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1. 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
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. 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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3. 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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4. 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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5. 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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  • [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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6. 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
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  • [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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7. 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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  • [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.
  • Higher levels of miR-196a were observed in EA, BE, and dysplastic lesions compared with normal squamous mucosa, and in high-grade dysplasia compared with BE and low-grade dysplasia.
  • [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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8. 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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  • [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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9. 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
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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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10. 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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  • [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.
  • Loss of Cdx2 function, or conditional deletion in the intestine, results in replacement of intestinal cells with a stratified squamous phenotype.
  • 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.
  • [MeSH-major] Barrett Esophagus / genetics. Esophagus / pathology. Homeodomain Proteins / physiology
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. CDX2 Transcription Factor. Esophageal Neoplasms / genetics. Esophageal Neoplasms / pathology. Humans. Metaplasia / genetics. Models, Biological

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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 / / MRC/ 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 Transcription Factor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins
  • [Number-of-references] 72
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11. 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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  • [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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12. 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).
  • Tumors were located close to the squamous-columnar junction.
  • 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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13. 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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14. Allameh A, Rasmi Y, Nasseri-Moghaddam S, Tavangar SM, Sharifi R, Sadreddini M: Immunohistochemical analysis of selected molecular markers in esophagus precancerous, adenocarcinoma and squamous cell carcinoma in Iranian subjects. Cancer Epidemiol; 2009 Jul;33(1):79-84
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  • [Title] Immunohistochemical analysis of selected molecular markers in esophagus precancerous, adenocarcinoma and squamous cell carcinoma in Iranian subjects.
  • AIM: To investigate changes in potential causative factors during progression of esophagus cancer in a population living in high-risk area in Iran.
  • SUBJECTS: Formalin-fixed, paraffin-embedded esophageal specimens (n=87) from patients with gastroesophageal reflux disease (GERD), Barrett's metaplasia, adenocarcinoma (ADC) and squamous cells carcinoma (SCC) were collected based on their pathological diagnosis.
  • RESULTS: P53 expression was not detected in esophageal tissues from normal and GERD samples, whereas it was found positive in Barrett's, ADC, and SCC samples.
  • CONCLUSION: The pathological changes in ADC and SCC samples which were associated with increasing frequency of NT and COX-2 provides further evidence for involvement of these inflammatory factors in progression of esophagus cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Precancerous Conditions / metabolism. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / metabolism. Barrett Esophagus / pathology. Case-Control Studies. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclooxygenase 2 / metabolism. Disease Progression. Esophagus / metabolism. Esophagus / pathology. Female. Gastroesophageal Reflux / metabolism. Gastroesophageal Reflux / pathology. Glutathione S-Transferase pi / metabolism. Humans. Immunohistochemistry. Iran. Male. Middle Aged. Tumor Suppressor Protein p53 / metabolism. Tyrosine / analogs & derivatives. Tyrosine / metabolism. Young Adult


15. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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16. 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.
  • In these animals, extensive esophagitis with squamous cell hyperplasia was found.
  • 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


17. 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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18. 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.
  • RESULTS: Only mild superficial staining of MUC1 was seen in normal squamous epithelium.
  • 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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19. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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20. 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.
  • We observed MM duplication in 46 of 50 (92%) BE resections, involving 5% to >90% of the Barrett segment, in contrast to none in 20 (0%) resected squamous cell carcinoma, P<0.0001.
  • The outer MM was continuous with the single MM beneath squamous epithelium, suggesting that outer MM represents the "original" muscle layer.
  • [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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21. 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 07;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 / / MRC/ MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Genetic Markers
  • [Other-IDs] NLM/ PMC2997982
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22. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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23. 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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  • [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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24. 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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  • [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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25. 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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26. 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.
  • In contrast to the normal squamous epithelium, enterocytes of the distal ileum are adapted to transport bile acids from the intestinal lumen.
  • 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).
  • RESULTS: Our immunohistochemical studies showed that all three bile acid transporters are expressed in BE glands, but not in squamous epithelium.
  • In addition, RT-PCR studies showed increased expression of mRNA coding for ASBT (6.1x), IBABP (9.1x), and MRP3 (2.4x) in BE (N=13) compared with normal squamous epithelium (N=15).
  • Significantly increased mRNA levels of IBABP (10.1x) and MRP3 (2.5x) were also detected in EAC (N=21) compared with normal squamous epithelium.

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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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27. 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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28. 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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29. 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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30. Tischoff I, Tannapfel A: Barrett's esophagus: can biomarkers predict progression to malignancy? Expert Rev Gastroenterol Hepatol; 2008 Oct;2(5):653-63
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  • [Title] Barrett's esophagus: can biomarkers predict progression to malignancy?
  • Barrett's esophagus (BE) is one of the most common premalignant lesions and can progress to esophageal adenocarcinoma.
  • It is characterized histologically by a specialized intestinal metaplasia that replaces the squamous epithelium of the distal esophagus, and is associated with chronic gastroesophageal reflux disease and obesity.
  • Similar to the adenoma-carcinoma sequence of colorectal carcinomas, esophageal adenocarcinoma develops through progression from BE to low- and high-grade dysplasia, then to adenocarcinoma with accumulation of genetic and epigenetic abnormalities.
  • Dysplasia is the most predictive marker for risk of esophageal adenocarcinoma, whereas endoscopic and histological diagnoses are still the gold standard for surveillance of patients with BE.
  • Several studies have identified candidate biomarkers that may have predictive value and may serve as additional factors for the risk assessment of esophageal adenocarcinoma.
  • This review discusses the role of biomarkers in the progression from BE to adenocarcinoma, focusing on clinical and molecular markers.
  • [MeSH-major] Barrett Esophagus / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Disease Progression. Humans. Predictive Value of Tests

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  • (PMID = 19072343.001).
  • [ISSN] 1747-4132
  • [Journal-full-title] Expert review of gastroenterology & hepatology
  • [ISO-abbreviation] Expert Rev Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 97
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31. Binato M, Gurski RR, Fagundes RB, Meurer L, Edelweiss MI: P53 and Ki-67 overexpression in gastroesophageal reflux disease--Barrett's esophagus and adenocarcinoma sequence. Dis Esophagus; 2009;22(7):588-95
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  • [Title] P53 and Ki-67 overexpression in gastroesophageal reflux disease--Barrett's esophagus and adenocarcinoma sequence.
  • Gastroesophageal reflux disease (GERD) is a major risk factor for the development of esophageal adenocarcinoma (ACE).
  • Many molecular alterations occur in esophageal carcinogenesis, yet the exact mechanism of ACE development remains unknown.
  • This study aims to determine p53 protein and Ki-67 expression in esophageal mucosa of patients with GERD and study the correlation between these markers and the progression from normal squamous epithelium to esophagitis, columnar epithelium with or without intestinal metaplasia and ACE.
  • Those biopsies were classified into five groups: (i) G1 normal squamous epithelium (58);.
  • (iii) G3 columnar epitheliums without intestinal metaplasia (30);.
  • (iv) G4, columnar epitheliums with intestinal metaplasia (32); and (v) G5 ACEs (35).
  • Linear correlation between p53/Ki67 expression and the multistep progression from squamous epithelium to ACE was observed (P < 0.001 and P < 0.05).

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  • (PMID = 19302208.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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32. Yeh RW, Triadafilopoulos G: Endoscopic therapy for Barrett's esophagus. Gastrointest Endosc Clin N Am; 2005 Jul;15(3):377-97, vii
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  • [Title] Endoscopic therapy for Barrett's esophagus.
  • With the increase in the rate of esophageal adenocarcinoma in the United States and the Western world matched with the high morbidity and mortality of esophagectomy, there is an increasing need for new and effective techniques to treat and prevent esophageal adenocarcinoma.
  • A wide variety of endoscopic mucosal ablative techniques have been developed for early esophageal neoplasia.
  • Most studies show that specialized intestinal metaplasia may persist underneath neo-squamous mucosa, posing a risk for subsequent neoplastic progression.
  • In this article we review current published literature on endoscopic therapies for the management of Barrett's esophagus.
  • [MeSH-major] Barrett Esophagus / therapy. Endoscopy, Gastrointestinal

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  • (PMID = 15990048.001).
  • [ISSN] 1052-5157
  • [Journal-full-title] Gastrointestinal endoscopy clinics of North America
  • [ISO-abbreviation] Gastrointest. Endosc. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 90
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33. Barbera M, Fitzgerald RC: Cellular mechanisms of Barrett's esophagus development. Surg Oncol Clin N Am; 2009 Jul;18(3):393-410
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  • [Title] Cellular mechanisms of Barrett's esophagus development.
  • Barrett's esophagus (BE) is a metaplastic premalignant disorder in which the normal stratified squamous epithelium of the lower esophagus is replaced by a columnar lined epithelium with intestinal differentiation.
  • BE generally occurs in the context of chronic gastroesophageal reflux disease and it is the primary risk factor for the development of esophageal adenocarcinoma, with a conversion rate of 0.5% to 1% per annum.
  • The dramatic increase of esophageal adenocarcinoma incidence in the western world over the last two decades justifies the strong interest in BE and its development with the aim to improve preventative and therapeutic clinical strategies.
  • [MeSH-major] Barrett Esophagus / etiology. Barrett Esophagus / pathology. Esophagus / pathology. Precancerous Conditions / etiology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / etiology. Aneuploidy. Animals. Cell Transdifferentiation / physiology. Cell Transformation, Neoplastic. Cocarcinogenesis. Disease Models, Animal. Epigenesis, Genetic. Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications. Humans. Inflammation. Metaplasia / etiology. Metaplasia / pathology. Multipotent Stem Cells / physiology. Mutation. Risk Factors. Stem Cells / physiology

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  • (PMID = 19500732.001).
  • [ISSN] 1558-5042
  • [Journal-full-title] Surgical oncology clinics of North America
  • [ISO-abbreviation] Surg. Oncol. Clin. N. Am.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 105
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34. Kim CW, Lee BI, Kim BW, Kim JI, Park SH, Kim JK, Han SW, Jung IS, Sun HS, Lee AW, Lee KY: [Immunohistochemical expression of the p53 and Ki-67 proteins in Barrett's esophagus in Korea]. Korean J Gastroenterol; 2005 Sep;46(3):189-95
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  • [Title] [Immunohistochemical expression of the p53 and Ki-67 proteins in Barrett's esophagus in Korea].
  • BACKGROUND/AIMS: Barrett's esophagus is a premalignant lesion of the esophagus in which normal squamous epithelium is replaced by intestinalized columnar epithelium.
  • In Korea, adenocarcinoma associated with Barrett's esophagus is rare compared with that of Western country.
  • The purpose of this study was to investigate the immunohistochemical expression of p53 and Ki-67 in Barrett's esophagus which had predictive value for cancer risk in Korea.
  • METHODS: Ninety five patients (43 male and 52 female, median age 44, range 21-75) who have been suspected to have Barrett's esophagus by endoscopic assessment were enrolled in this study.
  • Alcian blue (pH 2.5) and high ion diamine stain for the evaluation of specialized intestinal metaplasia (SIM) and immunohistochemical stain for p53 and Ki-67 were done.
  • RESULTS: 57.9% (55/95) of biopsies from the columnar lined esophagus showed SIM, but no dysplasia.
  • 56.4% (31/55) of Barrett's esophagus showed sulfomucin positive colonic metaplasia.
  • The p53 expression was observed in 10.9% (6/55) of the patients of Barrett's esophagus and all of them showed colonic metaplasia.
  • CONCLUSIONS: In Korea, 10.9% of Barrett's esophagus had p53 mutation and moreover all of them had colonic metaplasia.
  • Consequently, we expect that these patients have high risk of developing dysplasia and adenocarcinoma and need careful follow-up.
  • [MeSH-major] Barrett Esophagus / metabolism. Ki-67 Antigen / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / genetics. Adult. Aged. Esophageal Neoplasms / etiology. Esophageal Neoplasms / genetics. Female. Humans. Immunohistochemistry. Male. Middle Aged. Risk Factors

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  • (PMID = 16179838.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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35. Barbera M, Fitzgerald RC: Cellular origin of Barrett's metaplasia and oesophageal stem cells. Biochem Soc Trans; 2010 Apr;38(2):370-3
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  • [Title] Cellular origin of Barrett's metaplasia and oesophageal stem cells.
  • Barrett's oesophagus is a metaplastic pre-malignant disorder and the only established precursor lesion for oesophageal adenocarcinoma.
  • Barrett's oesophagus develops when the normal stratified squamous epithelium of the lower oesophagus is replaced by a columnar lined mucosa with intestinal differentiation, usually in the context of chronic gastro-oesophageal reflux disease.
  • Abnormal differentiation of multipotent stem cells in the squamous oesophagus, triggered by exposure to refluxate, is one potential mechanism.
  • These stem cells could be located in the basal layer of the squamous oesophageal epithelium and/or in the neck region of the oesophageal submucosal gland ducts; however, their exact location and identification are still matter of discussion.
  • Three-dimensional models combined with state-of-the-art imaging techniques are now applied to characterize the squamous epithelium in human oesophageal samples, and this could unveil essential information to identify these progenitor cells.
  • Locating stem cells in human squamous oesophagus could have important implications for our understanding of Barrett's oesophagus and remarkably improve our future strategies for its prevention.
  • [MeSH-major] Barrett Esophagus / etiology. Esophagus / cytology. Esophagus / pathology. Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Movement / physiology. Cell Transdifferentiation / physiology. Epithelial Cells / cytology. Epithelial Cells / physiology. Gastric Mucosa / cytology. Gastric Mucosa / pathology. Gastric Mucosa / physiology. Humans. Metaplasia / pathology

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  • (PMID = 20298185.001).
  • [ISSN] 1470-8752
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ MC/ U105365007; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 36
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36. Takubo K, Aida J, Naomoto Y, Sawabe M, Arai T, Shiraishi H, Matsuura M, Ell C, May A, Pech O, Stolte M, Vieth M: Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma. Hum Pathol; 2009 Jan;40(1):65-74
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  • [Title] Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma.
  • Many publications focusing on the background or original mucosa of Barrett adenocarcinoma have maintained that adenocarcinoma arises in intestinal-type mucosa with goblet cells in the columnar-lined esophagus, and this has become a central dogma.
  • The mucosa on each side of a series of 141 minute esophageal adenocarcinomas (almost all of which were mucosal carcinomas) resected by endoscopic mucosal resection was recorded as the background mucosa.
  • All 141 cases had endoscopic evidence of an esophageal origin, and for 113 of them, histologic evidence of an esophageal origin was also available.
  • The mucosae were classified into 4 types--squamous, cardiac, fundic, and intestinal--based on routine histology and immunohistochemical staining.
  • The present joint pathologic examination of the background mucosa of Barrett adenocarcinoma conducted by Japanese and German pathologists and gastroenterologists found that more than 70% of primary small adenocarcinomas (<2 cm) of the esophagus were adjacent to cardiac/fundic-type rather than intestinal-type mucosa.
  • Moreover, intestinal metaplasia was not observed in any areas of the endoscopic mucosal resection specimens in 64 (56.6%) of the 113 cases.
  • In other words, there was no evidence to support the previously held view that Barrett adenocarcinoma is nearly always accompanied and preceded by intestinal-type mucosa.
  • Our study has demonstrated a close relationship between esophageal adenocarcinoma and cardiac-type mucosa.
  • Therefore, it is not proven histogenetically that the background mucosa of esophageal adenocarcinoma is the intestinal type.
  • Also, it seems better to define Barrett esophagus as metaplastic columnar-lined esophagus alone, without requiring the presence of goblet cells, in accordance with histogenetic and practical standpoints.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cardia / pathology. Esophageal Neoplasms / pathology. Intestines / pathology
  • [MeSH-minor] Aged. Endoscopy. Female. Humans. Immunohistochemistry. Male. Metaplasia / complications. Metaplasia / pathology. Middle Aged

