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1. Brankley SM, Wang KK, Harwood AR, Miller DV, Legator MS, Lutzke LS, Kipp BR, Morrison LE, Halling KC: The development of a fluorescence in situ hybridization assay for the detection of dysplasia and adenocarcinoma in Barrett's esophagus. J Mol Diagn; 2006 May;8(2):260-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The development of a fluorescence in situ hybridization assay for the detection of dysplasia and adenocarcinoma in Barrett's esophagus.
  • The goal of this study was to identify a set of fluorescence in situ hybridization probes for the detection of dysplasia and adenocarcinoma in patients with Barrett's esophagus.
  • We examined 170 brushing specimens from 138 patients with Barrett's esophagus or a history of Barrett's esophagus using fluorescence in situ hybridization with probes to 5p15, 5q21-22, centromere 7, 7p12, 8q24.12-13, centromere 9, 9p21, centromere 17, 17p13.1, 17q11.2-12, 20q13.2, and centromere Y.
  • Receiver-operator curves were used to determine the sensitivity and specificity of various four-probe combinations for detecting low-grade dysplasia, high-grade dysplasia, and esophageal adenocarcinoma.
  • Of these, a set consisting of probes to 8q24, 9p21, 17q11.2, and 20q13.2 was found to have a sensitivity and specificity, respectively, of 70% and 89% for low-grade dysplasia, 84% and 93% for high-grade dysplasia, and 94% and 93% for esophageal adenocarcinoma.
  • This probe set was chosen for future prospective clinical evaluations based on its high sensitivity and specificity, its ability to distinguish adenocarcinoma and high-grade or low-grade dysplasia from lesser diagnostic categories, and the favorable signal quality for each of the probes.

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  • (PMID = 16645214.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097048; United States / NCI NIH HHS / CA / R0 1 CA97048-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1867582
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2. Tomizawa Y, Wang KK: Changes in screening, prognosis and therapy for esophageal adenocarcinoma in Barrett's esophagus. Curr Opin Gastroenterol; 2009 Jul;25(4):358-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changes in screening, prognosis and therapy for esophageal adenocarcinoma in Barrett's esophagus.
  • PURPOSE OF REVIEW: Significant changes in concepts of managing Barrett's esophagus have led to change in the recommendations concerning screening, surveillance, biomarkers, and therapies in this condition over the past several years.
  • RECENT FINDINGS: Narrow band imaging and esophageal capsule endoscopy are alternative methods to screen for Barrett's esophagus.
  • Esophageal capsule endoscopy is a new potential tool that allows a direct noninvasive visualization of esophagus.
  • Research efforts are currently directed towards risk stratification of patients and biomarkers have been developed to predict development of esophageal adenocarcinoma.
  • Recent studies have reported that frequent loss of heterozygosity (LOH) as well as allelic imbalances in chromosomes in esophageal adenocarcinoma.
  • Fluorescent in-situ hybridization technique, which uses fluorescently labeled DNA probes to detect chromosomal alterations in cells, obtained from cytology specimens has been developed.
  • Currently, many studies support the concept of endoscopic elimination of dysplastic lesions in the esophagus by a mucosal ablation therapy.
  • SUMMARY: Recent advances in screening; prognostication and therapy for esophageal adenocarcinoma in Barrett's esophagus have brought a significant new insight in clinical practices and will eventually ensure better patients outcomes.

