/10, 10.0%) (P<0.001).
  • These results show that the downregulation of TRAIL is associated with development of dysplasia in Barrett's esophagus.
  • Thus, the immunohistochemically detected downregulation of TRAIL expression appears to be a promising indicator of dysplasia in Barrett's esophagus.

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  • (PMID = 16785783.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TNF-Related Apoptosis-Inducing Ligand
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84. Leers JM, DeMeester SR, Chan N, Ayazi S, Oezcelik A, Abate E, Banki F, Lipham JC, Hagen JA, DeMeester TR: Clinical characteristics, biologic behavior, and survival after esophagectomy are similar for adenocarcinoma of the gastroesophageal junction and the distal esophagus. J Thorac Cardiovasc Surg; 2009 Sep;138(3):594-602; discussion 601-2
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  • [Title] Clinical characteristics, biologic behavior, and survival after esophagectomy are similar for adenocarcinoma of the gastroesophageal junction and the distal esophagus.
  • OBJECTIVE: The Siewert classification system differentiates between adenocarcinoma of the gastroesophageal junction and that of the distal esophagus.
  • METHODS: Records of all patients who underwent resection for adenocarcinoma of the distal esophagus or gastroesophageal junction from 1987 to 2007 were retrospectively reviewed.
  • Based on the endoscopic location of the epicenter of the tumor in relation to the gastroesophageal junction, tumors were categorized in 301 patients as being of the distal esophagus and in 208 as being of the gastroesophageal junction.
  • RESULTS: There were no significant differences in age, sex, or body mass index between patients with adenocarcinoma of the distal esophagus or gastroesophageal junction.
  • Patients with adenocarcinoma of the distal esophagus were more likely to have reflux symptoms (75% vs 53%, P < .0001) and peritumoral intestinal metaplasia (73% vs 51%, P < .0001) and be in a surveillance program (54% vs 9%, P = .0005) compared with patients with adenocarcinoma of the gastroesophageal junction.
  • However, the prevalence and location of nodal metastases was similar, and in node-positive patients mediastinal node involvement was present in more than 40% of the patients in each group (distal esophageal adenocarcinoma, 47%; gastroesophageal junction adenocarcinoma, 41%).
  • Survival was similar (5 years: distal esophageal adenocarcinoma, 45%; gastroesophageal junction adenocarcinoma, 38%; P = .14), as was the prevalence and type of recurrence.
  • CONCLUSION: The prevalence and distribution of lymph node metastases in patients with adenocarcinoma of the distal esophagus and gastroesophageal junction were similar, and after esophagectomy, there was no difference in overall survival or recurrence.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagectomy / mortality. Esophagogastric Junction / surgery. Neoplasm Recurrence, Local / classification

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  • (PMID = 19698841.001).
  • [ISSN] 1097-685X
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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85. Rygiel AM, Milano F, Ten Kate FJ, Schaap A, Wang KK, Peppelenbosch MP, Bergman JJ, Krishnadath KK: Gains and amplifications of c-myc, EGFR, and 20.q13 loci in the no dysplasia-dysplasia-adenocarcinoma sequence of Barrett's esophagus. Cancer Epidemiol Biomarkers Prev; 2008 Jun;17(6):1380-5
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  • [Title] Gains and amplifications of c-myc, EGFR, and 20.q13 loci in the no dysplasia-dysplasia-adenocarcinoma sequence of Barrett's esophagus.
  • The progression of Barrett's esophagus to esophageal adenocarcinoma is often characterized by the accumulation of genetic abnormalities.
  • The goal was to evaluate the copy number alterations of several oncogene loci, including 7p12 [epidermal growth factor receptor (EGFR)], 8q24 (c-myc), and 20q13 in the sequence of no dysplasia-dysplasia-adenocarcinoma of Barrett's esophagus.
  • Fluorescence in situ hybridization with DNA probes for the centromeric region of chromosome 7 and the locus-specific regions of 7p12 (EGFR), 8q24 (c-myc), and 20q13 was applied on 99 brush cytology specimens of patients with Barrett's esophagus with different stages of dysplasia or esophageal adenocarcinoma.
  • Gains (3-4 copies) of chromosome 17, 8q24 (c-myc), and 20q.13 loci were found in the low frequencies in nondysplastic Barrett's esophagus.
  • Their frequencies increased with the stage of dysplasia and reached a high incidence in esophageal adenocarcinoma.
  • Amplification (>4 copies) of at least 1 of the loci was observed in 14% of high-grade dysplasia and increased to 50% in esophageal adenocarcinoma (P = 0.015).
  • The most frequently amplified locus was c-myc (18%), followed by 20q13 (13%) and EGFR (11%) in the high-grade dysplasia/esophageal adenocarcinoma cases.
  • High amplification levels (>10 copies) of the loci were more frequent in esophageal adenocarcinoma (72%) compared with high-grade dysplasia (20%; P = 0.049).
  • Amplifications of the c-myc, EGFR, and 20q12 loci may serve as diagnostic markers to identify patients with Barrett's esophagus with high-grade dysplasia or esophageal adenocarcinoma.
  • Gains of the loci might be of value as prognostic markers because they are already present in nondysplasia cases and may precede the later event of the amplification as observed in high-grade dysplasia and esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Chromosomes, Human, Pair 20 / genetics. Esophageal Neoplasms / genetics. Genes, erbB-1 / genetics. Precancerous Conditions / genetics. Proto-Oncogene Proteins c-myc / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Chromosomes, Human, Pair 17 / genetics. Female. Gene Amplification. Humans. In Situ Hybridization, Fluorescence. Male. Metaplasia / pathology. Middle Aged. Prospective Studies