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  • [CommentIn] Hum Pathol. 2009 Dec;40(12):1820 [19913679.001]
  • [CommentIn] Hum Pathol. 2009 Aug;40(8):1208-9; author reply 1209-10 [19616700.001]
  • [CommentIn] Hum Pathol. 2009 Aug;40(8):1206-7; author reply 1207-8 [19616698.001]
  • (PMID = 18755496.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Wijnhoven BP, Hussey DJ, Watson DI, Tsykin A, Smith CM, Michael MZ, South Australian Oesophageal Research Group: MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma. Br J Surg; 2010 Jun;97(6):853-61
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  • [Title] MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND: The genetic changes that drive metaplastic progression from squamous oesophageal mucosa toward intestinal metaplasia and adenocarcinoma are unclear.
  • This study examined whether miRNAs play a role in the development of oesophageal adenocarcinoma.
  • METHODS: RNA was extracted from mucosa of normal oesophageal squamous epithelium, normal gastric epithelium, Barrett's oesophagus with intestinal metaplasia and oesophageal adenocarcinoma obtained from 16 individuals.
  • Tissue-specific expression profiles were observed, with miR-21, miR-143, miR-145, miR-194 and miR-215 significantly upregulated in columnar tissues compared with normal squamous epithelium.
  • Expression of miR-143, miR-145 and miR-215 was lower in oesophageal adenocarcinoma than in Barrett's oesophagus.
  • Levels of miR-203 and miR-205 were high in normal squamous epithelium and low in columnar epithelia.
  • MiR-205 levels were lower in gastric epithelium than in both Barrett's oesophagus and adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. MicroRNAs / analysis. RNA, Messenger / analysis

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  • (PMID = 20301167.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger
  • [Investigator] Wijnhoven BP; Hussey DJ; Watson DI; Smith CM; Mayne GC; Michael MZ; Astill D; Van der Hoek MB; Tsykin A; Tilanus HW; Wijnhoven BP
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38. Ling FC, Baldus SE, Khochfar J, Xi H, Neiss S, Brabender J, Metzger R, Drebber U, Dienes HP, Bollschweiler E, Hoelscher AH, Schneider PM: Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer. Histopathology; 2007 Jan;50(2):203-9
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  • [Title] Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer.
  • The aim of this study was to examine a possible association between COX-2 protein expression and the development and progression of the Barrett's metaplasia-dysplasia-carcinoma sequence and the type and degree of associated inflammatory reaction.
  • METHODS AND RESULTS: Squamous epithelium, metaplastic, low-grade, high-grade dysplastic lesions and tumour tissue of 49 resection specimens from patients with Barrett's adenocarcinoma were immunohistochemically analysed.
  • The most significant differences were detected between squamous epithelium and Barrett's metaplasia (P < 0.001) and from low- to high-grade dysplasia (P < 0.0001).
  • Active and chronic inflammation were significantly different between squamous epithelium and Barrett's metaplasia (P < 0.0001), but not during further progression in the sequence.
  • CONCLUSIONS: Increasing COX-2 expression in Barrett's metaplasia is significantly associated with a change in the local inflammatory reaction, but not during further progression through dysplasia to cancer.
  • [MeSH-major] Barrett Esophagus / enzymology. Cyclooxygenase 2 / genetics. Esophageal Neoplasms / enzymology. Inflammation / enzymology. Membrane Proteins / genetics

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  • [ErratumIn] Histopathology. 2007 Mar;50(4):531
  • (PMID = 17222248.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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39. Montgomery E, Mamelak AJ, Gibson M, Maitra A, Sheikh S, Amr SS, Yang S, Brock M, Forastiere A, Zhang S, Murphy KM, Berg KD: Overexpression of claudin proteins in esophageal adenocarcinoma and its precursor lesions. Appl Immunohistochem Mol Morphol; 2006 Mar;14(1):24-30
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  • [Title] Overexpression of claudin proteins in esophageal adenocarcinoma and its precursor lesions.
  • The authors identified upregulation of Claudins 3, 4, and 7 in gastric adenocarcinoma using Affymetrix U-133 oligonucleotide microarrays and immunohistochemistry (IHC).
  • While normal gastric mucosa lacked Claudin 3, 4, and 7 expression, intestinal metaplasia and dysplasia showed these proteins.
  • The authors hypothesized that Claudins would be similarly overexpressed in Barrett's esophagus (BE)/adenocarcinoma.
  • Claudins 3, 4, and 7 gene expression was analyzed by Affymetrix U-133 microarrays in three esophageal adenocarcinomas, one case of BE, and three normal esophagi.
  • IHC validation was performed using tissue microarrays constructed from esophageal resection specimens containing squamous (44 cases), gastric (40 cases), and non-dysplastic BE (16 cases), low-grade and high-grade dysplasia (16 and 26 cases), adenocarcinoma (58 cases), and nodal metastases (27 cases).
  • By microarray analysis, Claudin 3 showed a marked increase in mRNA expression compared with normal esophagus (approximately 100-fold).
  • By IHC, Claudin 3 expression was 1+ in most (>95%) normal squamous or gastric tissues and 2+ to 4+ in more than 80% of high-grade dysplasia, adenocarcinoma, and metastases specimens.
  • Claudin 4 protein expression was 2+ or less in most squamous and gastric mucosa (>90%) but 3+ or 4+ in BE, low- and high-grade dysplasia, adenocarcinoma, and metastases specimens (>90%).
  • Claudin 7 expression was minimal in squamous and gastric mucosa but strong (3+ to 4+) in BE and low-grade dysplasia.
  • In high-grade dysplasia, adenocarcinoma, and metastases, Claudin 7 was less intense, with 60% to 70% staining 3+ or 4+ and 30% to 40% staining weakly (1+ or 2+).
  • The findings suggest that alterations in Claudin proteins are an early event in tumorigenesis and may provide targets for diagnosis and directed therapy for esophageal adenocarcinoma and its precursors.

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  • (PMID = 16540726.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLDN3 protein, human; 0 / CLDN4 protein, human; 0 / CLDN7 protein, human; 0 / Claudin-3; 0 / Claudin-4; 0 / Claudins; 0 / Membrane Proteins; 0 / RNA, Messenger
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40. Finley JC, Reid BJ, Odze RD, Sanchez CA, Galipeau P, Li X, Self SG, Gollahon KA, Blount PL, Rabinovitch PS: Chromosomal instability in Barrett's esophagus is related to telomere shortening. Cancer Epidemiol Biomarkers Prev; 2006 Aug;15(8):1451-7
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  • [Title] Chromosomal instability in Barrett's esophagus is related to telomere shortening.
  • Barrett's esophagus is a useful model for the study of carcinogenesis, as the metaplastic columnar epithelium that replaces squamous esophageal epithelium is at elevated risk for development of adenocarcinoma.
  • We examined telomere length and chromosomal instability (CIN) in Barrett's esophagus biopsies using fluorescence in situ hybridization.
  • To study CIN, we selected centromere and locus-specific arm probes to chromosomes 17/17p (p53), 11/11q (cyclin D1), and 9/9p (p16 INK4A), loci reported to be involved in early stages of Barrett's esophagus neoplasia.
  • Telomere shortening was observed in Barrett's esophagus epithelium at all histologic grades, whereas CIN was highest in biopsies with dysplastic changes; there was, however, considerable heterogeneity between patients in each variable.
  • We conclude that CIN is related to telomere shortening in Barrett's esophagus but varies by chromosome.
  • Because telomere shortening and CIN are early events in Barrett's esophagus neoplastic progression and are highly variable among patients, it will be important to determine whether they identify a subset of patients that is at risk for more rapid neoplastic evolution.
  • [MeSH-major] Barrett Esophagus / genetics. Chromosomal Instability. Esophageal Neoplasms / genetics. Telomere / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Aged. Anaphase / genetics. Chromosomes, Human / genetics. Esophagus / metabolism. Flow Cytometry. Gastroesophageal Reflux / genetics. Gastroesophageal Reflux / pathology. Humans. In Situ Hybridization, Fluorescence / methods. Metaplasia / genetics. Middle Aged

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  • (PMID = 16896031.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P01CA91955; United States / NIA NIH HHS / AG / P30AG13280; United States / NCI NIH HHS / CA / T32CA09437
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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41. Williams LJ, Guernsey DL, Casson AG: Biomarkers in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma. Curr Oncol; 2006 Feb;13(1):33-43
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  • [Title] Biomarkers in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma.
  • Since the early 1970s, a dramatic change has occurred in the epidemiology of esophageal malignancy in both North America and Europe: the incidence of adenocarcinomas of the lower esophagus and esophagogastric junction is increasing.
  • Primary esophageal adenocarcinomas are thought to arise from Barrett esophagus, an acquired condition in which the normal esophageal squamous epithelium is replaced by a specialized metaplastic columnar-cell-lined epithelium.Today, gerd is recognized as an important risk factor in Barrett esophagus.
  • Progression of Barrett esophagus to invasive adenocarcinoma is reflected histologically by the metaplasia-dysplasia-carcinoma sequence.
  • Although several molecular alterations associated with progression of Barrett esophagus to invasive adenocarcinoma have been identified, relatively few will ultimately have clinical application.
  • Currently, the histologic finding of high-grade dysplasia remains the most reliable predictor of progression to invasive esophageal adenocarcinoma.
  • It is anticipated that models incorporating combinations of objective scores of sociodemographic and lifestyle risk factors (that is, age, sex, body mass index), severity of gerd, endoscopic and histologic findings, and a panel of biomarkers will be developed to better identify patients with Barrett esophagus at increased risk for malignant progression, leading to more rational endoscopic surveillance and screening programs.

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  • (PMID = 17576439.001).
  • [ISSN] 1198-0052
  • [Journal-full-title] Current oncology (Toronto, Ont.)
  • [ISO-abbreviation] Curr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC1891165
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42. Mehta S, Johnson IT, Rhodes M: Systematic review: the chemoprevention of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2005 Nov 1;22(9):759-68
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic review: the chemoprevention of oesophageal adenocarcinoma.
  • The incidence of oesophageal adenocarcinoma is increasing in the UK faster than any other malignancy.
  • Despite its relatively poor prognosis and the limited success of existing treatments, there is enthusiasm that chemopreventive agents might be able to stem the transition from normal squamous epithelium to adenocarcinoma.
  • We discuss gastro-oesophageal reflux as the main risk factor for the development of Barrett's metaplasia, the only known precursor of oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / prevention & control. Esophageal Neoplasms / prevention & control
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Arachidonic Acid / metabolism. Barrett Esophagus / complications. Diet. Disease Progression. Fatty Acids, Omega-3 / metabolism. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / drug therapy. Humans. Nitric Oxide / metabolism. Oxidative Stress / physiology. Proton Pump Inhibitors

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  • (PMID = 16225483.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Fatty Acids, Omega-3; 0 / Proton Pump Inhibitors; 27YG812J1I / Arachidonic Acid; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 96
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43. Oh DS, Demeester SR: Pathophysiology and treatment of Barrett's esophagus. World J Gastroenterol; 2010 Aug 14;16(30):3762-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathophysiology and treatment of Barrett's esophagus.
  • About 10%-15% of patients with GERD develop Barrett's esophagus, which can progress to adenocarcinoma, currently the most prevalent type of esophageal cancer.
  • The esophagus is normally lined by squamous mucosa, therefore, it is clear that for adenocarcinoma to develop, there must be a sequence of events that result in transformation of the normal squamous mucosa into columnar epithelium.
  • This article reviews the pathophysiology of Barrett's esophagus and implications for its treatment.
  • The effect of medical and surgical therapy of Barrett's esophagus is compared.
  • [MeSH-major] Barrett Esophagus / therapy. Digestive System Surgical Procedures. Esophageal Neoplasms / prevention & control. Esophagus / surgery. Gastrointestinal Agents / therapeutic use. Precancerous Conditions / therapy
  • [MeSH-minor] Disease Progression. Fundoplication. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / physiopathology. Gastroesophageal Reflux / therapy. Humans. Laparoscopy. Metaplasia. Risk Reduction Behavior. Treatment Outcome

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  • (PMID = 20698038.001).
  • [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
  • [Chemical-registry-number] 0 / Gastrointestinal Agents
  • [Other-IDs] NLM/ PMC2921087
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44. Shaheen NJ, Peery AF, Overholt BF, Lightdale CJ, Chak A, Wang KK, Hawes RH, Fleischer DE, Goldblum JR, AIM Dysplasia Investigators: Biopsy depth after radiofrequency ablation of dysplastic Barrett's esophagus. Gastrointest Endosc; 2010 Sep;72(3):490-496.e1
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biopsy depth after radiofrequency ablation of dysplastic Barrett's esophagus.
  • BACKGROUND: After endoscopic radiofrequency ablation (RFA) of dysplastic Barrett's esophagus (BE), endoscopic biopsy samples are obtained to assess response to therapy.
  • MAIN OUTCOME MEASUREMENTS: The proportion of biopsy samples demonstrating subepithelial structures, stratified by tissue type (columnar vs squamous) in sham- and RFA-treated subjects.
  • Squamous biopsy samples from RFA and sham subjects demonstrated subepithelium at similar rates (78.4% vs 79.1%, respectively, P = not significant [NS]).
  • Regardless of treatment assignment, more columnar than squamous biopsy samples demonstrated subepithelium (98.8% vs 78.5%, P < .001).
  • CONCLUSIONS: In both squamous and columnar tissue, endoscopic biopsy samples after RFA were as likely to demonstrate subepithelium as untreated controls.
  • Almost 80% of all biopsy samples were adequate to evaluate for subsquamous intestinal metaplasia.
  • The primary determinant of biopsy depth is the type of epithelium that underwent biopsy, with squamous less likely to yield subepithelium than columnar.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Catheter Ablation / methods. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagoscopy. Postoperative Complications / pathology. Postoperative Complications / surgery. Precancerous Conditions / pathology. Precancerous Conditions / surgery
  • [MeSH-minor] Aged. Biopsy. Disease Progression. Esophagus / pathology. Female. Follow-Up Studies. Humans. Male. Metaplasia. Middle Aged. Predictive Value of Tests. Treatment Outcome