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  • (PMID = 19461512.001).
  • [ISSN] 1531-7056
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21CA122426; United States / NCI NIH HHS / CA / R01CA097048; United States / NCI NIH HHS / CA / R01 CA097048-06A2; United States / NCI NIH HHS / CA / R01 CA111603; United States / NCI NIH HHS / CA / CA097048-06A2; United States / NCI NIH HHS / CA / R21 CA122426-02; United States / NCI NIH HHS / CA / CA122426-02; United States / NCI NIH HHS / CA / CA111603-05; United States / NCI NIH HHS / CA / R01 CA111603-05; United States / NCI NIH HHS / CA / R01 CA097048; United States / NCI NIH HHS / CA / R21 CA122426; United States / NCI NIH HHS / CA / R01CA111603
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Number-of-references] 54
  • [Other-IDs] NLM/ NIHMS181013; NLM/ PMC3762463
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3. Hao Y, Triadafilopoulos G, Sahbaie P, Young HS, Omary MB, Lowe AW: Gene expression profiling reveals stromal genes expressed in common between Barrett's esophagus and adenocarcinoma. Gastroenterology; 2006 Sep;131(3):925-33
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  • [Title] Gene expression profiling reveals stromal genes expressed in common between Barrett's esophagus and adenocarcinoma.
  • BACKGROUND & AIMS: Barrett's esophagus is a precursor of esophageal adenocarcinoma.
  • DNA microarrays that enable a genome-wide assessment of gene expression enhance the identification of specific genes as well as gene expression patterns that are expressed by Barrett's esophagus and adenocarcinoma compared with normal tissues.
  • Barrett's esophagus length has also been identified as a risk factor for progression to adenocarcinoma, but whether there are intrinsic biological differences between short-segment and long-segment Barrett's esophagus can be explored with microarrays.
  • METHODS: Gene expression profiles for endoscopically obtained biopsy specimens of Barrett's esophagus or esophageal adenocarcinoma and associated normal esophagus and duodenum were identified for 17 patients using DNA microarrays.
  • Barrett's esophagus and esophageal adenocarcinoma express a unique set of stromal genes that is distinct from normal tissues but similar to other cancers.
  • Adenocarcinoma also showed lower and higher expression for many genes compared with Barrett's esophagus.
  • No difference in gene expression was found between short-segment and long-segment Barrett's esophagus.
  • Stromal gene expression in Barrett's esophagus and adenocarcinoma is similar, indicating that these changes precede malignant transformation.

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  • (PMID = 16952561.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK056339; United States / NIDDK NIH HHS / DK / R01 DK063624; United States / NIDDK NIH HHS / DK / P30 DK56339; United States / NIDDK NIH HHS / DK / R01 DK 063624
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Chondroitin Sulfate Proteoglycans; 0 / Cspg2 protein, mouse; 0 / DNA, Neoplasm; 0 / Lectins, C-Type; 0 / POSTN protein, human; 0 / VCAN protein, human; 126968-45-4 / Versicans; 9007-34-5 / Collagen
  • [Other-IDs] NLM/ NIHMS12359; NLM/ PMC2575112
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4. Wong RK, Altekruse SF: Where are you and how do we find you? The dilemma of identifying Barrett's epithelium before adenocarcinoma of the esophagus. Am J Gastroenterol; 2009 Jun;104(6):1363-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Where are you and how do we find you? The dilemma of identifying Barrett's epithelium before adenocarcinoma of the esophagus.
  • The incidence of esophageal adenocarcinoma in white males has been increasing steadily over the past decade.
  • However, attempts to identify the precursor lesion, intestinal metaplasia of the esophagus, or early in-situ cancers have been dismal, with no increase in the diagnosis of early cancers over 9 years of follow-up, as noted in the study by Cooper et al.
  • Important predictors of survival,such as a previous diagnosis of gastroesophageal reflux disease, endoscopy, and the diagnosis of intestinal metaplasia, continue to represent a minority of patients who present with esophageal adenocarcinoma.
  • Over time, factors that encourage localized, distal esophageal reflux may be the insidious culprit that leads to intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Intestinal Mucosa / pathology. Precancerous Conditions / pathology. SEER Program