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  • (PMID = 18559552.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc
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86. Koppert LB, Wijnhoven BP, van Dekken H, Tilanus HW, Dinjens WN: The molecular biology of esophageal adenocarcinoma. J Surg Oncol; 2005 Dec 1;92(3):169-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The molecular biology of esophageal adenocarcinoma.
  • BACKGROUND: Barrett's esophagus is an acquired metaplastic change that occurs in the distal esophagus secondary to chronic gastroesophageal reflux.
  • This premalignant condition forms the most important risk factor for developing esophageal adenocarcinoma, which is an extremely aggressive tumor with a 5-year survival rate of less than 25%.
  • Carcinomas that arise in the setting of Barrett's esophagus are thought to develop as part of the metaplasia-dysplasia-carcinoma sequence.
  • OBJECTIVE: To review the current knowledge on the genomic alterations involved in the development of Barrett's esophagus and its progression to dysplasia and/or cancer.
  • RESULTS: Several changes in gene structure, gene expression, and protein structure are associated with the progression of Barrett's esophagus to adenocarcinoma.
  • Alterations in tumor suppressor genes, amongst which p53 and p16, are early events in the metaplasia-dysplasia-adenocarcinoma sequence, followed by loss of cell cycle checkpoints.
  • CONCLUSIONS: Within the multistep process of esophageal adenocarcinogenesis, to date no single molecular marker came forward able to predict who will and who will not develop cancer in the setting of Barrett's esophagus.
  • Identification of crucial molecular pathways involved in esophageal adenocarcinogenesis would ultimately improve therapy and facilitate development of new treatment strategies.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / pathology. Chromosome Aberrations. DNA, Neoplasm / genetics. Esophageal Neoplasms / genetics
  • [MeSH-minor] Apoptosis / genetics. Cyclin D1 / genetics. Epidermal Growth Factor / genetics. Gastroesophageal Reflux / complications. Gene Expression Regulation, Neoplastic. Humans. Metaplasia / pathology. Microsatellite Repeats. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics. Tumor Suppressor Protein p53 / genetics