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  • [Copyright] Copyright 2010 American Society for Gastrointestinal Endoscopy. Published by Mosby, Inc. All rights reserved.
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  • (PMID = 20598302.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00282672
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007634-15; United States / NIDDK NIH HHS / DK / T32 DK 07634; United States / NIDDK NIH HHS / DK / P30 DK034987; United States / NIDDK NIH HHS / DK / IH P30 DK034987; United States / NIDDK NIH HHS / DK / T32 DK007634
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS289916; NLM/ PMC3093936
  • [Investigator] Shaheen NJ; Madanick RD; Galanko JA; Sharma P; Overholt BF; Wolfsen HC; Sampliner RE; Wang KK; Falk GW; 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; Kimmey MB; Chak A; Lightdale CJ
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45. Rice TW, Mendelin JE, Goldblum JR: Barrett's esophagus: pathologic considerations and implications for treatment. Semin Thorac Cardiovasc Surg; 2005;17(4):292-300
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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 esophagus: pathologic considerations and implications for treatment.
  • Barrett's esophagus (BE) is a complication of chronic reflux that results in the replacement of esophageal squamous epithelium with columnar epithelium.
  • [MeSH-major] Barrett Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Disease Progression. Epithelium / pathology. Esophageal Neoplasms / pathology. Goblet Cells / pathology. Humans. Immunohistochemistry. Intestines / pathology. Metaplasia. Mucous Membrane / pathology

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  • (PMID = 16428035.001).
  • [ISSN] 1043-0679
  • [Journal-full-title] Seminars in thoracic and cardiovascular surgery
  • [ISO-abbreviation] Semin. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 38
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46. Cook MB, Wild CP, Everett SM, Hardie LJ, Bani-Hani KE, Martin IG, Forman D: Risk of mortality and cancer incidence in Barrett's esophagus. Cancer Epidemiol Biomarkers Prev; 2007 Oct;16(10):2090-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk of mortality and cancer incidence in Barrett's esophagus.
  • BACKGROUND: There are very few prospective follow-up studies of Barrett esophagus (BE) cohorts assessing the risk of extraesophageal cancer incidence or mortality.
  • RESULTS: All-cause mortality was found to be elevated in patients with BE [SMR, 1.21; 95% confidence interval (95% CI), 1.06, 1.37] and remained so after esophageal cancers were excluded (SMR, 1.16; 95% CI, 1.01-1.32).
  • Increased mortality risks were also found for malignant neoplasms of the esophagus (SMR, 7.26; 95% CI, 3.87-12.42) and diseases of the digestive system (SMR, 2.03; 95% CI, 1.11-3.40).
  • Circulatory disease mortality was borderline statistically significant (SMR, 1.24; 95% CI, 1.00-1.52; P = 0.053) for those with a specialized intestinal metaplasia diagnosis of BE.
  • In the cancer incidence analyses, esophageal malignancies (SIR, 8.66; 95% CI, 4.73-14.53) and esophageal adenocarcinomas (SIR, 14.29; 95% CI, 7.13-22.56) were found to be increased in BE.
  • CONCLUSIONS: This study has shown evidence of an increased risk of esophageal cancer incidence and mortality in BE.
  • It has also shown that those who have a histologic BE diagnosis may also have an increased risk of circulatory disease mortality.
  • [MeSH-major] Adenocarcinoma / mortality. Barrett Esophagus / mortality. Carcinoma, Squamous Cell / mortality. Esophageal Neoplasms / mortality. Neoplasms, Multiple Primary / mortality. Precancerous Conditions / mortality

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  • (PMID = 17890521.001).
  • [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
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47. Vallböhmer D, Peters JH, Kuramochi H, Oh D, Yang D, Shimizu D, DeMeester SR, Hagen JA, Chandrasoma PT, Danenberg KD, Danenberg PV, DeMeester TR: Molecular determinants in targeted therapy for esophageal adenocarcinoma. Arch Surg; 2006 May;141(5):476-81; discussion 481-2
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  • [Title] Molecular determinants in targeted therapy for esophageal adenocarcinoma.
  • HYPOTHESIS: Cyclooxygenase 2 (COX-2), vascular endothelial growth factor (VEGF), and epidermal growth factor receptor (EGFR) are useful biological determinants in targeted therapy for esophageal adenocarcinoma.
  • PATIENTS: Sixteen patients with squamous mucosa and normal results of a pH study without mucosal injury (control group), 15 with Barrett esophagus (metaplasia group), and 44 with adenocarcinoma (carcinoma group).
  • After laser-capture microdissection, quantitative real-time polymerase chain reaction was used to measure gene expression across the spectrum of the metaplasia-dysplasia-carcinoma sequence.
  • RESULTS: Expression of both COX-2 and VEGF was significantly up-regulated in patients with metaplasia, dysplasia, and cancer compared with controls (P<.01).
  • Expression levels of both were significantly higher in cancer than in the metaplasia group (P<.05) and increased sequentially from metaplasia to dysplasia to cancer.
  • No change in expression levels of EGFR was seen in the histologic progression to esophageal adenocarcinoma.
  • CONCLUSION: Gene expression data suggest that pharmacologic inhibition of COX-2 and VEGF may be useful adjuncts in targeted therapy for esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Antineoplastic Agents / therapeutic use. Cyclooxygenase 2 / metabolism. Esophageal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Receptor, Epidermal Growth Factor / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16702519.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA84424-02
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / RNA, Neoplasm; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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48. Gaddam S, Sharma P: Advances in endoscopic diagnosis and treatment of Barrett's esophagus. J Dig Dis; 2010 Dec;11(6):323-33
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  • [Title] Advances in endoscopic diagnosis and treatment of Barrett's esophagus.
  • Barrett's esophagus (BE) is defined as abnormal specialized columnar metaplasia with intestinalization in place of the normal squamous esophageal epithelium.
  • Patients with high grade dysplasia (HGD) and early cancer have a high rate of progression to invasive adenocarcinoma and traditionally these patients were treated with esophagectomy.
  • [MeSH-major] Adenocarcinoma. Barrett Esophagus. Endoscopy, Digestive System / trends. Esophageal Neoplasms

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  • [Copyright] © 2010 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.
  • (PMID = 21091894.001).
  • [ISSN] 1751-2980
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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49. Li M, Anastassiades CP, Joshi B, Komarck CM, Piraka C, Elmunzer BJ, Turgeon DK, Johnson TD, Appelman H, Beer DG, Wang TD: Affinity peptide for targeted detection of dysplasia in Barrett's esophagus. Gastroenterology; 2010 Nov;139(5):1472-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Affinity peptide for targeted detection of dysplasia in Barrett's esophagus.
  • BACKGROUND & AIMS: Dysplasia is a premalignant condition in Barrett's esophagus that is difficult to detect on endoscopy because of its flat architecture and patchy distribution.
  • We aim to select and validate an affinity peptide that binds to esophageal dysplasia for future clinical studies.
  • METHODS: Peptide selection was performed using phage display by removing nonspecific binders using Q-hTERT (intestinal metaplasia) cells and achieving specific binding against OE33 (esophageal adenocarcinoma) cells.
  • On esophageal specimens (n = 12), the fluorescence intensity (mean ± SEM) in 1-mm intervals classified histologically as squamous (n = 145), intestinal metaplasia (n = 83), dysplasia (n = 61), and gastric mucosa (n = 69) was 46.5 ± 1.6, 62.3 ± 5.8, 100.0 ± 9.0, and 42.4 ± 3.0 arb units, respectively.
  • CONCLUSIONS: The peptide sequence SNFYMPL binds specifically to dysplasia in Barrett's esophagus and can be fluorescence labeled to target premalignant mucosa on imaging.

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  • [Copyright] Copyright © 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • [Cites] Am J Med. 2002 Oct 15;113(6):499-505 [12427500.001]
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  • (PMID = 20637198.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U54 CA163059; United States / NCI NIH HHS / CA / U54 CA163059-01; United States / NCI NIH HHS / CA / U54 CA13642; United States / NCI NIH HHS / CA / U54 CA136429; United States / NCI NIH HHS / CA / U54 CA136429-01
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Affinity Labels; 0 / Carrier Proteins
  • [Other-IDs] NLM/ NIHMS365874; NLM/ PMC3319360
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50. Long KB, Hornick JL: SOX2 is highly expressed in squamous cell carcinomas of the gastrointestinal tract. Hum Pathol; 2009 Dec;40(12):1768-73
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  • [Title] SOX2 is highly expressed in squamous cell carcinomas of the gastrointestinal tract.
  • SOX2 is a high-mobility group box embryonic stem cell transcription factor that is expressed in the developing foregut and normal gastric epithelium and is downregulated in intestinal metaplasia of the stomach and esophagus.
  • In addition, SOX2 colocalizes with p63 in the basal layer and plays a critical role in the maintenance of the stratified squamous epithelium of the esophagus.
  • SOX2 expression in squamous cell carcinomas of the gastrointestinal tract has not been previously evaluated.
  • The purpose of this study was to determine whether SOX2 is differentially expressed in squamous cell carcinomas versus adenocarcinomas of the esophagus and rectum/anal canal and to compare its expression to p63, cytokeratin 5/6, and CDX2.
  • In total, 93 tumors were evaluated: 26 esophageal squamous cell carcinomas, 23 esophageal adenocarcinomas, 21 squamous cell carcinomas of the anal canal, and 23 rectal adenocarcinomas.
  • SOX2 was expressed in 81% of esophageal squamous cell carcinomas and 91% of anal canal squamous cell carcinomas, compared to 13% and 17% of esophageal and rectal adenocarcinomas, respectively. p63 was expressed in 96% of esophageal squamous cell carcinomas and 100% of anal canal squamous cell carcinomas; the single squamous cell carcinoma negative for p63 was strongly positive for SOX2.
  • Cytokeratin 5/6 was expressed in most esophageal and anal canal squamous cell carcinomas, but was also positive in 43% of esophageal adenocarcinomas and 13% of rectal adenocarcinomas.
  • In summary, SOX2 is preferentially expressed in squamous cell carcinomas of the esophagus and anal canal compared to adenocarcinomas from these sites.
  • SOX2 may be useful in an immunohistochemical panel to differentiate between squamous cell carcinomas and adenocarcinomas of the gastrointestinal tract.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / metabolism. Gastrointestinal Neoplasms / metabolism. SOXB1 Transcription Factors / biosynthesis
  • [MeSH-minor] Adenocarcinoma / metabolism. Diagnosis, Differential. Homeodomain Proteins / biosynthesis. Humans. Immunohistochemistry. Keratin-5 / biosynthesis. Keratin-6 / biosynthesis. Membrane Proteins / biosynthesis

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  • (PMID = 19716157.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / CKAP4 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-5; 0 / Keratin-6; 0 / Membrane Proteins; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors
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51. Jaquet Y, Pilloud R, Grosjean P, Radu A, Monnier P: Extended endoscopic mucosal resection in the esophagus and hypopharynx: a new rigid device. Eur Arch Otorhinolaryngol; 2007 Jan;264(1):57-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extended endoscopic mucosal resection in the esophagus and hypopharynx: a new rigid device.
  • We present a new device allowing for the diagnosis and treatment of extended superficial lesions of the esophagus and hypopharynx such as early squamous cell carcinoma, intestinal metaplasia with high grade intraepithelial neoplasia or early adenocarcinoma arising in Barrett's esophagus.
  • The deep resection margin was precisely located at the submucosal level, a prerequisite for a safe resection of superficial cancers of the esophagus and hypopharynx.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / surgery. Endoscopy / methods. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Hypopharyngeal Neoplasms / pathology. Hypopharyngeal Neoplasms / surgery. Minimally Invasive Surgical Procedures / instrumentation
  • [MeSH-minor] Barrett Esophagus / pathology. Barrett Esophagus / surgery. Early Diagnosis. Equipment Design. Humans. Mucous Membrane / pathology

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  • (PMID = 17043858.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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52. Maezato K, Nishimaki T, Oshiro M, Yamashiro T, Sasaki H, Sashida Y: Signet-ring cell carcinoma of the esophagus associated with Barrett's epithelium: report of a case. Surg Today; 2007;37(12):1096-101
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  • [Title] Signet-ring cell carcinoma of the esophagus associated with Barrett's epithelium: report of a case.
  • We herein report a case of infiltrative esophageal signet-ring cell carcinoma resembling gastric signet-ring cell carcinoma.
  • Grossly, the tumor was a diffusely infiltrative carcinoma involving the lower esophagus measuring 11 cm in diameter.
  • Histologically, the tumor was signet-ring cell carcinoma covered with normal squamous epithelium.
  • However, the most superficial part of the tumor center contained a region of Barrett's mucosa with incomplete-type intestinal metaplasia and a well-differentiated adenocarcinoma component with goblet cells.
  • The expression of cytokeratins 7 and 20 also indicated that both the Barrett's mucosa and the signet-ring cell carcinoma had an esophageal origin.
  • Esophageal signet-ring cell carcinoma with diffuse infiltrative growth is quite rare, and may need a special treatment strategy because of its highly aggressive behavior and poor treatment outcome.
  • [MeSH-major] Barrett Esophagus / complications. Carcinoma, Signet Ring Cell / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy. Diagnosis, Differential. Esophagectomy. Fatal Outcome. Humans. Male

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  • (PMID = 18030574.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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53. Lurje G, Vallbohmer D, Collet PH, Xi H, Baldus SE, Brabender J, Metzger R, Heitmann M, Neiss S, Drebber U, Holscher AH, Schneider PM: COX-2 mRNA expression is significantly increased in acid-exposed compared to nonexposed squamous epithelium in gastroesophageal reflux disease. J Gastrointest Surg; 2007 Sep;11(9):1105-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] COX-2 mRNA expression is significantly increased in acid-exposed compared to nonexposed squamous epithelium in gastroesophageal reflux disease.
  • BACKGROUND: Little is known about the role of cyclooxygenase (COX)-2 in gastroesophageal reflux disease (GERD) and the development of Barrett's metaplasia.
  • The objectives of this study were to further analyze COX-2 mRNA expression in patients with GERD compared to Barrett's esophagus (BE) and Barrett's cancer (BC).
  • Also, 24-h pH monitoring was performed in all patients of the GERD study group and the DeMeester composite score was used to match COX-2 mRNA expression with the severity of acid exposure in the lower esophagus.
  • RESULTS: COX-2 mRNA is progressively upregulated within the metaplasia-dysplasia-adenocarcinoma (MDA) sequence (p = 0.001).
  • COX-2 levels of the squamous epithelium in the distal esophagus from patients with GERD and a pathologic mean DeMeester score (>14.72) were significantly higher than in patients with normal DeMeester scores (p = 0.01).
  • CONCLUSION: In summary our findings suggest that alterations in COX-2 mRNA expression occur independently of endoscopic or histologic signs of GERD in the acid-exposed squamous epithelium of the distal esophagus.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Cyclooxygenase 2 / metabolism. Esophageal Neoplasms / metabolism. Gastroesophageal Reflux / metabolism