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  • [CommentOn] Am J Gastroenterol. 2009 Jun;104(6):1356-62 [19491849.001]
  • (PMID = 19436281.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
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5. Rygiel AM, Milano F, Ten Kate FJ, Schaap A, Wang KK, Peppelenbosch MP, Bergman JJ, Krishnadath KK: Gains and amplifications of c-myc, EGFR, and 20.q13 loci in the no dysplasia-dysplasia-adenocarcinoma sequence of Barrett's esophagus. Cancer Epidemiol Biomarkers Prev; 2008 Jun;17(6):1380-5
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  • [Title] Gains and amplifications of c-myc, EGFR, and 20.q13 loci in the no dysplasia-dysplasia-adenocarcinoma sequence of Barrett's esophagus.
  • The progression of Barrett's esophagus to esophageal adenocarcinoma is often characterized by the accumulation of genetic abnormalities.
  • The goal was to evaluate the copy number alterations of several oncogene loci, including 7p12 [epidermal growth factor receptor (EGFR)], 8q24 (c-myc), and 20q13 in the sequence of no dysplasia-dysplasia-adenocarcinoma of Barrett's esophagus.
  • Fluorescence in situ hybridization with DNA probes for the centromeric region of chromosome 7 and the locus-specific regions of 7p12 (EGFR), 8q24 (c-myc), and 20q13 was applied on 99 brush cytology specimens of patients with Barrett's esophagus with different stages of dysplasia or esophageal adenocarcinoma.
  • Gains (3-4 copies) of chromosome 17, 8q24 (c-myc), and 20q.13 loci were found in the low frequencies in nondysplastic Barrett's esophagus.
  • Their frequencies increased with the stage of dysplasia and reached a high incidence in esophageal adenocarcinoma.
  • Amplification (>4 copies) of at least 1 of the loci was observed in 14% of high-grade dysplasia and increased to 50% in esophageal adenocarcinoma (P = 0.015).
  • The most frequently amplified locus was c-myc (18%), followed by 20q13 (13%) and EGFR (11%) in the high-grade dysplasia/esophageal adenocarcinoma cases.
  • High amplification levels (>10 copies) of the loci were more frequent in esophageal adenocarcinoma (72%) compared with high-grade dysplasia (20%; P = 0.049).
  • Amplifications of the c-myc, EGFR, and 20q12 loci may serve as diagnostic markers to identify patients with Barrett's esophagus with high-grade dysplasia or esophageal adenocarcinoma.
  • Gains of the loci might be of value as prognostic markers because they are already present in nondysplasia cases and may precede the later event of the amplification as observed in high-grade dysplasia and esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Chromosomes, Human, Pair 20 / genetics. Esophageal Neoplasms / genetics. Genes, erbB-1 / genetics. Precancerous Conditions / genetics. Proto-Oncogene Proteins c-myc / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Chromosomes, Human, Pair 17 / genetics. Female. Gene Amplification. Humans. In Situ Hybridization, Fluorescence. Male. Metaplasia / pathology. Middle Aged. Prospective Studies

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  • (PMID = 18559552.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc
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6. Ooi A, Zen Y, Ninomiya I, Tajiri R, Suzuki S, Kobayashi H, Imoto I, Dobashi Y: Gene amplification of ERBB2 and EGFR in adenocarcinoma in situ and intramucosal adenocarcinoma of Barrett's esophagus. Pathol Int; 2010 Jun;60(6):466-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene amplification of ERBB2 and EGFR in adenocarcinoma in situ and intramucosal adenocarcinoma of Barrett's esophagus.
  • We examined 11 cases of carcinoma arising from Barrett's esophagus consisting of two adenocarcinomas in situ (ACIS), two intramucosal adenocarcinomas, and seven overt invasive adenocarcinomas.
  • Overexpression of p53 (implying a mutation of the p53 gene), ERBB2, and EGFR was measured by immunohistochemistry, and gene amplification of ERBB2 and EGFR was measured by fluorescence in situ hybridization (FISH).
  • In all cases of ACIS and the intramucosal adenocarcinomas, almost all cancer cells overexpressed p53, however the populations overexpressing ERBB2 and EGFR varied in different cases: in one ACIS, ERBB2 was coexpressed in all the cancer cells, in the other ACIS and one intramucosal adenocarcinoma, ERBB2 was overexpressed in about 50% and only 10% of the p53-positive cells respectively.
  • EGFR was co-expressed in 20% in the other intramucosal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Carcinoma in Situ / genetics. Gene Amplification. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics
  • [MeSH-minor] Esophagus / metabolism. Esophagus / pathology. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Mucous Membrane / metabolism. Mucous Membrane / pathology. Neoplasm Invasiveness / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 20518902.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
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7. Fritcher EG, Brankley SM, Kipp BR, Voss JS, Campion MB, Morrison LE, Legator MS, Lutzke LS, Wang KK, Sebo TJ, Halling KC: A comparison of conventional cytology, DNA ploidy analysis, and fluorescence in situ hybridization for the detection of dysplasia and adenocarcinoma in patients with Barrett's esophagus. Hum Pathol; 2008 Aug;39(8):1128-35
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  • [Title] A comparison of conventional cytology, DNA ploidy analysis, and fluorescence in situ hybridization for the detection of dysplasia and adenocarcinoma in patients with Barrett's esophagus.
  • New detection methods with prognostic power are needed for early identification of dysplasia and esophageal adenocarcinoma (EA) in patients with Barrett's esophagus (BE).
  • This study assessed the relative sensitivity and specificity of conventional cytology, DNA ploidy analysis with digital image analysis (DIA), and fluorescence in situ hybridization (FISH) for the detection of dysplasia and adenocarcinoma in endoscopic brushing specimens from 92 patients undergoing endoscopic surveillance for BE.