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16299787.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  • [Number-of-references] 252
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87. Piazuelo E, Cebrián C, Escartín A, Jiménez P, Soteras F, Ortego J, Lanas A: Superoxide dismutase prevents development of adenocarcinoma in a rat model of Barrett's esophagus. World J Gastroenterol; 2005 Dec 21;11(47):7436-43
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  • [Title] Superoxide dismutase prevents development of adenocarcinoma in a rat model of Barrett's esophagus.
  • AIM: To test whether antioxidant treatment could prevent the progression of Barrett's esophagus to adenocarcinoma.
  • Rat's esophagus was assessed by histological analysis, superoxide anion and peroxinitrite generation, SOD levels and DNA oxidative damage.
  • RESULTS: All rats undergoing esophagojejunostomy developed extensive esophageal mucosal ulceration and inflammation by mo 4.
  • The process was associated with a progressive presence of intestinal metaplasia beyond the anastomotic area (9% 1st mo and 50% 4th mo) (94% at the anastomotic level) and adenocarcinoma (11% 1st mo and 60% 4th mo).
  • Exogenous administration of SOD decreased mucosal superoxide levels, increased mucosal SOD levels and reduced the risk of developing intestinal metaplasia beyond the anastomotic area (odds ratio = 0.326; 95%CI: 0.108-0.981; P = 0.046), and esophageal adenocarcinoma (odds ratio = 0.243; 95%CI: 0.073-0.804; P = 0.021).
  • CONCLUSION: Superoxide dismutase prevents the progression of esophagitis to Barrett's esophagus and adenocarcinoma in this rat model of gastrointestinal reflux, supporting a role of antioxidants in the chemoprevention of esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / drug therapy. Esophageal Neoplasms / prevention & control. Free Radical Scavengers / pharmacology. Superoxide Dismutase / pharmacology

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  • (PMID = 16437713.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Free Radical Scavengers; EC 1.15.1.1 / Superoxide Dismutase
  • [Other-IDs] NLM/ PMC4725177
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88. Lastraioli E, Taddei A, Messerini L, Comin CE, Festini M, Giannelli M, Tomezzoli A, Paglierani M, Mugnai G, De Manzoni G, Bechi P, Arcangeli A: hERG1 channels in human esophagus: evidence for their aberrant expression in the malignant progression of Barrett's esophagus. J Cell Physiol; 2006 Nov;209(2):398-404
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  • [Title] hERG1 channels in human esophagus: evidence for their aberrant expression in the malignant progression of Barrett's esophagus.
  • We investigated the expression of hERG1 K+ channels in the human upper gastrointestinal tract, focusing our attention on the lower esophagus.
  • In particular, we analyzed by both Reverse transcription and polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) endoscopic samples obtained from normal subjects, from patients suffering from gastroesophageal reflux, associated or not with esophagitis, and from patients affected by Barrett's esophagus (BE), that is, intestinal metaplasia.
  • None of the normal samples, nor those from patients with gastro-esophageal reflux symptoms and reflux esophagitis expressed the hERG1 protein.
  • Data here reported, support the hypothesis that hERG1 expression marks an early step of the progression of normality to cancer in the human esophagus through a metaplastic and dysplastic stage.
  • [MeSH-major] Barrett Esophagus / pathology. Esophagus / metabolism. Ether-A-Go-Go Potassium Channels / genetics. Ether-A-Go-Go Potassium Channels / metabolism
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Gene Expression Regulation. Humans. Male. Metaplasia. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16883575.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ether-A-Go-Go Potassium Channels; 0 / KCNH1 protein, human; 0 / RNA, Messenger
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89. Asthana N, Mandich D, Ligato S: Esophageal polypoid dysplasia of gastric foveolar phenotype with focal intramucosal carcinoma associated with Barrett's esophagus. Am J Surg Pathol; 2008 Oct;32(10):1581-5
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  • [Title] Esophageal polypoid dysplasia of gastric foveolar phenotype with focal intramucosal carcinoma associated with Barrett's esophagus.
  • We describe a rare case of esophageal polypoid dysplasia with gastric phenotype and focal intramucosal carcinoma associated with Barrett's esophagus.
  • Screening upper gastrointestinal endoscopic evaluation revealed a large intraluminal polypoid lesion occluding the distal portion of the esophagus.
  • Surgery was performed with resection of the distal esophagus and proximal stomach.
  • A few residual foci of specialized intestinal metaplasia consistent with Barrett's esophagus without dysplasia were identified at the proximal and distal ends of the lesion.
  • In our opinion, this case represents a precursor lesion of an extremely well-differentiated adenocarcinoma of gastric foveolar phenotype that has been previously documented in the stomach and in the duodenum and that now for the first time we report in the esophagus in association with Barrett's intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Cell Differentiation. Esophagoscopy. Humans. Immunohistochemistry. Male. Metaplasia. Mucous Membrane / pathology. Phenotype