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  • (PMID = 17619937.001).
  • [ISSN] 1091-255X
  • [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, Messenger; EC 1.14.99.1 / Cyclooxygenase 2
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54. Gomes LI, Esteves GH, Carvalho AF, Cristo EB, Hirata R Jr, Martins WK, Marques SM, Camargo LP, Brentani H, Pelosof A, Zitron C, Sallum RA, Montagnini A, Soares FA, Neves EJ, Reis LF: Expression profile of malignant and nonmalignant lesions of esophagus and stomach: differential activity of functional modules related to inflammation and lipid metabolism. Cancer Res; 2005 Aug 15;65(16):7127-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profile of malignant and nonmalignant lesions of esophagus and stomach: differential activity of functional modules related to inflammation and lipid metabolism.
  • Adenocarcinomas of stomach and esophagus are frequently associated with preceding inflammatory alterations of the normal mucosa.
  • Whereas intestinal metaplasia of the gastric mucosa is associated with higher risk of malignization, Barrett's disease is a risk factor for adenocarcinoma of the esophagus.
  • Barrett's disease is characterized by the substitution of the squamous mucosa of the esophagus by a columnar tissue classified histopathologically as intestinal metaplasia.
  • Using cDNA microarrays, we determined the expression profile of normal gastric and esophageal mucosa as well as intestinal metaplasia and adenocarcinomas from both organs.
  • Data were explored to define functional alterations related to the transformation from squamous to columnar epithelium and the malignant transformation from intestinal metaplasia to adenocarcinomas.
  • Based on their expression profile, adenocarcinomas of the esophagus showed stronger correlation with intestinal metaplasia of the stomach than with Barrett's mucosa.
  • Whereas the lipid metabolism module is active in samples representing intestinal metaplasia and inactive in adenocarcinomas, the cytokine module is inactive in samples representing normal esophagus and esophagitis.
  • Exploitation of the data presented herein will help in the precise molecular characterization of adenocarcinoma from the distal esophagus, avoiding the topographical and descriptive classification that is currently adopted, and help with the proper management of patients with Barrett's disease.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Esophageal Neoplasms / genetics. Esophageal Neoplasms / metabolism. Lipid Metabolism. Stomach Neoplasms / genetics. Stomach Neoplasms / metabolism

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  • (PMID = 16103062.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
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55. Lu S, Lowe AW, Triadafilopoulos G, Hsiung PL, Hao Y, Crawford JM, Wang TD: Endoscopic evaluation of esophago-gastro-jejunostomy in rat model of Barrett's esophagus. Dis Esophagus; 2009;22(4):323-30
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  • [Title] Endoscopic evaluation of esophago-gastro-jejunostomy in rat model of Barrett's esophagus.
  • Endoscopy can be used to monitor the onset of metaplastic transformation and to observe the progression of neoplasia in small animal models of Barrett's esophagus.
  • We aim to characterize the endoscopic features of esophageal mucosa at various stages of the metaplasia-dysplasia-carcinoma sequence in a rat reflux model of Barrett's for comparison with histology.
  • Endoscopic examination of the distal esophagus was performed in 24 surgically altered and 4 control rats, between weeks 24 and 36 after the operation in 4-week intervals, and all rats were biopsied and sacrificed at 36 weeks.
  • Endoscopic images were classified based on the surface mucosal patterns of the distal esophagus and then compared with histology.
  • (ii) intestinal metaplasia, defined as elevated plaques/ridges, deep grooves, and thin linear folds;.
  • The endoscopic criteria for intestinal metaplasia yielded a sensitivity of 100% in comparison with histology.
  • Intestinal metaplasia with high-grade dysplasia was found in two rats and with low-grade dysplasia in three rats.
  • Both focally invasive squamous cell carcinoma and invasive adenocarcinoma were found in one rat.
  • Small animal endoscopy in a rat model of Barrett's esophagus can be used to perform surveillance, classify mucosal patterns, observe the onset of intestinal metaplasia, and monitor the progression of neoplastic transformation, representing a useful tool for studying the natural history of this disease.

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  • (PMID = 19473210.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R33 CA109988-05; United States / NIDDK NIH HHS / DK / P30 DK56339; United States / NIDDK NIH HHS / DK / K08 DK067618; United States / NCI NIH HHS / CA / U54 CA105296-05; United States / NIDDK NIH HHS / DK / R01 DK063624; United States / NIDDK NIH HHS / DK / K08 DK067618-06; United States / NCI NIH HHS / CA / U54 CA105296; United States / NCI NIH HHS / CA / R33 CA109988; United States / NCI NIH HHS / CA / U54 CA136429; United States / NIDDK NIH HHS / DK / P30 DK056339-10; United States / NIDDK NIH HHS / DK / P30 DK056339; United States / NCI NIH HHS / CA / U54 CA136429-01; United States / NIDDK NIH HHS / DK / R01 DK063624-09
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS247578; NLM/ PMC3221518
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56. Vallböhmer D, Peters JH, Oh D, Kuramochi H, Shimizu D, Demeester SR, Hagen JA, Chandrasoma PT, Danenberg KD, DeMeester TR, Danenberg P: Survivin, a potential biomarker in the development of Barrett's adenocarcinoma. Surgery; 2005 Oct;138(4):701-6; discussion 706-7
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  • [Title] Survivin, a potential biomarker in the development of Barrett's adenocarcinoma.
  • BACKGROUND: Survivin, a member of the inhibitor-of-apoptosis family, is reported to be overexpressed in esophageal cancer but no data are available about its status in the metaplastic/dysplastic sequence.
  • The aim of this study was to measure survivin gene expression in normal squamous/columnar epithelium and in the various stages of development of Barrett's adenocarcinoma.
  • (1) squamous epithelium from 3 cm above the gastroesophageal junction in patients with a negative pH study and no histologic injury (n = 17, pH- control);.
  • (3) specialized intestinal metaplasia from patients with Barrett's esophagus (n = 16; Barrett's group);.
  • (4) low- or high-grade dysplasia (n = 12, dysplasia group), and (5) adenocarcinoma (n = 45 cancer group).
  • RESULTS: Survivin gene expression was greater in columnar (antral) compared with squamous (pH-) control tissues (P = .03).
  • Expression levels in dysplastic epithelium were greater than in squamous control (P = .01) and Barrett's tissues (P = .04), but not higher than columnar control tissues, whereas expression in adenocarcinoma was greater than all tissues except dysplasia (P < .001).
  • CONCLUSIONS: Survivin expression may be a biomarker in the development of Barrett's adenocarcinoma that is able to distinguish between quiescent Barrett's, dysplastic Barrett's, and Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Barrett Esophagus / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / etiology. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Esophagus / metabolism. Esophagus / pathology. Female. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Mucous Membrane / metabolism. Mucous Membrane / pathology

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  • (PMID = 16269299.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA84424-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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57. Miyashita T, Ohta T, Fujimura T, Ninomiya I, Fushida S, Hattori T, Miwa K: Duodenal juice stimulates oesophageal stem cells to induce Barrett's oesophagus and oesophageal adenocarcinoma in rats. Oncol Rep; 2006 Jun;15(6):1469-75
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  • [Title] Duodenal juice stimulates oesophageal stem cells to induce Barrett's oesophagus and oesophageal adenocarcinoma in rats.
  • the present study was performed to examine the sequential process of the development of Barrett's oesophagus (BE) and oesophageal adenocarcinoma (ADC) induced by duodeno-oesophageal reflux (DER) in rats.
  • Severe squamous oesophagitis with erosion, regenerative thickening (RT), and basal cell hyperplasia (BCH) were observed on the 10th week after surgery.
  • On the 20th week, glandular structures that stained positively with Galactose oxidase-Schiff (foveolar metaplasia) were observed in the basal layer of the oesophageal squamous epithelium.
  • On the 30th week, the glands developed and formed cysts that stained positively with concanavalin A (pyloric glandular metaplasia) and/or high-iron diamine and Alcian blue (intestinal metaplasia).
  • Persistent stimulation with DER can alter the stem cells in the squamous epithelial basal layer leading to the formation of columnar-lined cells and subsequent ADC.
  • Foveolar metaplasia was observed as part of the sequence of events leading to the development of columnar-lined epithelium (CLE), followed by the appearance of pyloric glandular metaplasia and intestinal metaplasia, completing the histogenesis of BE.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / etiology. Duodenogastric Reflux / complications. Duodenum / secretion. Esophageal Neoplasms / etiology. Esophagus / pathology. Gastroesophageal Reflux / complications. Stem Cells / pathology

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  • (PMID = 16685381.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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58. Muldoon TJ, Anandasabapathy S, Maru D, Richards-Kortum R: High-resolution imaging in Barrett's esophagus: a novel, low-cost endoscopic microscope. Gastrointest Endosc; 2008 Oct;68(4):737-44
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  • [Title] High-resolution imaging in Barrett's esophagus: a novel, low-cost endoscopic microscope.
  • BACKGROUND: This report describes the clinical evaluation of a novel, low-cost, high-resolution endoscopic microscope for obtaining fluorescent images of the cellular morphology of the epithelium of regions of the esophagus with Barrett's metaplasia.
  • PATIENTS, INTERVENTIONS, AND MAIN OUTCOME MEASUREMENTS: The tissue samples studied in this report were obtained by endoscopic resection from patients with previous diagnoses of either high-grade dysplasia or esophageal adenocarcinoma.
  • RESULTS: Three distinct tissue types were observed ex vivo with the endoscopic microscope: normal squamous mucosa, Barrett's metaplasia, and high-grade dysplasia.
  • Squamous tissue was identified by bright nuclei surrounded by dark cytoplasm in an ordered pattern.
  • Barrett's metaplasia could be identified by large glandular structures with intact nuclear polarity.
  • Future improvement and integration with widefield endoscopic techniques will aid in improving the sensitivity of detection of dysplasia and early cancer development in the esophagus.

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  • (PMID = 18926182.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB007594-02; United States / NCI NIH HHS / CA / CA103830; United States / NCI NIH HHS / CA / R01 CA103830-05; United States / NIDDK NIH HHS / DK / P30 DK56338; United States / NIBIB NIH HHS / EB / EB007594-02; United States / NIDDK NIH HHS / DK / P30 DK056338; United States / NCI NIH HHS / CA / R01 CA103830; United States / NIBIB NIH HHS / EB / R01 EB007594; United States / NIBIB NIH HHS / EB / R01 EB002179
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Other-IDs] NLM/ NIHMS187221; NLM/ PMC2869299
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59. Majka J, Rembiasz K, Migaczewski M, Budzynski A, Ptak-Belowska A, Pabianczyk R, Urbanczyk K, Zub-Pokrowiecka A, Matlok M, Brzozowski T: Cyclooxygenase-2 (COX-2) is the key event in pathophysiology of Barrett's esophagus. Lesson from experimental animal model and human subjects. J Physiol Pharmacol; 2010 Aug;61(4):409-18
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  • [Title] Cyclooxygenase-2 (COX-2) is the key event in pathophysiology of Barrett's esophagus. Lesson from experimental animal model and human subjects.
  • Mixed reflux of the gastroduodenal contents induces the esophageal mucosal damage and inflammation progressing chronic esophagitis and premalignant Barrett's esophagus (BE).
  • The role of cyclooxygenase-2 (COX-2) and chronic inflammation in the progression of BE toward adenocarcinoma of the esophagus has not been extensively studied in experimental models of BE in animals and in human subjects.
  • Expression of COX-2 was evaluated in fresh-frozen biopsy specimens obtained from the distal esophagus in all 60 patients before and 12 months after treatment.
  • At 4 months, the esophageal damage in EGDA rats was evaluated by macroscopic and histological index score, the plasma IL-1beta and TNF-alpha levels was determined by ELISA and the mucosal expression of COX-2 mRNA and COX-2 protein were assessed by RT-PCR and Western Blot, respectively.
  • Histology revealed extensive esophageal ulcerations with development of columnar epithelium, formation of mucus glands in squamous epithelium, intestinal metaplasia distant to anastomosis consisting of goblet cells, infiltration of inflammatory cells including plasma cells and lymphocytes.
  • COX-2 mRNA was absent in the esophageal mucosa of sham-control animals but strongly upregulated in metaplastic Barrett's epithelium.
  • We conclude that 1) EGDA rats serve as the suitable model of the chronic esophagitis by the gastrointestinal refluxate resembling many features of those observed in human Barrett's esophagus, as confirmed by severe morphology changes, excessive release of proinflammatory cytokines TNF-alpha and IL-1beta and overexpression of COX-2, and 2) the significant correlation of the degree of COX-2 overexpression with histopathological findings indicates the usefulness of this inducible biomarker as a valuable indicator of the risk of malignant transformation in patients with BE.
  • [MeSH-major] Barrett Esophagus / enzymology. Barrett Esophagus / physiopathology. Cyclooxygenase 2 / physiology. Disease Models, Animal
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Adult. Aged. Animals. Biomarkers / metabolism. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Esophageal Neoplasms / enzymology. Esophageal Neoplasms / pathology. Esophageal Neoplasms / physiopathology. Female. Humans. Male. Middle Aged. Rats. Rats, Wistar

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  • (PMID = 20814068.001).
  • [ISSN] 1899-1505
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers; EC 1.14.99.1 / Cyclooxygenase 2
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60. Szentpáli K, Széll M, Paszt A, Wolfárd A, Dobozy A, Németh I, Tiszlavicz L, Iván L, Boros M: Simultaneous adeno- and squamous cell carcinoma with different phenotypic profiles in a rat model of chronic gastroesophageal reflux. Dis Esophagus; 2007;20(4):305-10
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  • [Title] Simultaneous adeno- and squamous cell carcinoma with different phenotypic profiles in a rat model of chronic gastroesophageal reflux.
  • The aim of our study was to investigate the incidence of duodeno-gastroesophageal reflux-induced malignant transformation in a series of duodeno-esophageal anastomosis operations in rats.
  • This surgical method provides a model for reflux-induced esophageal pathologies, without carcinogen administration.
  • Thirty weeks of duodeno-gastroesophageal reflux disease significantly increased the risk of the development of Barrett's esophagus, and reflux-induced esophageal adenocarcinoma formation was evident in four animals.
  • In one of these particular cases, a superficial squamous cell cancer was noted in close vicinity to the adenocarcinoma formation.
  • The immunophenotypes revealed cyclin D1 expression (nuclear positivity in 35% of all the squamous cells), p53 protein accumulation (50% nuclear positivity), with a low expression of cox-2, and negative c-erbB2 staining in the squamous carcinoma cells.
  • The specialized intestinal metaplasia and mucinous adenocarcinoma cells exhibited exclusively diffuse cox-2 positivity (90% of all glandular cells) and weak focal c-erbB2 (5%) staining, without cyclin D1 expression or p53 protein accumulation.
  • The most dramatic changes were observed in the level of expression of cyclin D1 (a 9.08-fold expression as compared with the non-treated esophagus samples), while the p53 and cox-2 gene expressions were increased by 1.61 and 2.45-fold, respectively, relative to the non-treated samples.


61. Abdel-Latif MM, O'Riordan JM, Ravi N, Kelleher D, Reynolds JV: Activated nuclear factor-kappa B and cytokine profiles in the esophagus parallel tumor regression following neoadjuvant chemoradiotherapy. Dis Esophagus; 2005;18(4):246-52
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  • [Title] Activated nuclear factor-kappa B and cytokine profiles in the esophagus parallel tumor regression following neoadjuvant chemoradiotherapy.
  • Esophageal adenocarcinoma is increasing in incidence; it relates to chronic gastroesophageal reflux, it is difficult to cure, and treatment modalities increasingly use chemotherapy and radiation therapy prior to resectional surgery.
  • Nuclear factor-kappa B (NF-kappaB) is a pleiotropic transcription factor that regulates several genes for cytokines and enzymes involved in inflammation and immunity, and we have previously described sequential expression of NF-kappaB from the normal esophagus through Barrett's metaplasia to adenocarcinoma.
  • The aim of this exploratory study was to assess the NF-kappaB status and cytokine profiles pre- and post-chemoradiotherapy for esophageal adenocarcinoma.
  • Fresh biopsy specimens obtained from 20 patients with esophageal adenocarcinoma and normal adjacent squamous epithelium were obtained pre-, during and post-chemoradiotherapy, and NF-kappaB expression was analyzed by electrophoretic mobility shift assay.
  • NF-kappaB was constitutively activated in tumor tissues from esophageal adenocarcinoma but was not detected in adjacent normal esophageal mucosa.