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  • (PMID = 18602665.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA09704; United States / NCI NIH HHS / CA / R01 CA097048-01; United States / NCI NIH HHS / CA / CA85992-01; United States / NCI NIH HHS / CA / R01 CA111603; United States / NCI NIH HHS / CA / R01 CA111603-01A1; United States / NCI NIH HHS / CA / R01 CA097048; United States / NCI NIH HHS / CA / R01 CA085992
  • [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 / DNA, Neoplasm
  • [Other-IDs] NLM/ NIHMS84339; NLM/ PMC2614867
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8. Messmann H: [Barrett's esophagus carcinoma]. Praxis (Bern 1994); 2006 Jun 21;95(25-26):1029-35
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  • [Title] [Barrett's esophagus carcinoma].
  • The incidence of Barrett's esophagus, long segment as well as short segment, has increased over the last few years.
  • However there is a simultaneous increase of Barrett's adenocarcinoma in the Western world, while the number of squamous epithelium cancer decreases.
  • Besides improved endoscopic diagnosis other exogenous factors such as nutrition, reflux or adipositas play an important role.
  • Due to available data it is clear that the risk of Barrett's esophagus has been overestimated, mainly because of a publication bias.
  • The risk of a Barrett's esophagus carcinoma has been published with 0.5%/year.
  • The diagnosis of Barrett's esophagus is made endoscopically and histologically, this means 4 quadrant biopsies every 1-2 cm are gold standard.
  • Staining with methylene blue or acetic acid in combination with zoom endoscopy may improve the diagnosis.
  • In patients with proven Barrett's esophagus regular surveillance endoscopies depending on the presence of intraepithelial neoplasia are recommended.
  • While patients with Barrett's esophagus and no or with low grade intraepithelial neoplasia need only surveillance, those with high grade intraepithelial neoplasia should be treated.
  • Non visible lesions can be treated promisingly by PDT.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Biopsy. Carcinoma in Situ / diagnosis. Carcinoma in Situ / pathology. Carcinoma in Situ / therapy. Endosonography. Esophagoscopy. Esophagus / pathology. Humans. Mass Screening. Prognosis

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  • (PMID = 16836063.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Switzerland
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9. Abraham SC, Wang H, Wang KK, Wu TT: Paget cells in the esophagus: assessment of their histopathologic features and near-universal association with underlying esophageal adenocarcinoma. Am J Surg Pathol; 2008 Jul;32(7):1068-74
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  • [Title] Paget cells in the esophagus: assessment of their histopathologic features and near-universal association with underlying esophageal adenocarcinoma.
  • Pagetoid spread of primary esophageal melanomas and several cases of pagetoid esophageal squamous cell carcinoma are known.
  • However, true esophageal Paget disease (intraepithelial growth of neoplastic cells with glandular differentiation) has only rarely been reported.
  • We encountered 3 endoscopic biopsy specimens containing Paget cells in squamous epithelium associated with adenocarcinomas in Barrett esophagus (BE) and in the esophagogastric junction.
  • To determine the prevalence of Paget cells in the esophagus, we studied 81 endoscopic mucosal resections and 27 esophagectomies from patients with invasive or intramucosal adenocarcinoma, and compared the findings to a control group of 47 endoscopic mucosal resections and 25 esophagectomies from patients with high-grade dysplasia in BE.
  • A computerized search for primary Paget disease using the terms "Paget's and esophagus" or "pagetoid and esophagus" from 1994 to 2007 did not yield any additional cases.
  • Morphologically, all adenocarcinomas with Paget cells contained at least a component of diffuse, poorly differentiated adenocarcinoma, and 1 was a signet ring cell carcinoma.
  • These results demonstrate a low but significant prevalence (4.9%) of Paget cells in esophageal and esophagogastric junction adenocarcinomas.
  • Unlike previously described cases of mammary, vulvar, and perianal Paget disease, esophageal Paget cells are almost universally associated with underlying adenocarcinoma and not with high grade dysplasia ("in situ" disease) or primary Paget disease.
  • A commonality among cases with Paget cells is the presence of focal or diffuse, poorly differentiated adenocarcinoma with discohesive cells.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Paget Disease, Extramammary / pathology