90. Nunobe S, Nakanishi Y, Taniguchi H, Sasako M, Sano T, Kato H, Yamagishi H, Sekine S, Shimoda T: Two distinct pathways of tumorigenesis of adenocarcinomas of the esophagogastric junction, related or unrelated to intestinal metaplasia. Pathol Int; 2007 Jun;57(6):315-21
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  • [Title] Two distinct pathways of tumorigenesis of adenocarcinomas of the esophagogastric junction, related or unrelated to intestinal metaplasia.
  • It is still uncertain whether intestinal metaplasia (IM) of the esophagogastric junction (EGJ) plays a role in the development of adenocarcinoma of the esophagogastric junction (AEGJ).
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Esophagogastric Junction / pathology. Gastric Mucosa / pathology. Intestinal Mucosa / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / metabolism. Barrett Esophagus / pathology. Biomarkers, Tumor / metabolism. Female. Humans. Lymphatic Metastasis. Male. Metaplasia / metabolism. Metaplasia / pathology. Middle Aged. Phenotype

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  • [CommentIn] Z Gastroenterol. 2008 Nov;46(11):1333-4 [19012205.001]
  • (PMID = 17539961.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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91. Takubo K, Vieth M, Aida J, Sawabe M, Kumagai Y, Hoshihara Y, Arai T: Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia. Digestion; 2009;80(4):248-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia.
  • METHODS: Here we discuss four such important differences: the definition of the esophagogastric junction (EGJ), the possible precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus (BE), and the histologic criteria for mucosal adenocarcinoma.
  • If an area of columnar-lined esophagus (CLE) is only partially involved by intestinal metaplasia, then the latter cannot always be demonstrated in biopsy specimens.
  • Therefore, we do not think that a definition of BE as CLE with histologic intestinal metaplasia is practical.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Gastroenterology / standards. Precancerous Conditions / diagnosis. Terminology as Topic
  • [MeSH-minor] Esophagogastric Junction / pathology. Esophagoscopy. Gastroscopy. Humans. Stomach Neoplasms / diagnosis

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  • [Copyright] 2009 S. Karger AG, Basel.
  • (PMID = 19828957.001).
  • [ISSN] 1421-9867
  • [Journal-full-title] Digestion
  • [ISO-abbreviation] Digestion
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 59
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92. Kelty CJ, Gough MD, Van Wyk Q, Stephenson TJ, Ackroyd R: Barrett's oesophagus: intestinal metaplasia is not essential for cancer risk. Scand J Gastroenterol; 2007 Nov;42(11):1271-4
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  • [Title] Barrett's oesophagus: intestinal metaplasia is not essential for cancer risk.
  • OBJECTIVE: Barrett's oesophagus is the main identifiable risk factor for oesophageal adenocarcinoma.
  • It has been suggested that only patients with intestinal metaplasia are at risk of cancer, but the British Society of Gastroenterology (BSG) guidelines suggest that glandular mucosa is all that is needed.
  • The aim of this study was to quantify the risk of adenocarcinoma in columnar-lined lower oesophagus, with or without specialized intestinal metaplasia.
  • All histological specimens were re-examined and reported according to whether they contained columnar epithelial-lined lower oesophagus, glandular mucosa, with or without intestinal metaplasia.
  • The primary outcome measure was the development of adenocarcinoma.
  • Of these, 379 (55.1%) were found to have specialized intestinal metaplasia (SIM), and the remaining 309 (44.9%, p = NS) were reported as having glandular mucosa (GM).
  • Twenty-eight patients went on to develop adenocarcinoma (4.1%) during the follow-up period - 17 in the SIM group (4.5%) and 11 in the GM group (3.6%, p =NS).
  • CONCLUSIONS: Patients who have glandular mucosa on biopsy without intestinal metaplasia have a similar cancer risk to those with specialized intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Barrett Esophagus / complications. Barrett Esophagus / pathology. Esophageal Neoplasms / etiology. Esophageal Neoplasms / pathology. Esophagus / pathology
  • [MeSH-minor] Biopsy. Female. Humans. Incidence. Male. Metaplasia. Mucous Membrane / pathology. Risk Factors