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  • (PMID = 16128781.001).
  • [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] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Interleukin-1; 0 / Interleukin-8; 0 / NF-kappa B; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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62. Dumot JA, Vargo JJ 2nd, Falk GW, Frey L, Lopez R, Rice TW: An open-label, prospective trial of cryospray ablation for Barrett's esophagus high-grade dysplasia and early esophageal cancer in high-risk patients. Gastrointest Endosc; 2009 Oct;70(4):635-44
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  • [Title] An open-label, prospective trial of cryospray ablation for Barrett's esophagus high-grade dysplasia and early esophageal cancer in high-risk patients.
  • BACKGROUND: Endoscopic ablation of Barrett's esophagus (BE) is a treatment option for patients with high-grade dysplasia (HGD) and intramucosal carcinoma (IMCA).
  • MAIN OUTCOME MEASUREMENTS: Histologic response was defined by the worst pathology obtained at any level of the esophagus or gastric cardia in 1 of 3 categories:.
  • (1) incremental = absence of HGD and IMCA in all biopsy specimens, (2) partial = residual IMCA with absence of any dysplasia, and (3) complete = absence of any intestinal metaplasia or dysplasia.
  • [MeSH-major] Adenocarcinoma / therapy. Barrett Esophagus / therapy. Carcinoma, Squamous Cell / therapy. Cryosurgery / methods. Esophageal Neoplasms / therapy

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  • (PMID = 19559428.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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63. Guo M, House MG, Suzuki H, Ye Y, Brock MV, Lu F, Liu Z, Rustgi AK, Herman JG: Epigenetic silencing of CDX2 is a feature of squamous esophageal cancer. Int J Cancer; 2007 Sep 15;121(6):1219-26
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  • [Title] Epigenetic silencing of CDX2 is a feature of squamous esophageal cancer.
  • Mice heterozygously disrupted for CDX2 develop disorganized polypoid hamartomas with glandular epithelium and stratified squamous metaplasia resembling foregut mucosa.
  • Eleven of 17 squamous esophageal cancer cell lines lacked expression of CDX2 that was restored following treatment with 5-aza-2'-deoxycytidine, while all colorectal cancer cell lines expressed CDX2.
  • Methylation of CDX2 was rare in primary colorectal (1 of 44 tumors, 2%) and esophageal adenocarcinoma neoplasms (2 of 43 tumors, 5%), but was common in esophageal squamous carcinoma (24 of 45 tumors, 49%).
  • Using semi-quantitative RT-PCR, expression of CDX2 was found in low level in normal esophagus, at higher levels in primary adenocarcinoma of the esophagus, but not in primary squamous cancers of the esophagus.
  • Our results suggest that the inactivation of CDX2 in esophageal cancer associated with DNA methylation may be an important determinant of the squamous or non-adenomatous phenotype.
  • [MeSH-major] Adenocarcinoma / genetics. Cell Transformation, Neoplastic / genetics. Esophageal Neoplasms / genetics. Gene Silencing. Homeodomain Proteins / genetics. Neoplasms, Squamous Cell / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17534889.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84986
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / DNA, Neoplasm; 0 / Homeodomain Proteins; 0 / MUC2 protein, human; 0 / Muc2 protein, mouse; 0 / Mucin-2; 0 / Mucins; 0 / RNA, Small Interfering
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64. Hu Y, Williams VA, Gellersen O, Jones C, Watson TJ, Peters JH: The pathogenesis of Barrett's esophagus: secondary bile acids upregulate intestinal differentiation factor CDX2 expression in esophageal cells. J Gastrointest Surg; 2007 Jul;11(7):827-34
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  • [Title] The pathogenesis of Barrett's esophagus: secondary bile acids upregulate intestinal differentiation factor CDX2 expression in esophageal cells.
  • INTRODUCTION: Clinical evidence strongly suggests that bile acids are important in the development of Barrett's esophagus, although the mechanism remains unknown.
  • Caudal-related homeobox 2 (CDX2) is a transcription factor recently implicated in early differentiation and maintenance of normal intestinal epithelium and is suggested to play a key role in the pathogenesis of intestinal metaplasia in Barrett's esophagus.
  • OBJECTIVE: The aim of this study was to investigate the effect of primary and secondary bile acids on CDX2 mRNA expression in human esophageal cells.
  • METHODS: Human esophageal cells:.
  • (1) squamous, immortalized by SV40 (Het-1A);.
  • (2) adenocarcinoma (SEG-1); and (3) squamous cell carcinoma (HKESC-1 & HKESC-2), were exposed in cell culture for 1-24 h to 100-1,000 microM deoxycholic, chenodeoxycholic, and glycocholic acids.
  • The maximal induction of CDX2 expression was seen in SEG-1 adenocarcinoma cells.
  • Expression in Het-1A cells also increased significantly as did expression in HKESC-1,2 cells, although to a lesser extent than in adenocarcinoma.
  • They further support the role of bile acids in the pathogenesis of Barrett's esophagus and link the clinical evidence of a high prevalence of luminal bile acids in Barrett's to expression of the gene thought to be responsible for the phenotypic expression of intestinal metaplasia.
  • [MeSH-major] Barrett Esophagus / etiology. Bile Acids and Salts / physiology. Esophagus / pathology. Homeodomain Proteins / genetics. Intestines / microbiology. Mucins / genetics. RNA, Messenger / biosynthesis

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  • [CommentIn] Arch Surg. 2008 Aug;143(8):807 [18711046.001]
  • [ErratumIn] J Gastrointest Surg. 2008 Feb;12(2):400 [18071834.001]
  • (PMID = 17458588.001).
  • [ISSN] 1091-255X
  • [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] Duplicate Publication; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / MUC2 protein, human; 0 / Mucin-2; 0 / Mucins; 0 / RNA, Messenger
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65. da Rocha JR, Ribeiro U Jr, Sallum RA, Szachnowicz S, Cecconello I: Barrett's esophagus (BE) and carcinoma in the esophageal stump (ES) after esophagectomy with gastric pull-up in achalasia patients: a study based on 10 years follow-up. Ann Surg Oncol; 2008 Oct;15(10):2903-9
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  • [Title] Barrett's esophagus (BE) and carcinoma in the esophageal stump (ES) after esophagectomy with gastric pull-up in achalasia patients: a study based on 10 years follow-up.
  • AIM: To analyze late clinical, endoscopic, and pathologic findings in the esophageal stump (ES) mucosa after subtotal esophagectomy in patients treated for advanced chagasic achalasia.
  • RESULTS: The incidence of esophagitis in the esophageal stump (45.9% at 1 year; 71.9% at 5 years, and 70.0% at 10 years follow-up); gastritis in the transposed stomach (20.4% at 1 year, 31.0% at 5 years, and 40.0% at 10 or more years follow-up), and the occurrence of ectopic columnar metaplasia and Barrett's Esophagus in the ES (none until 1 year; 10.9% between 1 and 5 years; 29.5% between 5 and 10 years; and 57.5% at 10 or more years follow-up), all rose over time.
  • Esophageal stump cancer was detected in the setting of chronic esophagitis in five patients: three squamous cell carcinomas and two adenocarcinomas. CONCLUSION:.
  • (1) Esophagitis and Barrett's esophagus in the esophageal stump rose over time. (2) These mucosal alterations and the development of squamous cell carcinoma and adenocarcinoma are probably due to exposure to duodenogastric reflux, and progressively higher acid output in the transposed stomach.
  • [MeSH-major] Barrett Esophagus / etiology. Esophageal Achalasia / surgery. Esophageal Neoplasms / etiology. Esophagectomy. Gastroplasty. Postoperative Complications
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Adenocarcinoma / surgery. Adolescent. Adult. Aged. Carcinoma, Squamous Cell / etiology. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / surgery. Duodenogastric Reflux / complications. Duodenogastric Reflux / pathology. Duodenogastric Reflux / surgery. Esophagitis / etiology. Esophagitis / surgery. Female. Follow-Up Studies. Gastroesophageal Reflux / pathology. Gastroesophageal Reflux / surgery. Humans. Male. Middle Aged. Prognosis. Prospective Studies


66. Estensen RD, Anderson WR, Galbraith AR, Hartle DE, Jordan MM, Ondrey FG, Wattenberg LW: A method of producing carcinoma in upper aerodigestive tree and esophagus of the Syrian golden hamster using wounding and instillation of N-methylnitrosourea. Cancer Epidemiol Biomarkers Prev; 2007 Aug;16(8):1644-50
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  • [Title] A method of producing carcinoma in upper aerodigestive tree and esophagus of the Syrian golden hamster using wounding and instillation of N-methylnitrosourea.
  • The method produces a majority of squamous carcinomas of the trachea and glottis that follow squamous metaplasia of respiratory epithelium.
  • Squamous carcinomas of the digestive epithelium arise in primary squamous epithelium.
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Animals. Anticarcinogenic Agents / therapeutic use. Carcinoma, Squamous Cell / etiology. Carcinoma, Squamous Cell / pathology. Chemoprevention. Cricetinae. Epithelium / pathology. Esophageal Neoplasms / etiology. Esophageal Neoplasms / pathology. Glottis / pathology. Laryngeal Neoplasms / etiology. Laryngeal Neoplasms / pathology. Mesocricetus. Metaplasia. Mucous Membrane / pathology. Pharyngeal Neoplasms / etiology. Pharyngeal Neoplasms / pathology. Respiratory Mucosa / pathology

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  • (PMID = 17684140.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Carcinogens; 684-93-5 / Methylnitrosourea
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67. Chen X, Qin R, Liu B, Ma Y, Su Y, Yang CS, Glickman JN, Odze RD, Shaheen NJ: Multilayered epithelium in a rat model and human Barrett's esophagus: similar expression patterns of transcription factors and differentiation markers. BMC Gastroenterol; 2008 Jan 11;8:1
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  • [Title] Multilayered epithelium in a rat model and human Barrett's esophagus: similar expression patterns of transcription factors and differentiation markers.
  • BACKGROUND: In rats, esophagogastroduodenal anastomosis (EGDA) without concomitant chemical carcinogen treatment leads to gastroesophageal reflux disease, multilayered epithelium (MLE, a presumed precursor in intestinal metaplasia), columnar-lined esophagus, dysplasia, and esophageal adenocarcinoma.
  • Previously we have shown that columnar-lined esophagus in EGDA rats resembled human Barrett's esophagus (BE) in its morphology, mucin features and expression of differentiation markers (Lab. Invest. 2004;84:753-765).
  • Tissue sections were immunohistochemically stained for a variety of transcription factors and differentiation markers of esophageal squamous epithelium and intestinal columnar epithelium.
  • As expected, both rat and human squamous epithelium, but not intestinal metaplasia, expressed squamous transcription factors and differentiation markers (p63, Sox2, CK14 and CK4) in all cases.
  • Both rat and human intestinal metaplasia, but not squamous epithelium, expressed intestinal transcription factors and differentiation markers (Cdx2, GATA4, HNF1alpha, villin and Muc2) in all cases.
  • CONCLUSION: These data indicate that rat MLE shares similar properties to human MLE in its expression pattern of these markers, not withstanding small differences, and support the concept that MLE may be a transitional stage in the metaplastic conversion of squamous to columnar epithelium in BE.

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  • (PMID = 18190713.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA75683; United States / NIDDK NIH HHS / DK / R21 DK063650; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / U56 CA092077; United States / NIDDK NIH HHS / DK / DK63650; United States / NCI NIH HHS / CA / CA092077; United States / NCI NIH HHS / CA / R01 CA075683
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2267197
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68. Alvarez H, Rojas PL, Yong KT, Ding H, Xu G, Prasad PN, Wang J, Canto M, Eshleman JR, Montgomery EA, Maitra A: Mesothelin is a specific biomarker of invasive cancer in the Barrett-associated adenocarcinoma progression model: translational implications for diagnosis and therapy. Nanomedicine; 2008 Dec;4(4):295-301
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  • [Title] Mesothelin is a specific biomarker of invasive cancer in the Barrett-associated adenocarcinoma progression model: translational implications for diagnosis and therapy.
  • Esophageal adenocarcinoma arises in the backdrop of Barrett metaplasia-dysplasia sequence, with the vast majority of patients presenting with late-stage malignancy.
  • Mesothelin expression was assessed in esophageal tissue microarrays encompassing the entire histological spectrum of Barrett-associated dysplasia and adenocarcinoma.
  • In contrast, normal squamous and cardiac mucosa, as well as noninvasive Barrett lesions, failed to label with mesothelin.
  • Mesothelin was expressed in the esophageal adenocarcinoma cell line JH-EsoAd1 but not in primary human esophageal epithelial cells.
  • Anti-mesothelin antibody-conjugated nanoparticles can be useful for the diagnosis and therapy of mesothelin-overexpressing esophageal adenocarcinomas.

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  • (PMID = 18691948.001).
  • [ISSN] 1549-9642
  • [Journal-full-title] Nanomedicine : nanotechnology, biology, and medicine
  • [ISO-abbreviation] Nanomedicine
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA119397-04; United States / NCI NIH HHS / CA / R01 CA119397; United States / NCI NIH HHS / CA / R01 CA119397-04; United States / NCI NIH HHS / CA / R01CA119397
  • [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 / Antibodies; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / mesothelin
  • [Other-IDs] NLM/ NIHMS79893; NLM/ PMC2606904
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69. Jin Z, Mori Y, Yang J, Sato F, Ito T, Cheng Y, Paun B, Hamilton JP, Kan T, Olaru A, David S, Agarwal R, Abraham JM, Beer D, Montgomery E, Meltzer SJ: Hypermethylation of the nel-like 1 gene is a common and early event and is associated with poor prognosis in early-stage esophageal adenocarcinoma. Oncogene; 2007 Sep 20;26(43):6332-40
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  • [Title] Hypermethylation of the nel-like 1 gene is a common and early event and is associated with poor prognosis in early-stage esophageal adenocarcinoma.
  • The nel-like1 (NELL1) gene maps to chromosome 11p15, which frequently undergoes loss of heterozygosity in esophageal adenocarcinoma (EAC).
  • NELL1 promoter hypermethylation was examined by real-time methylation-specific polymerase chain reaction in 259 human esophageal tissues.
  • Hypermethylation of this promoter showed highly discriminative receiver-operator characteristic curve profiles, clearly distinguishing esophageal squamous cell carcinoma (ESCC) and EAC from normal esophagus (NE) (P<0.001).
  • NELL1 normalized methylation values were significantly higher in Barrett's metaplasia (BE), dysplastic Barrett's (D) and EAC than in NE (P<0.0000001).
  • Promoter hypermethylation of NELL1 is a common, tissue-specific event in human EAC, occurs early during Barrett's-associated esophageal neoplastic progression, and is a potential biomarker of poor prognosis in early-stage EAC.