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  • (PMID = 18496141.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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10. Li H, Zhang L, Lou H, Ding I, Kim S, Wang L, Huang J, Di Sant'Agnese PA, Lei JY: Overexpression of decoy receptor 3 in precancerous lesions and adenocarcinoma of the esophagus. Am J Clin Pathol; 2005 Aug;124(2):282-7
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  • [Title] Overexpression of decoy receptor 3 in precancerous lesions and adenocarcinoma of the esophagus.
  • Overexpression of decoy receptor (DcR) 3 protein, a recently discovered member of the tumor necrosis factor receptor superfamily, was examined in 40 esophagogastrectomy specimens containing areas of Barrett esophagus (n = 27), low-grade dysplasia (n = 27), high-grade dysplasia or carcinoma in situ (n = 22), and esophageal adenocarcinoma (EAC; n = 28) with immunohistochemical analysis.
  • The results revealed significantly more overexpression of DcR3 in high-grade dysplasia or carcinoma in situ and EAC than in benign esophageal mucosa (both P < .0001), Barrett esophagus (both P < .001), and low-grade dysplasia (P < .01 and P = .033, respectively).
  • Low-grade dysplasia also showed significant overexpression of DcR3 compared with benign esophagus (P < .05) but not with Barrett esophagus (P > .05).
  • Our results suggest that overexpression of DcR3 protein might aid in the diagnosis of high-grade dysplasia or carcinoma in situ and EAC and also might serve as a potential therapeutic target.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / analysis. Esophageal Neoplasms / metabolism. Membrane Glycoproteins / biosynthesis. Precancerous Conditions / metabolism. Receptors, Cell Surface / biosynthesis. Receptors, Tumor Necrosis Factor / biosynthesis

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  • (PMID = 16040301.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / TNFRSF6B protein, human
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11. Reichelt U, Duesedau P, Tsourlakis MCh, Quaas A, Link BC, Schurr PG, Kaifi JT, Gros SJ, Yekebas EF, Marx A, Simon R, Izbicki JR, Sauter G: Frequent homogeneous HER-2 amplification in primary and metastatic adenocarcinoma of the esophagus. Mod Pathol; 2007 Jan;20(1):120-9
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  • [Title] Frequent homogeneous HER-2 amplification in primary and metastatic adenocarcinoma of the esophagus.
  • In order to evaluate the potential role of such a treatment in esophageal cancers, HER-2 amplification and overexpression was investigated in primary and metastatic cancers of the esophagus.
  • A tissue microarray was constructed from 255 primary esophageal cancers (110 adenocarcinomas and 145 squamous cell carcinomas), 89 nodal and 33 distant metastases.
  • DAKO) and fluorescence in situ hybridization (FISH; PathVysion; Vysis-Abbott) for HER-2 amplification and overexpression.
  • Amplification was unrelated to survival, grading, pT, pN, pM or UICC stage.
  • We conclude that esophageal adenocarcinomas belong to those cancer types with relevant frequency high-level HER-2 gene amplification clinical trials or individual case studies investigating the response of metastatic HER-2-positive esophageal cancers to Herceptin((R)) should be undertaken.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Gene Amplification. Gene Expression Regulation, Neoplastic. Genes, erbB-2. Receptor, ErbB-2 / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Kaplan-Meier Estimate. Male. Matched-Pair Analysis. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Time Factors. Tissue Array Analysis. Up-Regulation