93. Csendes A, Bragheto I, Burdiles P, Smok G, Henriquez A, Parada F: Regression of intestinal metaplasia to cardiac or fundic mucosa in patients with Barrett's esophagus submitted to vagotomy, partial gastrectomy and duodenal diversion. A prospective study of 78 patients with more than 5 years of follow up. Surgery; 2006 Jan;139(1):46-53
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  • [Title] Regression of intestinal metaplasia to cardiac or fundic mucosa in patients with Barrett's esophagus submitted to vagotomy, partial gastrectomy and duodenal diversion. A prospective study of 78 patients with more than 5 years of follow up.
  • BACKGROUND: Regression of intestinal metaplasia to cardiac mucosa in patients with Barrett's (BE) esophagus could alter the natural history of BE.
  • OBJECTIVE: To determine the regression of intestinal metaplasia to cardiac mucosa in patients followed more than 5 years after operation, by repeated endoscopy with biopsy.
  • One patient progressed to low grade dysplasia, but no patient progressed to high-grade dysplasia or adenocarcinoma.
  • CONCLUSIONS: Vagotomy and antrectomy combined with duodenal bile diversion abolish acid and duodenal reflux into the distal esophagus in patients with BE, which is accompanied by a regression of BE from intestinal to cardiac or fundic mucosa in about 60% of patients.
  • [MeSH-major] Barrett Esophagus / surgery. Cardia / pathology. Duodenum / surgery. Gastrectomy. Gastric Fundus / pathology. Intestines / pathology. Vagotomy
  • [MeSH-minor] Adolescent. Adult. Aged. Anastomosis, Roux-en-Y. Female. Gastroesophageal Reflux / etiology. Gastroesophageal Reflux / physiopathology. Humans. Longitudinal Studies. Male. Metaplasia. Middle Aged. Postoperative Period. Prospective Studies. Remission Induction

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  • [CommentIn] Surgery. 2006 Sep;140(3):479 [16934615.001]
  • (PMID = 16364717.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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94. Belova GV, Mel'chenko DS, Reshetova NV, Frank GA, Sokolov VV: [Barrett's esophagus: endoscopic and immunomorphological parallels]. Eksp Klin Gastroenterol; 2010;(10):46-50
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  • [Title] [Barrett's esophagus: endoscopic and immunomorphological parallels].
  • Barrett esophagus is the most serious sequela of the gastroesophageal reflux disease being an obligate precancer with a high index of the neoplastic transformation as to an adenocarcinoma esophagus.
  • THE PURPOSE OF THE PAPER: To reveal the extent of the susceptibility to oncogenesis of the Barrett esophagus-patients and to determine high-risk groups.
  • MATERIALS AND METHODS: Our paper has shown the examination results of the 55 Barrett esophagus-patients (29 women and 26 men at the age of 39 to 62 years old), including 40 intestinal metaplasia-patients and 15 patients of the intestinal metaplasia + dysplasia of long clinical course given corresponding correcting cure.
  • In our investigation a DNA-flow cytometry was a method of determining the adenocarcinoma esophagus risk secondary to the Barrett esophagus as well as an index of the proliferation and an index of the aneuploidy were the factors analyzed.
  • THE RESULTS:. 1) As the pathosis histology-progresses from metaplasia to dysplasia and adenocarcinoma esophagus the increase in the aneuploidy rate, the proliferation index, and S-cycling state cells portion is observed;.
  • 3) the increased aneuploidy index in the presence of the intestinal metaplasia free of esophagus dysplasia can serve as an objective factor for neoplastic progression.
  • [MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aneuploidy. Cell Cycle / drug effects. Cell Proliferation / drug effects. Endoscopy, Gastrointestinal. Female. Flow Cytometry. Humans. Immunohistochemistry. Male. Metaplasia. Middle Aged. Photochemotherapy. Predictive Value of Tests. Prospective Studies. Retrospective Studies. Risk. Treatment Outcome