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  • (PMID = 17452981.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK067872; United States / NCI NIH HHS / CA / CA001808; United States / NCI NIH HHS / CA / CA085069; United States / NCI NIH HHS / CA / CA106763
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NELL1 protein, human; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 65-47-4 / Cytidine Triphosphate; 72052-96-1 / 5-aza-2'-deoxycytidine-5'-triphosphate; M801H13NRU / Azacitidine
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70. Chandrasoma P, Wijetunge S, Demeester SR, Hagen J, Demeester TR: The histologic squamo-oxyntic gap: an accurate and reproducible diagnostic marker of gastroesophageal reflux disease. Am J Surg Pathol; 2010 Nov;34(11):1574-81
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  • This study provides a method to develop a histologic definition of GERD based on biopsies obtained from the affected esophagus.
  • Biopsies were obtained from the esophagus, around the gastroesophageal junction and the stomach: proximal, body, and antrum.
  • Patients who had oxyntocardiac±cardiac±intestinal epithelia between the squamous epithelium proximally and the proximal limit of gastric oxyntic mucosa distally were defined as having a squamo-oxyntic gap.
  • Only oxyntocardiac epithelium was seen in 190 (11.5%) of the patients, oxyntocardiac and cardiac epithelia in 898 (54.3%), and intestinal metaplasia in addition to the other 2 epithelial types in 567 (34.2%).
  • The prevalence of intestinal metaplasia was directly proportional to length of the squamo-oxyntic gap, being 24.3% (340/1399) when the length was <1 cm, and 83.5% (147/176) with length 1 to 5 cm.
  • All patients with a length more than 5 cm had intestinal metaplasia.
  • The distribution of the 3 epithelia was constant irrespective of the length of the squamocolumnar gap; intestinal metaplasia, when present, was seen maximally in the proximal region of the gap, cardiac epithelium intermediate and oxyntocardiac epithelium in the most distal segment of the gap.
  • The squamo-oxyntic gap started in a dilated region distal to the end of the tubular esophagus and distal to the proximal limit of the rugal folds and extended into the tubular esophagus.
  • Distal gastric biopsies showed no evidence of significant inflammation, intestinal metaplasia or Helicobacter pylori infection in 1543 (93.2%) of the patients, indicating that the squamo-oxyntic gap was largely independent of gastric pathology.
  • We provide evidence that the squamo-oxyntic gap is equivalent to the columnar-lined esophagus.
  • The presence of intestinal metaplasia within the squamo-oxyntic gap is the most accurate risk indicator for esophageal adenocarcinoma and defines Barrett esophagus.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Epithelial Cells / pathology. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Gastroesophageal Reflux / diagnosis. Parietal Cells, Gastric / pathology. Precancerous Conditions / diagnosis
  • [MeSH-minor] Biopsy. California. Endoscopy, Gastrointestinal. Humans. Metaplasia. Predictive Value of Tests. Reproducibility of Results. Retrospective Studies. Risk Assessment. Risk Factors. Severity of Illness Index

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  • [CommentIn] Am J Surg Pathol. 2011 May;35(5):773; author reply 773-4 [21502913.001]
  • (PMID = 20871393.001).
  • [ISSN] 1532-0979
  • [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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71. Dias Pereira A, Suspiro A, Chaves P: Cancer risk in Barrett's oesophagus. Eur J Gastroenterol Hepatol; 2007 Nov;19(11):915-8

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  • )Barrett's oesophagus results from the replacement of the normal squamous lining of the oesophagus by a columnar epithelium.
  • It is the sole known premalignant condition for oesophageal adenocarcinoma.
  • The prerequisite of the presence of intestinal metaplasia for the diagnosis of Barrett's oesophagus, although widely accepted, is questioned by some authors.
  • How adenocarcinoma incidence is influenced by requiring or not intestinal metaplasia for Barrett's oesophagus diagnosis is unknown.
  • Data on adenocarcinoma incidence in short segments (<3 cm) are very scarce, but it is believed to be lower than in long segments.
  • Frequently, therapeutic intervention is performed when high-grade dysplasia is diagnosed, preventing progression to adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / pathology. Esophagus / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Disease Progression. Esophageal Neoplasms / pathology. Esophagoscopy. Humans. Incidence. Intestines / pathology. Metaplasia. Risk

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  • (PMID = 18049157.001).
  • [ISSN] 0954-691X
  • [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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72. Micev M, Cosić-Micev M: [Pathology and pathobiology of the oesophageal carcinoma]. Acta Chir Iugosl; 2010;57(2):15-26
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  • Identification of dysplasia in mucosal biopsies is the most reliable pathologic indicator of an increased risk of development of squamous cell carcinoma and passes through the sequence of chronic esophagitis, low-grade and high-grade dysplasia and invasive carcinoma.
  • Although Barrett's esophagus is a precursor to esophageal adenocarcinoma and have a well described sequence of carcinogenesis: the Barrett's metaplasia-dysplasia-adenocarcinoma sequence, not all patients with this disorder require intensive surveillance.
  • More studies are needed to define other early nonmorphologic biomarkers for risk of squamous cell carcinoma.
  • [MeSH-major] Esophageal Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Barrett Esophagus / complications. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / pathology. Humans

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  • (PMID = 20954310.001).
  • [ISSN] 0354-950X
  • [Journal-full-title] Acta chirurgica Iugoslavica
  • [ISO-abbreviation] Acta Chir Iugosl
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Serbia
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73. Punia RS, Arya S, Mohan H, Duseja A, Bal A: Spectrum of clinico-pathological changes in Barrett oesophagus. J Assoc Physicians India; 2006 Mar;54:187-9
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  • OBJECTIVES: Barrett oesophagus is replacement of squamous epithelium to specialised intestinal metaplasia.
  • It is associated with an increased risk for adenocarcinoma which develops through dysplasia.
  • On histology examination, in 6 cases, squamous epithelium was replaced by intestinal epithelium containing goblet cells and in 7 cases it was replaced by gastric epithelium.
  • Associated dysplasia was not seen in any of the case, while one case showed associated adenocarcinoma.
  • There is a paucity of patients with pure dysplasia in Barrett metaplasia.
  • Despite the fact that there are a number of patients presenting with Barrett esophagus and carcinoma, very few patients present with dysplasia, indicating that Barrett oesophagus is a silent disease presenting later as a carcinoma.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / pathology. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology
  • [MeSH-minor] Adult. Age Factors. Aged. Biopsy. Esophagoscopy. Female. Humans. India. Male. Metaplasia. Middle Aged. Retrospective Studies. Sex Factors. Staining and Labeling

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  • (PMID = 16800342.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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74. Hao J, Liu B, Yang CS, Chen X: Gastroesophageal reflux leads to esophageal cancer in a surgical model with mice. BMC Gastroenterol; 2009 Jul 23;9:59
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  • [Title] Gastroesophageal reflux leads to esophageal cancer in a surgical model with mice.
  • BACKGROUND: Esophago-gastroduodenal anastomosis with rats mimics the development of human Barrett's esophagus and esophageal adenocarcinoma by introducing mixed reflux of gastric and duodenal contents into the esophagus.
  • Therefore, a mouse model of esophageal adenocarcinoma is needed.
  • RESULTS: At week 20, we observed metaplasia in wild-type mice (5%, 1/20) and p53A135V mice (5.3%, 1/19).
  • At week 40, metaplasia was found in wild-type mice (16.2%, 6/37), p53A135V mice (4.8%, 2/42), and wild-type mice also receiving gastrectomy and iron (6.7%, 1/15).
  • Esophageal squamous cell carcinoma developed in INK4a/Arf+/- mice (7.1%, 1/14), and wild-type mice receiving gastrectomy and iron (21.4%, 3/14).
  • Among 13 wild-type mice which were given iron from week 40 to 80, twelve (92.3%) developed squamous cell carcinoma at week 80.
  • None of these mice developed esophageal adenocarcinoma.
  • CONCLUSION: Surgically induced gastroesophageal reflux produced esophageal squamous cell carcinoma, but not esophageal adenocarcinoma, in mice.
  • Dominant negative p53 mutation, heterozygous loss of INK4a/Arf, antacid treatment, iron supplementation, or gastrectomy failed to promote esophageal adenocarcinoma in these mice.
  • Further studies are needed in order to develop a mouse model of esophageal adenocarcinoma.

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  • (PMID = 19627616.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / R01 CA75683; United States / NCI NIH HHS / CA / R03 CA125804; United States / NCI NIH HHS / CA / U56 CA092077
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Protein p53; E1UOL152H7 / Iron; KG60484QX9 / Omeprazole
  • [Other-IDs] NLM/ PMC2723127
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75. Chandrasoma P: Controversies of the cardiac mucosa and Barrett's oesophagus. Histopathology; 2005 Apr;46(4):361-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Confusion regarding the diagnosis of Barrett's oesophagus exists because of a false dogma that cardiac mucosa is normally present in the gastro-oesophageal junctional region.
  • Recent data indicate that the only normal epithelia in the oesophagus and proximal stomach are squamous epithelium and gastric oxyntic mucosa.
  • When this fact is recognized, it becomes easy to develop precise histological definitions for the normal state (presence of only squamous and oxyntic mucosa), metaplastic oesophageal columnar epithelium (cardiac mucosa with and without intestinal metaplasia, and oxynto-cardiac mucosa), the gastro-oesophageal junction (the proximal limit of gastric oxyntic mucosa), the oesophagus (that part of the foregut lined by squamous and metaplastic columnar epithelium), reflux disease (the presence of metaplastic columnar epithelium), and Barrett's oesophagus (cardiac mucosa with intestinal metaplasia).
  • It is also possible to assess accurately the severity of reflux which is directly proportional to the amount of metaplastic columnar epithelium, and the risk of adenocarcinoma which is related to the amount of dysplasia in intestinal metaplastic epithelium present within the columnar lined segment of the oesophagus.
  • Histopathological precision cannot be matched by any other modality and can convert the confusion that exists regarding diagnosis of Barrett's oesophagus to complete lucidity in a manner that is simple, accurate, and reproducible.
  • [MeSH-major] Barrett Esophagus / pathology. Cardia / pathology. Gastric Mucosa / pathology
  • [MeSH-minor] Esophagogastric Junction / pathology. Humans. Metaplasia

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  • [CommentIn] Histopathology. 2006 Jul;49(1):97-8; author reply 98 [16842257.001]
  • (PMID = 15810947.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 48
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76. Cooper BT, Chapman W, Neumann CS, Gearty JC: Continuous treatment of Barrett's oesophagus patients with proton pump inhibitors up to 13 years: observations on regression and cancer incidence. Aliment Pharmacol Ther; 2006 Mar 15;23(6):727-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM: To determine if longer periods of treatment with proton pump inhibitors lead to significant regression of Barrett's oesophagus, and to determine the incidence of oesophageal adenocarcinoma in the proton pump inhibitor-treated patients.
  • RESULTS: 188 patients with Barrett's oesophagus and intestinal metaplasia, were treated for 1-13 years with a proton pump inhibitor (966 years of treatment; mean 5.1 years).
  • No change in length was seen during treatment but 48% of patients developed squamous islands (25% after 1-3 years; 100% at 12-13 years).
  • Squamous islands correlated with treatment duration and male sex but not with proton pump inhibitor dose or patient age.
  • Six patients developed dysplasia and three males developed adenocarcinoma during treatment (cancer incidence 0.31%).
  • CONCLUSIONS: Proton-pump inhibitor treatment over 1-13 years does not shorten the Barrett's oesophagus segment but squamous islands appear in many patients.
  • The incidence of oesophageal adenocarcinoma was low in these proton pump inhibitor-treated patients compared with published series.
  • [MeSH-major] Barrett Esophagus / drug therapy. Enzyme Inhibitors / administration & dosage. Proton Pump Inhibitors
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles. Adenocarcinoma / chemically induced. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Drug Administration Schedule. Esophageal Diseases / chemically induced. Esophageal Diseases / pathology. Esophageal Neoplasms / chemically induced. Esophageal Neoplasms / pathology. Female. Humans. Lansoprazole. Long-Term Care. Male. Middle Aged. Omeprazole / administration & dosage. Omeprazole / analogs & derivatives. Prospective Studies. Sex Factors. Treatment Outcome

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  • [CommentIn] Nat Clin Pract Gastroenterol Hepatol. 2006 Dec;3(12):658-9 [17130871.001]
  • (PMID = 16556174.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Enzyme Inhibitors; 0 / Proton Pump Inhibitors; 0K5C5T2QPG / Lansoprazole; KG60484QX9 / Omeprazole
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77. Jin Z, Hamilton JP, Yang J, Mori Y, Olaru A, Sato F, Ito T, Kan T, Cheng Y, Paun B, David S, Beer DG, Agarwal R, Abraham JM, Meltzer SJ: Hypermethylation of the AKAP12 promoter is a biomarker of Barrett's-associated esophageal neoplastic progression. Cancer Epidemiol Biomarkers Prev; 2008 Jan;17(1):111-7
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  • [Title] Hypermethylation of the AKAP12 promoter is a biomarker of Barrett's-associated esophageal neoplastic progression.
  • We examined AKAP12 promoter hypermethylation using real-time methylation-specific PCR in 259 human esophageal tissues.
  • AKAP12 hypermethylation showed highly discriminative receiver-operator characteristic (ROC) curve profiles, clearly distinguishing esophageal adenocarcinoma (EAC) from esophageal squamous cell carcinoma and normal esophagus (P < 0.0001).
  • AKAP12-normalized methylation values were significantly higher in Barrett's metaplasia (BE), dysplastic Barrett's, and EAC than in normal esophagus (P < 0.0000001).
  • AKAP12 hypermethylation frequency was zero in normal esophagus but increased early during neoplastic progression, to 38.9% in BE from patients with Barrett's alone, 52.5% in dysplastic Barrett's metaplasia, and 52.2% in EAC.
  • AKAP12 hypermethylation levels were significantly higher in normal esophageal epithelia from patients with EAC (mean = 0.00082) than in normal esophagi from patients without Barrett's or esophageal cancer (mean = 0.00007; P = 0.006).
  • In contrast, only 2 (7.7%) of 26 esophageal squamous cell carcinomas exhibited AKAP12 hypermethylation.
  • We conclude that promoter hypermethylation of AKAP12 is a common, tissue-specific event in human EAC, occurs early during Barrett's-associated esophageal neoplastic progression, and is a potential biomarker for the early detection of EAC.

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  • (PMID = 18199717.001).
  • [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
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK067872; United States / NCI NIH HHS / CA / CA 001808; United States / NCI NIH HHS / CA / CA 106763; United States / NCI NIH HHS / CA / CA 85069
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / A Kinase Anchor Proteins; 0 / AKAP12 protein, human; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / RNA, Messenger
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78. Basseri B, Conklin JL, Mertens RB, Lo SK, Bellack GS, Shaye OA: Heterotopic gastric mucosa (inlet patch) in a patient with laryngopharyngeal reflux (LPR) and laryngeal carcinoma: a case report and review of literature. Dis Esophagus; 2009;22(4):E1-5
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  • The inlet patch is an area of heterotopic gastric mucosa most commonly located in the postcricoid portion of the esophagus at, or just below, the level of the upper esophageal sphincter.
  • Esophageal and supraesophageal symptoms are commonly associated with inlet patch, while esophageal adenocarcinoma rarely complicates it.
  • Laryngeal adenocarcinoma associated with inlet patch is not described in the literature.
  • Upper endoscopy at our institution revealed an upper esophageal stricture and a 1 cm inlet patch.
  • Biopsies showed columnar mucosa (predominantly gastric cardiac/fundic type) consistent with inlet patch, with focal intestinal metaplasia.
  • Dysphagia and regurgitation were improved by serial dilatations of the upper esophageal stricture.