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  • (PMID = 17143264.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, ErbB-2
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12. Villanacci V, Rossi E, Grisanti S, Bassotti G, Ferrari VD, Missale G, Minelli L, Cengia P, Marini G, Cestari R: Targeted therapy with trastuzumab in dysplasia and adenocarcinoma arising in Barrett's esophagus: a translational approach. Minerva Gastroenterol Dietol; 2008 Dec;54(4):347-53
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  • [Title] Targeted therapy with trastuzumab in dysplasia and adenocarcinoma arising in Barrett's esophagus: a translational approach.
  • AIM: Human epidermal growth factor receptor (HER2) protooncogene, overexpressed/ amplified in preneoplastic lesions and in adenocarcinoma (ADC) of the esophagus, can be considered a target for treatment of esophageal dysplasia/ADC.
  • The aim of this study was to evaluate the therapeutic role of the anti-HER2 monoclonal antibody, trastuzumab, in the management of ADC originating from HER2-positive Barrett's esophagus (BE).
  • METHODS: Two patients with high-grade dysplasia and ADC of the esophagus after esophageal mucosectomy and no metastatic disease were studied.
  • HER2 status was assessed by immunohistochemistry and fluorescence in situ hybridization.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / drug therapy. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Barrett Esophagus / complications. Esophageal Neoplasms / complications. Esophageal Neoplasms / drug therapy


13. Martinek J, Benes M, Brandtl P, Hucl T, Vasicek M, Voska L, Lanska V, Nosek V, Spicak J: Low incidence of adenocarcinoma and high-grade intraepithelial neoplasia in patients with Barrett's esophagus: a prospective cohort study. Endoscopy; 2008 Sep;40(9):711-6
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  • [Title] Low incidence of adenocarcinoma and high-grade intraepithelial neoplasia in patients with Barrett's esophagus: a prospective cohort study.
  • BACKGROUND AND STUDY AIMS: Barrett's esophagus is a premalignant condition.
  • The risk of developing high grade intraepithelial neoplasia (HGIN) or adenocarcinoma is currently a matter of debate.
  • The main aim of our study was to investigate the incidence of HGD and adenocarcinoma in a cohort of patients with Barrett's esophagus.
  • PATIENTS AND METHODS: In a prospective, cohort study, all patients had intestinal metaplasia and macroscopic evidence of short- or long-segment (< 3 cm or > or = 3 cm) Barrett's esophagus.
  • Simultaneous HGIN and adenocarcinoma were detected in two patients with long-segment Barrett's esophagus (1.5%; 2 and 6 years after the index endoscopy).
  • Our study shows an incidence of HGIN/adenocarcinoma of 1/350 patient-years.
  • Endoscopic regression of Barrett's esophagus was seen in 20.7% of patients.
  • CONCLUSION: The incidence of HGIN/adenocarcinoma is low in patients with adequately treated Barrett's esophagus.
  • The annual risk of developing HGIN/adenocarcinoma is 0.21% (1.6% in long-segment Barrett's esophagus).
  • [MeSH-major] Adenocarcinoma / epidemiology. Barrett Esophagus / epidemiology. Carcinoma in Situ / epidemiology