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  • (PMID = 21434371.001).
  • [ISSN] 1682-8658
  • [Journal-full-title] Ėksperimental'nai︠a︡ i klinicheskai︠a︡ gastroėnterologii︠a︡ = Experimental & clinical gastroenterology
  • [ISO-abbreviation] Eksp Klin Gastroenterol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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95. Zaninotto G, Rizzetto C: Surgical options and outcomes in Barrett's esophagus. Curr Opin Gastroenterol; 2007 Jul;23(4):452-5
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  • [Title] Surgical options and outcomes in Barrett's esophagus.
  • PURPOSE OF REVIEW: Barrett's esophagus is a complication of chronic gastroesophageal reflux that results in the replacement of normal stratified squamous epithelium in the distal esophagus by metaplastic columnar mucosa and it carries a 30-fold to 125-fold risk of progression to esophageal adenocarcinoma.
  • RECENT FINDINGS: Laparoscopic antireflux surgery has proved durable and effective in treating reflux and reflux-related symptoms in patients with Barrett's esophagus.
  • SUMMARY: Recent studies have disproved the widely held assumption that, once established, Barrett's esophagus does not change.
  • Antireflux surgery can achieve a regression of intestinal metaplasia to cardiac mucosa in patients with Barrett's esophagus and may thus alter the natural history of the disease.
  • [MeSH-major] Barrett Esophagus / surgery
  • [MeSH-minor] Esophagus / pathology. Esophagus / surgery. Fundoplication / methods. Humans. Laparoscopy. Metaplasia

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  • (PMID = 17545785.001).
  • [ISSN] 0267-1379
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 22
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96. Siewert JR, Stein HJ, Feith M: Adenocarcinoma of the esophago-gastric junction. Scand J Surg; 2006;95(4):260-9
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  • [Title] Adenocarcinoma of the esophago-gastric junction.
  • BACKGROUND: The border between the esophagus and stomach gives rise to many discrepancies in the current literature regarding the etiology, classification and surgical treatment of adenocarcinoma arising at the esophago-gastric junction.
  • We have consequently used the AEG-criteria (adenocarcinoma of the esophago-gastric junction) for classification and have based the selection of the surgical approach on the anatomic topographic subclassification.
  • METHODS: In the following we report an analysis of a large and homogeneously classified population of 1602 consecutive patients with adenocarcinoma of the esophago-gastric junction, with an emphasis on the surgical approach, the pattern of lymphatic spread, the outcome after surgical treatment and the prognostic factors.
  • RESULTS: The study confirms the marked differences in sex distribution, associated specialized intestinal metaplasia in the esophagus, tumor grading, tumor growth pattern, lymphatic spread, and stage between the three tumor entities.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / surgery. Esophageal Neoplasms / classification. Esophageal Neoplasms / surgery. Esophagogastric Junction. Stomach Neoplasms / classification. Stomach Neoplasms / surgery

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  • (PMID = 17249275.001).
  • [ISSN] 1457-4969
  • [Journal-full-title] Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society
  • [ISO-abbreviation] Scand J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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97. Shaheen NJ, Sharma P, Overholt BF, Wolfsen HC, Sampliner RE, Wang KK, Galanko JA, Bronner MP, Goldblum JR, Bennett AE, Jobe BA, Eisen GM, Fennerty MB, Hunter JG, Fleischer DE, Sharma VK, Hawes RH, Hoffman BJ, Rothstein RI, Gordon SR, Mashimo H, Chang KJ, Muthusamy VR, Edmundowicz SA, Spechler SJ, Siddiqui AA, Souza RF, Infantolino A, Falk GW, Kimmey MB, Madanick RD, Chak A, Lightdale CJ: Radiofrequency ablation in Barrett's esophagus with dysplasia. N Engl J Med; 2009 May 28;360(22):2277-88
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  • [Title] Radiofrequency ablation in Barrett's esophagus with dysplasia.
  • BACKGROUND: Barrett's esophagus, a condition of intestinal metaplasia of the esophagus, is associated with an increased risk of esophageal adenocarcinoma.
  • We assessed whether endoscopic radiofrequency ablation could eradicate dysplastic Barrett's esophagus and decrease the rate of neoplastic progression.
  • METHODS: In a multicenter, sham-controlled trial, we randomly assigned 127 patients with dysplastic Barrett's esophagus in a 2:1 ratio to receive either radiofrequency ablation (ablation group) or a sham procedure (control group).
  • Randomization was stratified according to the grade of dysplasia and the length of Barrett's esophagus.
  • Primary outcomes at 12 months included the complete eradication of dysplasia and intestinal metaplasia.
  • Overall, 77.4% of patients in the ablation group had complete eradication of intestinal metaplasia, as compared with 2.3% of those in the control group (P<0.001).
  • In the ablation group, one patient had upper gastrointestinal hemorrhage, and five patients (6.0%) had esophageal stricture.
  • CONCLUSIONS: In patients with dysplastic Barrett's esophagus, radiofrequency ablation was associated with a high rate of complete eradication of both dysplasia and intestinal metaplasia and a reduced risk of disease progression. (ClinicalTrials.gov number, NCT00282672. )
  • [MeSH-major] Barrett Esophagus / surgery. Catheter Ablation. Esophagus / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Disease Progression. Female. Humans. Logistic Models. Male. Metaplasia / surgery. Middle Aged. Treatment Outcome