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  • (PMID = 19473208.001).
  • [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] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 30
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79. Leeuwenburgh I, Haringsma J, Van Dekken H, Scholten P, Siersema PD, Kuipers EJ: Long-term risk of oesophagitis, Barrett's oesophagus and oesophageal cancer in achalasia patients. Scand J Gastroenterol Suppl; 2006;(243):7-10
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  • Stasis and fermentation can also lead to inflammation of the oesophageal mucosa, giving rise to hyperplasia of the epithelium, multifocal dysplasia and in some patients eventually squamous cell carcinoma.
  • Although it is generally accepted that achalasia is a pre-malignant disorder, the reported increased risk of patients with achalasia developing a squamous cell carcinoma varies from 0 to 140 times that of the normal population.
  • In addition, achalasia may predispose to Barrett's metaplasia and oesophageal adenocarcinoma, which have been described in case reports after myotomy.
  • [MeSH-major] Barrett Esophagus / etiology. Esophageal Achalasia / complications. Esophageal Neoplasms / etiology. Esophagitis / etiology
  • [MeSH-minor] Adenocarcinoma / etiology. Carcinoma, Squamous Cell / etiology. Endoscopy, Gastrointestinal. Humans. Risk Factors. Time Factors

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  • (PMID = 16782616.001).
  • [ISSN] 0085-5928
  • [Journal-full-title] Scandinavian journal of gastroenterology. Supplement
  • [ISO-abbreviation] Scand. J. Gastroenterol. Suppl.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Norway
  • [Number-of-references] 35
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80. Sato F, Meltzer SJ: CpG island hypermethylation in progression of esophageal and gastric cancer. Cancer; 2006 Feb 1;106(3):483-93
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  • [Title] CpG island hypermethylation in progression of esophageal and gastric cancer.
  • The upper gastrointestinal (GI) cancers have various carcinogenic pathways and precursor lesions, such as dysplasia for esophageal squamous cell carcinoma, Barrett esophagus for esophageal adenocarcinoma, and intestinal metaplasia for the intestinal-type of gastric cancer.
  • In this review, a variety of information is summarized regarding gene hypermethylation in esophageal and gastric cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Squamous Cell / pathology. CpG Islands / genetics. Esophageal Neoplasms / pathology. Stomach Neoplasms / pathology

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  • [Copyright] Copyright (c) 2005 American Cancer Society.
  • [ErratumIn] Cancer. 2006 Apr 1;106(7):1641
  • (PMID = 16362978.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 138
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81. Gyorffy H: [Study of claudins and prognostic factors in some gastrointestinal diseases]. Magy Onkol; 2009 Dec;53(4):377-83
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  • I. We explored the changes of CLDN expression in Barrett's esophagus and related adenocarcinoma.
  • CLDN2 and -3 expression in Barrett's esophagus was higher than in normal foveolar epithelium.
  • Adenocarcinoma showed higher CLDN2 and -3 expression compared with normal and Barrett's epithelia.
  • The similar CLDN expression profile of Barrett's esophagus and adenocarcinoma supports their sequential development.
  • II. Gastric intestinal metaplasia showed higher expression of CLDN2, -3 and -4 as compared with normal antral foveolar mucosa.
  • Colorectal adenoma and adenocarcinoma could not be differentiated according to their CLDN profile.
  • Intestinal metaplasias of Barrett's esophagus and stomach show similar CLDN profile to small bowel epithelium.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adolescent. Adult. Aged. Aged, 80 and over. Barrett Esophagus / metabolism. Carcinoma, Squamous Cell / metabolism. Child. Child, Preschool. Claudin-3. Female. Fluorescent Antibody Technique. Gastrointestinal Stromal Tumors / metabolism. Gene Expression Regulation, Neoplastic. Hemangiosarcoma / metabolism. Humans. Immunohistochemistry. Leiomyosarcoma / metabolism. Male. Membrane Proteins / metabolism. Middle Aged. Predictive Value of Tests. Prognosis. RNA, Messenger / metabolism. Risk Factors. Young Adult

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  • (PMID = 20071310.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLDN3 protein, human; 0 / Claudin-3; 0 / Claudins; 0 / Membrane Proteins; 0 / RNA, Messenger
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82. Roman S, Pétré A, Thépot A, Hautefeuille A, Scoazec JY, Mion F, Hainaut P: Downregulation of p63 upon exposure to bile salts and acid in normal and cancer esophageal cells in culture. Am J Physiol Gastrointest Liver Physiol; 2007 Jul;293(1):G45-53
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  • [Title] Downregulation of p63 upon exposure to bile salts and acid in normal and cancer esophageal cells in culture.
  • p63 is a member of the p53 protein family that regulates differentiation and morphogenesis in epithelial tissues and is required for the formation of squamous epithelia.
  • Barrett's mucosa is a glandular metaplasia of the squamous epithelium that develops in the lower esophagus in the context of chronic, gastroesophageal reflux and is considered as a precursor for adenocarcinoma.
  • Normal or squamous cancer esophageal cells were exposed to deoxycholic acid (DCA, 50, 100, or 200 microM) and chenodeoxycholic and taurochenodeoxycholic acid at pH 5. p63 and cyclooxygenase-2 (COX-2) expressions were studied by Western blot and RT-PCR.
  • These results show that combined exposure to bile salt and acid downregulates a critical regulator of squamous differentiation, providing a mechanism to explain the replacement of squamous epithelium by a glandular metaplasia upon exposure of the lower esophagus to gastric reflux.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. Deoxycholic Acid / pharmacology. Esophageal Neoplasms / metabolism. Esophagus / metabolism. Trans-Activators / biosynthesis. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Acetylcysteine / analogs & derivatives. Acetylcysteine / pharmacology. Apoptosis. Barrett Esophagus / physiopathology. Carcinoma, Squamous Cell / metabolism. Cell Line, Tumor. Cells, Cultured. Chenodeoxycholic Acid / pharmacology. Cyclooxygenase 2 / biosynthesis. Down-Regulation. Doxorubicin / pharmacology. Fluorescent Antibody Technique. Humans. Hydrogen-Ion Concentration. Leupeptins / pharmacology. Proteasome Inhibitors. Taurochenodeoxycholic Acid / pharmacology. Transcription Factors

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  • (PMID = 17615180.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Leupeptins; 0 / Proteasome Inhibitors; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 005990WHZZ / Deoxycholic Acid; 0GEI24LG0J / Chenodeoxycholic Acid; 133343-34-7 / lactacystin; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 516-35-8 / Taurochenodeoxycholic Acid; 80168379AG / Doxorubicin; EC 1.14.99.1 / Cyclooxygenase 2; WYQ7N0BPYC / Acetylcysteine
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83. Deviere J: Barrett's oesophagus: the new endoscopic modalities have a future. Gut; 2005 Mar;54 Suppl 1:i33-7
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  • Barrett's oesophagus is defined as the replacement of squamous oesophageal epithelium by intestinal metaplasia in the distal oesophagus.
  • GORD is essential for the development of Barrett's oesophagus.1 Intestinal metaplasia is a premalignant lesion that may further develop into dysplasia and lead to adenocarcinoma of the oesophagus.
  • Patients with Barrett's oesophagus have a 2-25% risk of developing mild to severe dysplasia and a 2-5% risk of having adenocarcinoma: 30-150 times higher than the risk in the general population.
  • Forty to fifty per cent of Barrett's oesophagus patients with severe dysplasia would present adenocarcinoma within 5 years.
  • [MeSH-major] Barrett Esophagus / surgery
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma / surgery. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagoscopy / methods. Esophagus / pathology. Esophagus / surgery. Humans. Metaplasia / surgery. Mucous Membrane / pathology. Mucous Membrane / surgery. Photochemotherapy / methods. Postoperative Complications / etiology. Precancerous Conditions / drug therapy. Precancerous Conditions / pathology. Precancerous Conditions / surgery

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  • (PMID = 15711006.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 50
  • [Other-IDs] NLM/ PMC1867791
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84. di Pietro M, Fitzgerald RC: Barrett's oesophagus: an ideal model to study cancer genetics. Hum Genet; 2009 Aug;126(2):233-46
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  • Chronic gastro-oesophageal reflux disease can induce a metaplastic change of the distal oesophagus called Barrett's oesophagus whereby the normal squamous epithelium is substituted by a columnar epithelium.
  • Patients with Barrett's oesophagus are at increased risk of oesophageal adenocarcinoma which occurs through dysplastic stages with increasing degree of cellular and architectural disorganization.
  • Here, we review the knowledge acquired so far on the genetic and molecular alterations along the oesophageal metaplasia-dysplasia-carcinoma sequence.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics
  • [MeSH-minor] Carcinoma / diagnosis. Carcinoma / genetics. Cell Transformation, Neoplastic. Endoscopy / methods. Female. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Humans. Male. Medical Oncology / methods. Metaplasia. Models, Biological. Prognosis

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  • (PMID = 19365640.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 220
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85. Chlumská A, Boudová L, Benes Z, Zámecník M: Histopathologic changes in gastroesophageal reflux disease. A study of 126 bioptic and autoptic cases. Cesk Patol; 2007 Oct;43(4):142-7
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  • The histologic diagnosis of reflux esophagitis is still complicated by the lack of a consensus opinion on what is the normal mucosa in the area of the gastroesophageal junction (GEJ).
  • Most authors consider GEJ as the junction between the squamous and the cardiac epithelium.
  • These glands are in fact indistinguishable from metaplastic mucosa that arises in the distal esophagus in consequence of gastroesophageal reflux (GER).
  • In our series of 120 endoscopic biopsies of the GEJ and distal esophagus the cardia type mucosa (CM) was always present.
  • In 17 cases, CM displayed intestinal metaplasia (IM) predominantly of incomplete type and no dysplasia.
  • In one specimen of esophagus resected for adenocarcinoma, CM with incomplete IM was found in the vicinity of the tumor.
  • Squamous metaplastic epithelium was often seen near the orifices of submucosal esophageal glands in these areas, indicating the metaplastic nature of the glandular mucosa in the distal esophagus.
  • [MeSH-minor] Adult. Cardia / pathology. Esophagogastric Junction / pathology. Esophagus / pathology. Female. Humans. Male. Middle Aged

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  • (PMID = 18188921.001).
  • [ISSN] 1210-7875
  • [Journal-full-title] Československá patologie
  • [ISO-abbreviation] Cesk Patol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
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86. Räsänen JV, Sihvo EI, Ahotupa MO, Färkkilä MA, Salo JA: The expression of 8-hydroxydeoxyguanosine in oesophageal tissues and tumours. Eur J Surg Oncol; 2007 Dec;33(10):1164-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the present study we investigated whether DNA damage linked to oxidative stress (as 8-OHdG) is present in Barrett's mucosa with or without associated adenocarcinoma or high-grade dysplasia and in normal controls' squamous mucosa.
  • EXPERIMENTAL DESIGN: We measured 8-OHdG in 51 patients (13 Barrett's metaplasia, six Barrett's oesophagus with high-grade dysplasia, 18 adenocarcinoma of the distal oesophagus/oesophagogastric junction and 14 normal controls).
  • RESULTS: Analysis revealed that 8-OHdG was present in both Barrett's metaplasia with and without dysplasia as well as in adenocarcinoma of the oesophagus/oesophagogastric junction.
  • Although the study group was small the amount of 8-OHdG was significantly increased in the distal oesophagus both in Barrett's epithelium 1.26 (0.08-29.47) and in high-grade dysplasia 1.35 (1.04-1.65) as well as in adenocarcinoma of oesophagus/oesophagogastric junction 1.08 (0.59-1.94) compared to controls 0.06 (0-4.08) (p=0.002, p=0.012, p=0.001, respectively).
  • CONCLUSIONS: Our results show the presence of oxidative DNA damage in the distal oesophagus of patients with Barrett's oesophagus and adenocarcinoma of the oesophagus/oesophagogastric junction.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. DNA Damage / physiology. Deoxyguanosine / analogs & derivatives. Esophageal Neoplasms / metabolism. Esophagus / metabolism

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  • (PMID = 17467227.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
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87. Menke V, van Es JH, de Lau W, van den Born M, Kuipers EJ, Siersema PD, de Bruin RW, Kusters JG, Clevers H: Conversion of metaplastic Barrett's epithelium into post-mitotic goblet cells by gamma-secretase inhibition. Dis Model Mech; 2010 Jan-Feb;3(1-2):104-10

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Barrett's esophagus (BE) affects approximately 2% of the Western population and progresses to esophageal adenocarcinoma (EAC) in 0.5% of these patients each year.
  • Immunohistochemistry confirmed the presence of an intact and activated Notch signaling pathway in metaplastic BE epithelium, but not in the normal human esophagus.
  • As we have shown previously in normal intestinal epithelium, Notch inhibition converted the proliferative Barrett's epithelial cells into terminally differentiated goblet cells, whereas the squamous epithelium remained intact.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Barrett Esophagus / enzymology. Barrett Esophagus / pathology. Epithelium / pathology. Goblet Cells / pathology. Mitosis
  • [MeSH-minor] Animals. Biopsy. Cell Line, Tumor. Cell Proliferation / drug effects. Colon / drug effects. Colon / metabolism. Colon / pathology. Dibenzazepines / pharmacology. Disease Models, Animal. Gene Expression Regulation / drug effects. Humans. Metaplasia. Rats. Receptors, Notch / antagonists & inhibitors. Receptors, Notch / genetics. Receptors, Notch / metabolism. Signal Transduction / drug effects

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  • (PMID = 20075383.001).
  • [ISSN] 1754-8411
  • [Journal-full-title] Disease models & mechanisms
  • [ISO-abbreviation] Dis Model Mech
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dibenzazepines; 0 / Receptors, Notch; 0 / dibenzazepine; EC 3.4.- / Amyloid Precursor Protein Secretases
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88. Beck P, Mayne GC, Astill D, Irvine T, Watson DI, Dijckmeester WA, Wijnhoven BP, Hussey DJ: Accuracy of identification of tissue types in endoscopic esophageal mucosal biopsies used for molecular biology studies. Clin Exp Gastroenterol; 2009;2:1-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Accuracy of identification of tissue types in endoscopic esophageal mucosal biopsies used for molecular biology studies.
  • OBJECTIVES: To determine if histopathologic assessment of esophageal biopsies harvested for research study is justified due to the heterogeneity of tissues in the esophagus, and the consequent histopathologic mis-matches with the clinical histopathology of biopsies taken at the same level.
  • METHODS: Since 2004, patients undergoing upper endoscopy for a variety of clinical conditions were invited to provide additional esophageal biopsies; those were collected for research purpose at the same level as biopsies collected for clinical histopathology.
  • Clinical histopathology summaries classified 123 levels (32.6%) as squamous epithelium, 84 levels (22.3%) as metaplastic columnar-lined epithelium, 135 levels (35.8%) as columnar-lined epithelium with intestinal metaplasia, 30 levels (8%) as dysplasia, and 5 levels (1.3%) as adenocarcinoma.
  • Research histopathology matched to clinical summaries on 120 of 123 (97.5%) levels for squamous epithelium, 52 of 84 (61.9%) for metaplastic columnar-lined epithelium, and 94 of 135 (69.5%) for columnar-lined epithelium with intestinal metaplasia.
  • On 59 (70.2%) metaplastic columnar-lined epithelium levels and on 62 (46%) columnar-lined epithelium with intestinal metaplasia levels, tissue heterogeneity was observed in clinical histopathology, with portions of squamous epithelium within the samples.
  • Matches with pure tissue samples in both clinical and research histopathology levels were observed on 22 (26.2%) levels of metaplastic columnar-lined epithelium and in 55 (40.7%) levels of columnar-lined epithelium with intestinal metaplasia.
  • CONCLUSIONS: The high proportion of mismatches and tissue heterogeneity observed, especially among columnar-lined epithelium with intestinal metaplasia and dysplasia, points to the necessity of determining the histopathology of the research samples to avoid sampling errors during molecular studies.