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  • (PMID = 18698534.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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14. McCluggage WG, Shah R, Connolly LE, McBride HA: Intestinal-type cervical adenocarcinoma in situ and adenocarcinoma exhibit a partial enteric immunophenotype with consistent expression of CDX2. Int J Gynecol Pathol; 2008 Jan;27(1):92-100
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  • [Title] Intestinal-type cervical adenocarcinoma in situ and adenocarcinoma exhibit a partial enteric immunophenotype with consistent expression of CDX2.
  • Most cases of cervical adenocarcinoma in situ (AIS) and adenocarcinoma are of the usual or endocervical type.
  • However, intestinal types of AIS and adenocarcinoma exist.
  • With an intestinal-type adenocarcinoma in the cervix, the question may arise as to whether one is dealing with a primary cervical neoplasm or direct or secondary spread from an intestinal adenocarcinoma.
  • In organs such as the ovary, urinary bladder, esophagus, and gallbladder, intestinal-type glandular epithelium often expresses enteric markers, but this has hardly been studied in the cervix.
  • The purpose of this study was to investigate whether intestinal-type AIS and adenocarcinoma in the cervix express enteric markers and to ascertain whether these antibodies are of value in the distinction from a metastatic intestinal adenocarcinoma.
  • Cases included were AIS of usual type (n = 6), primary cervical adenocarcinoma of usual type (n = 6), AIS of intestinal type (n = 21), primary cervical adenocarcinoma of intestinal type (n = 3), primary cervical adenocarcinoma with signet ring cells (n = 2), and colorectal adenocarcinoma involving the cervix (n = 5).
  • The 3 cases of primary cervical intestinal-type adenocarcinoma were diffusely CK7 positive, focally or diffusely positive with CK20 and CDX2, and focally positive with CEA.
  • Intestinal types of cervical AIS and adenocarcinoma exhibit a partial enteric immunophenotype, usually with diffuse expression of CDX2 and, in some cases, staining with CK20.
  • Although there is immunophenotypic overlap, focal staining with CK20 together with diffuse CK7 and sometimes p16 positivity helps to distinguish intestinal types of cervical adenocarcinoma from involvement by a colorectal adenocarcinoma; CEA and CDX2 are of no value in this regard.
  • Using a set of cases of AIS diagnosed in a single institution over a 7-year period (77 usual type; 13 intestinal type), intestinal type was more likely to be associated with early invasive adenocarcinoma than usual type (31% vs 17%), suggesting that intestinal differentiation may be a risk factor for invasion in premalignant cervical glandular lesions.
  • [MeSH-major] Adenocarcinoma / metabolism. Homeodomain Proteins / biosynthesis. Intestinal Neoplasms / metabolism. Uterine Cervical Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Carcinoembryonic Antigen / biosynthesis. Carcinoma in Situ / metabolism. Carcinoma in Situ / pathology. Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Immunophenotyping. Keratin-20 / biosynthesis. Keratin-7 / biosynthesis

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  • (PMID = 18156982.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Carcinoembryonic Antigen; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / Keratin-7
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15. Nomura T, Yamashita K, Miyashita M, Tajiri T: [Argon plasma coagulation in Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1458-62
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  • [Title] [Argon plasma coagulation in Barrett's esophagus].
  • Recently, it has been reported that Barrett's esophagus and Barrett's adenocarcinoma in situ could be successfully managed by APC.
  • The aims of this treatment are to prevent the developing of adenocarcinoma and to promote the restitution of normal squamous epithelium.
  • In patient with Barrett's esophagus, APC offers an effective, minimally invasive alternative to other treatments previously performed.
  • [MeSH-major] Argon / therapeutic use. Barrett Esophagus / surgery. Electrocoagulation / methods
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Combined Modality Therapy. Enzyme Inhibitors / therapeutic use. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / surgery. Humans. Proton Pump Inhibitors

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  • (PMID = 16101240.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Proton Pump Inhibitors; 67XQY1V3KH / Argon
  • [Number-of-references] 15
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16. 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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17. Rossi E, Villanacci V, Bassotti G, Casa DD, Missale G, Minelli L, Cestari R: Her-2/neu in barrett esophagus: a comparative study between histology, immunohistochemistry, and fluorescence in situ hybridization. Diagn Mol Pathol; 2006 Sep;15(3):125-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Her-2/neu in barrett esophagus: a comparative study between histology, immunohistochemistry, and fluorescence in situ hybridization.
  • Her-2/neu is a protooncogene frequently overexpressed in breast cancer, recently found to be also overexpressed in carcinoma arising on Barrett esophagus (BE).
  • Immunohistochemistry and fluorescence in situ hybridization (FISH) are conventionally used for Her-2 testing in carcinomas, but a single assay is not yet accepted as a "gold standard" in BE.
  • To evaluate the correlation between histopathology variables and gene expression/amplification in the sequence BE-low grade dysplasia-high grade dysplasia-adenocarcinoma, fifty esophageal specimens from patients with a diagnosis of BE (21 BE, 4 low-grade dysplasia, 12 high-grade dysplasia, and 13 adenocarcinomas) were evaluated.
  • [MeSH-major] Barrett Esophagus / diagnosis. Receptor, ErbB-2 / analysis. Receptor, ErbB-2 / genetics
  • [MeSH-minor] Aged. Female. Gene Amplification. Gene Expression. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. RNA, Messenger / analysis. RNA, Messenger / metabolism