98. Brown IS, Whiteman DC, Lauwers GY: Foveolar type dysplasia in Barrett esophagus. Mod Pathol; 2010 Jun;23(6):834-43
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  • [Title] Foveolar type dysplasia in Barrett esophagus.
  • Adenocarcinoma of the lower esophagus and esophagogastric junction is increasing in incidence in Western countries.
  • A metaplasia (Barrett esophagus)-dysplasia-carcinoma sequence induced by gastroesophageal reflux disease is established.
  • Esophagogastrectomy cases from 41 patients with glandular dysplasia with and without associated invasive adenocarcinoma of the lower esophagus were evaluated for expression of MUC2, MUC5AC, CDX2, villin, Ki67 and p53.
  • In addition, clinicopathological parameters including the presence and extent of background intestinal metaplasia were also evaluated.
  • In conclusion, our study provides evidence for a non intestinal pathway to neoplastic development in Barrett esophagus, that is, gastric metaplasia-foveolar dysplasia-adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Cell Differentiation. Disease Progression. Female. Homeodomain Proteins / analysis. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Male. Metaplasia. Microfilament Proteins / analysis. Middle Aged. Mucin 5AC / analysis. Mucin-2 / analysis. Prognosis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 20228780.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Ki-67 Antigen; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Microfilament Proteins; 0 / Mucin 5AC; 0 / Mucin-2; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / villin
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99. Szachnowicz S, Cecconello I, Ribeiro U, Iriya K, El Ibrahim R, Takeda FR, Corbett CE, Vaz Safatle-Ribeiro A: Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study. World J Surg Oncol; 2009;7:27
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  • [Title] Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study.
  • BACKGROUND: Mucin immunoexpression in adenocarcinoma arising in Barrett's esophagus (BE) may indicate the carcinogenesis pathway.
  • The aim of this study was to evaluate resected specimens of adenocarcinoma in BE for the pattern of mucins and to correlate to the histologic classification.
  • METHODS: Specimens were retrospectively collected from thirteen patients who underwent esophageal resection due to adenocarcinoma in BE.
  • Sections were scored for the grade of intestinal metaplasia.
  • Specialized epithelium with intestinal metaplasia was present in all adjacent mucosas.
  • CONCLUSION: Barrett's esophagus adenocarcinoma shows either gastric or intestinal type pattern of mucin expression.
  • The two types of tumors developed in Barrett's esophagus may reflect the original cell type involved in the malignant transformation.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Mucin 5AC / analysis. Mucin-2 / analysis

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  • (PMID = 19272137.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucin-2
  • [Other-IDs] NLM/ PMC2662840
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100. Kuramochi H, Uchida K, Peters JH, Shimizu D, Vallbohmer D, Schneider S, Danenberg KD, Danenberg PV: Loss of heterozygosity at thymidylate synthase locus in Barrett's metaplasia, dysplasia, and carcinoma sequences. BMC Cancer; 2009 May 21;9:157
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  • [Title] Loss of heterozygosity at thymidylate synthase locus in Barrett's metaplasia, dysplasia, and carcinoma sequences.
  • The aim of this study was to analyze the frequency and timing of LOH at the TS locus in Barrett-associated adenocarcinoma (BA) and its precursory lesions, such as intestinal metaplasia (IM) and dysplasia.
  • Biopsies were obtained from the lower esophageal mucosa/IM/dysplasia/BA, when available.
  • Normal squamous tissue from the upper esophagus was taken as a control.
  • RESULTS: Among the patients with informative heterozygous genotype in their control samples, no sample with LOH at the TS locus was observed in the lower esophageal mucosa in GERD patients (0/22 samples).

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  • (PMID = 19460136.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA84424
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.1.1.45 / Thymidylate Synthase
  • [Other-IDs] NLM/ PMC2694818
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