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  • (PMID = 21694820.001).
  • [ISSN] 1178-7023
  • [Journal-full-title] Clinical and experimental gastroenterology
  • [ISO-abbreviation] Clin Exp Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3108633
  • [Keywords] NOTNLM ; Barrett’s esophagus / columnar-lined epithelium / endoscopy / esophageal biopsies
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89. Zhou G, Sun YG, Wang HB, Wang WQ, Wang XW, Fang DC: Acid and bile salt up-regulate BMP4 expression in human esophageal epithelium cells. Scand J Gastroenterol; 2009;44(8):926-32

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acid and bile salt up-regulate BMP4 expression in human esophageal epithelium cells.
  • OBJECTIVE: Barrett's esophagus (BE) with an intestinal-type epithelium is thought to be a precancerous lesion of adenocarcinoma of the esophagus.
  • The pathophysiology of Barrett's metaplasia is poorly understood.
  • Bone morphogenetic protein 4 (BMP4), a factor determining the fate of cells, is up-regulated in BE and esophagitis mucosa when compared with normal squamous or non-goblet cell-containing cardiac epithelium.
  • The aim of this study was to demonstrate that BMP4 is a molecular mediator that links etiological agents of BE to the phenotypic changes in human esophagus epithelium cells (HEECs).
  • [MeSH-major] Barrett Esophagus / metabolism. Bile Acids and Salts / metabolism. Bone Morphogenetic Protein 4 / biosynthesis. Esophagus / metabolism

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  • (PMID = 19488929.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bile Acids and Salts; 0 / Bone Morphogenetic Protein 4
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90. Ponsot P: [Barrett's oesophagus: endoscopic diagnosis and follow-up]. Ann Chir; 2006 Jan;131(1):3-6
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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: endoscopic diagnosis and follow-up].
  • Barrett's oesophagus (BO), or replacement of the squamous mucosa by a specialized intestinal metaplasia due to gastro-oesophageal reflux disease (GORD), predisposes to adenocarcinoma.
  • Macroscopic diagnosis of BO is sometimes difficult and, in case of doubt, endoscopy should be redone after a period of efficient anti-secretory treatment.
  • Diagnosis of BO is histological and should be confirmed by biopsies.
  • The incidence of adenocarcinoma is globally estimated at 0.5% patient by year of follow-up, and exists for both short and long BO.
  • Due to this low incidence, screening for BO is only justified in patients at high risk for adenocarcinoma (male gender, age > 50 ans, old GORD in a young patient).
  • Low-grade dysplasia (LGD) then high-grade dysplasia (HGD) precedes adenocarcinoma.
  • Histological diagnosis of LGD is difficult: the main cause of confusion is inflammation so diagnosis of LGD must be confirmed after a 3-month high-dose anti-secretory treatment.
  • Diagnosis of HGD is easier but multiple biopsies are needed to determine the focal or multifocal disposition of HGD.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal. Esophageal Neoplasms / etiology
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Gastroesophageal Reflux / complications. Humans. Prognosis. Risk Factors

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  • (PMID = 16376849.001).
  • [ISSN] 0003-3944
  • [Journal-full-title] Annales de chirurgie
  • [ISO-abbreviation] Ann Chir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 16
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91. Grimm M, Lazariotou M, Kircher S, Stuermer L, Reiber C, Höfelmayr A, Gattenlöhner S, Otto C, Germer CT, von Rahden BH: MMP-1 is a (pre-)invasive factor in Barrett-associated esophageal adenocarcinomas and is associated with positive lymph node status. J Transl Med; 2010;8:99
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  • [Title] MMP-1 is a (pre-)invasive factor in Barrett-associated esophageal adenocarcinomas and is associated with positive lymph node status.
  • BACKGROUND: Esophageal adenocarcinomas (EACs) arise due to gastroesophageal reflux, with Barrett's esophagus (BE) regarded as precancerous lesion.
  • METHODS: Expression of MMP-1 and -13 was analyzed in esophageal cancer (n = 41 EAC with BE, n = 19 EAC without BE, and n = 10 esophageal squamous-cell carcinomas, ESCC), furthermore in BE without intraepithelial neoplasia (IN) (n = 18), and the cell line OE-33.
  • MMP-1 was co-labelled with Ki-67 (proliferation), Cdx-2 (marker for intestinal metaplasia, BE) and analyzed on mRNA level.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / pathology. Esophageal Neoplasms / enzymology. Lymphatic Metastasis. Matrix Metalloproteinase 1 / metabolism

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  • (PMID = 20946664.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.24.7 / Matrix Metalloproteinase 1
  • [Other-IDs] NLM/ PMC2967517
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92. Liu T, Zhang X, So CK, Wang S, Wang P, Yan L, Myers R, Chen Z, Patterson AP, Yang CS, Chen X: Regulation of Cdx2 expression by promoter methylation, and effects of Cdx2 transfection on morphology and gene expression of human esophageal epithelial cells. Carcinogenesis; 2007 Feb;28(2):488-96
The Lens. Cited by Patents in .

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  • [Title] Regulation of Cdx2 expression by promoter methylation, and effects of Cdx2 transfection on morphology and gene expression of human esophageal epithelial cells.
  • Caudal-related homeobox 2 (Cdx2) has been suggested as an early marker of Barrett's esophagus (BE), which is the premalignant lesion of esophageal adenocarcinoma (EAC).
  • However, the mechanism of ectopic Cdx2 expression in the esophageal epithelial cells and its role in the development of BE remained unclear.
  • RT-PCR, pyrosequencing and methylation-specific PCR were used to determine expression and promoter methylation of Cdx2 in human esophageal epithelial cells (HET1A and SEG1) after treatment with 5-aza-2'-deoxycytidine (DAC), acid, bile acids and their combination.
  • We found Cdx2 was expressed in most human EAC cell lines, but not in squamous epithelial cell lines.
  • Our data suggest that exposure to acid and/or bile acids may activate Cdx2 expression in human esophageal epithelial cells through promoter demethylation, and ectopic Cdx2 expression in esophageal squamous epithelial cells may contribute to intestinal metaplasia of the esophagus.
  • [MeSH-major] DNA Methylation. Esophagus / metabolism. Gene Expression Regulation. Homeodomain Proteins / genetics. Promoter Regions, Genetic

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  • (PMID = 16990345.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / 5T32ES07148; United States / NCI NIH HHS / CA / CA092077; United States / NCI NIH HHS / CA / CA75683; United States / NIDDK NIH HHS / DK / DK63650
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / CDX2 protein, human; 0 / DNA Primers; 0 / Homeodomain Proteins; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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93. Agnese V, Cabibi D, Calcara D, Terrasi M, Pantuso G, Fiorentino E, Intrivici C, Colucci G, Aragona F, Gebbia N, Bazan V, Russo A: Aurora-A overexpression as an early marker of reflux-related columnar mucosa and Barrett's oesophagus. Ann Oncol; 2007 Jun;18 Suppl 6:vi110-5
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  • BACKGROUND: The development of oesophageal adenocarcinoma is generally closely associated with the presence of a specialised intestinal-type epithelium such as that found in Barrett's oesophagus (BO).
  • A particular histological condition is when the distal oesophagus showing cardiac and/or fundic mucosa without intestinal metaplasia cannot be defined as 'Barrett's mucosa' [condition that we call 'columnar-lined oesophagus' (CLO)] and up till now, there has been no agreement in literature about the management of this condition.
  • As controls, two more biopsies were obtained, one on the normal-appearing squamous oesophagus above the GOJ, as far as possible from the columnar mucosa (controls A), and one taken 1 cm below the GOJ (controls B).

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  • (PMID = 17591802.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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94. Ingravallo G, Dall'Olmo L, Segat D, Fassan M, Mescoli C, Dazzo E, Castoro C, Polimeno L, Rizzetto C, Baroni MD, Zaninotto G, Ancona E, Rugge M: CDX2 hox gene product in a rat model of esophageal cancer. J Exp Clin Cancer Res; 2009;28:108
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  • [Title] CDX2 hox gene product in a rat model of esophageal cancer.
  • BACKGROUND: Barrett's mucosa is the precursor of esophageal adenocarcinoma.
  • Experimental models of longstanding esophageal reflux of duodenal-gastric contents may provide important information on the biological sequence of the Barrett's oncogenesis.
  • RESULTS: No Cdx2 expression was detected in either squamous epithelia of the proximal esophagus or squamous cell carcinomas.
  • De novo Cdx2 expression was consistently documented in the proliferative zone of the squamous epithelium close to reflux ulcers (Group A: 68%; Group B: 64%; Group C: 80%), multilayered epithelium and intestinal metaplasia (Group A: 9%; Group B: 41%; Group C: 60%), and esophageal adenocarcinomas (Group B: 36%; Group C: 35%).
  • CONCLUSION: De novo expression of Cdx2 is an early event in the spectrum of the lesions induced by experimental gastro-esophageal reflux and should be considered as a key step in the morphogenesis of esophageal adenocarcinoma.
  • [MeSH-major] Esophageal Neoplasms / genetics. Homeodomain Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. Barrett Esophagus / pathology. Disease Models, Animal. Esophagus / pathology. Gastroesophageal Reflux / pathology. Male. Rats. Rats, Wistar

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  • (PMID = 19664209.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cdx2 protein, rat; 0 / Homeodomain Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC3225830
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95. Chandrasoma P, Makarewicz K, Wickramasinghe K, Ma Y, Demeester T: A proposal for a new validated histological definition of the gastroesophageal junction. Hum Pathol; 2006 Jan;37(1):40-7
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  • Present definitions of the gastroesophageal junction (GEJ) are the point of flaring of the tubular esophagus and the proximal limit of the gastric rugal folds.
  • This study aims to validate the location of the true GEJ using the criterion of esophageal submucosal glands.
  • Ten esophagogastrectomy specimens, in which there was a well-defined point of flaring of the tubular esophagus that coincided with the proximal limit of gastric rugal folds, were examined by complete histological mapping to evaluate the distribution of esophageal submucosal glands and surface epithelial types.
  • Oxyntocardiac and cardiac mucosa with or without intestinal metaplasia were present under rugal folds distal to the end of tubular esophagus in all patients to a length of 0.31 to 2.05 cm.
  • Submucosal glands were present in the tubular esophagus and in the proximal pouch distal to the tubular esophagus in a distribution that closely coincided with squamous epithelium, oxyntocardiac, cardiac, and intestinal epithelia.
  • We conclude that a variable part of the saccular region distal to the tubular esophagus contains esophageal submucosal glands, therefore representing reflux-damaged distal esophagus.
  • This results in an error, where up to 2.05 cm of distal reflux-damaged dilated esophagus can be mistaken as proximal stomach when presently accepted definitions for the GEJ are used.
  • [MeSH-minor] Adenocarcinoma / pathology. Aged. Epithelial Cells / pathology. Esophageal Neoplasms / pathology. Esophagectomy. Female. Gastric Mucosa / pathology. Humans. Male. Middle Aged. Mucous Membrane / pathology

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  • (PMID = 16360414.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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96. Fassan M, Pizzi M, Battaglia G, Giacomelli L, Parente P, Bocus P, Ancona E, Rugge M: Programmed cell death 4 (PDCD4) expression during multistep Barrett's carcinogenesis. J Clin Pathol; 2010 Aug;63(8):692-6
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  • METHODS: PDCD4 immunohistochemical expression was assessed in 88 biopsy samples obtained from histologically proven long-segment Barrett's mucosa (BM; 25 non-intestinal columnar metaplasia, 25 intestinal metaplasia (IM), 16 low-grade intraepithelial neoplasia (LG-IEN), 12 high-grade IEN (HG-IEN) and 10 Barrett's adenocarcinoma (BAc)).
  • Normal basal squamous epithelial layers featured strong PDCD4 nuclear immunoreaction (mostly coexisting with weak-moderate cytoplasmic staining).
  • Non-intestinal columnar metaplasia and intestinal metaplasia preserved a strong nuclear immunostaining; conversely, a significant decrease in PDCD4 nuclear expression was seen in dysplastic (LG-IEN and HG-IEN) and neoplastic lesions.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Precancerous Conditions / metabolism. RNA-Binding Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biopsy. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Disease Progression. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. MicroRNAs / genetics. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Oligonucleotide Array Sequence Analysis / methods. RNA, Neoplasm / genetics. Retrospective Studies

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  • (PMID = 20702469.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / MIRN21 microRNA, human; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / PDCD4 protein, human; 0 / RNA, Neoplasm; 0 / RNA-Binding Proteins
  • [Other-IDs] NLM/ PMC2976066
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97. Pavlov K, Maley CC: New models of neoplastic progression in Barrett's oesophagus. Biochem Soc Trans; 2010 Apr;38(2):331-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Research in Barrett's oesophagus, and neoplastic progression to OAC (oesophageal adenocarcinoma), is hobbled by the lack of good pre-clinical models that capture the evolutionary dynamics of Barrett's cell populations.
  • Tissue culture models include squamous cell lines, Barrett's oesophagus cell lines and OAC cell lines, although it was recognized recently that BIC-1, SEG-1 and TE-7 are not true OAC cell lines.
  • The most realistic, but least tractable, model is a canine surgical model that generates reflux and leads to an intestinal metaplasia.

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  • (PMID = 20298178.001).
  • [ISSN] 1470-8752
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA010815; United States / NCI NIH HHS / CA / R03 CA137811-01; United States / NCI NIH HHS / CA / CA091955-089005; United States / NCI NIH HHS / CA / P01 CA091955; United States / NCI NIH HHS / CA / P01 CA091955-089005; United States / NCI NIH HHS / CA / CA140657-01; United States / NCI NIH HHS / CA / R01 CA140657-01; United States / NCI NIH HHS / CA / CA137811-01; United States / NCI NIH HHS / CA / R03 CA137811; United States / NCI NIH HHS / CA / R03 CA137811-02; United States / NCI NIH HHS / CA / P01 CA91955; United States / NCI NIH HHS / CA / R01 CA140657; United States / NCI NIH HHS / CA / R01 CA119224
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 53
  • [Other-IDs] NLM/ NIHMS199218; NLM/ PMC2866622
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98. di Pietro M, Peters CJ, Fitzgerald RC: Clinical puzzle: Barrett's oesophagus. Dis Model Mech; 2008 Jul-Aug;1(1):26-31
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