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  • (PMID = 16932066.001).
  • [ISSN] 1052-9551
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.1 / Receptor, ErbB-2
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18. Rygiel AM, Milano F, Ten Kate FJ, Bergman JJ, Krishnadath KK: Low Level of Her-2 Locus Amplification by Fluorescent In Situ Hybridization Does Not Correlate with Her-2 Protein Overexpression by Immunohistochemistry in Barrett's Esophagus. J Oncol; 2010;2010:382582
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  • [Title] Low Level of Her-2 Locus Amplification by Fluorescent In Situ Hybridization Does Not Correlate with Her-2 Protein Overexpression by Immunohistochemistry in Barrett's Esophagus.
  • The aim of the study was to correlate Her-2 locus (17q11.2) amplification and chromosome 17 gains as assessed by fluorescent in situ hybridization (FISH) with Her-2 protein overexpression by immunohistochemistry (IHC) in patients with Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC).

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  • (PMID = 20628513.001).
  • [ISSN] 1687-8469
  • [Journal-full-title] Journal of oncology
  • [ISO-abbreviation] J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2902046
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19. Wongsurawat VJ, Finley JC, Galipeau PC, Sanchez CA, Maley CC, Li X, Blount PL, Odze RD, Rabinovitch PS, Reid BJ: Genetic mechanisms of TP53 loss of heterozygosity in Barrett's esophagus: implications for biomarker validation. Cancer Epidemiol Biomarkers Prev; 2006 Mar;15(3):509-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic mechanisms of TP53 loss of heterozygosity in Barrett's esophagus: implications for biomarker validation.
  • BACKGROUND AND AIMS: 17p (TP53) loss of heterozygosity (LOH) has been reported to be predictive of progression from Barrett's esophagus to esophageal adenocarcinoma, but the mechanism by which TP53 LOH develops is unknown.
  • If an alternative biomarker assay, such as fluorescence in situ hybridization (FISH), provided equivalent results, then translation to the clinic might be accelerated, because LOH genotyping is presently limited to research centers.
  • CONCLUSIONS: LOH develops by multiple chromosome mechanisms in Barrett's esophagus, all of which can be detected by genotyping.
  • FISH will require validation in adequately powered longitudinal studies before implementation as a clinical diagnostic for esophageal adenocarcinoma risk prediction.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Genes, p53. Loss of Heterozygosity. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Esophagectomy. Esophagoscopy. Female. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Staging. Prognosis. Retrospective Studies. Risk Assessment. Sensitivity and Specificity. Survival Rate

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  • (PMID = 16537709.001).
  • [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 / P01 CA91955
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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20. Maley CC, Galipeau PC, Finley JC, Wongsurawat VJ, Li X, Sanchez CA, Paulson TG, Blount PL, Risques RA, Rabinovitch PS, Reid BJ: Genetic clonal diversity predicts progression to esophageal adenocarcinoma. Nat Genet; 2006 Apr;38(4):468-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic clonal diversity predicts progression to esophageal adenocarcinoma.
  • Here, in a prospective study, we show that clonal diversity measures adapted from ecology and evolution can predict progression to adenocarcinoma in the premalignant condition known as Barrett's esophagus, even when controlling for established genetic risk factors, including lesions in TP53 (p53; ref.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics
  • [MeSH-minor] Disease Progression. Genes, p16. Genes, p53. Humans. In Situ Hybridization, Fluorescence. Loss of Heterozygosity


21. Wolfsen HC: Present status of photodynamic therapy for high-grade dysplasia in Barrett's esophagus. J Clin Gastroenterol; 2005 Mar;39(3):189-202
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  • [Title] Present status of photodynamic therapy for high-grade dysplasia in Barrett's esophagus.
  • BACKGROUND: Barrett's esophagus is thought to be the result of long-standing gastroesophageal reflux disease and is known to be the most important risk factor for the development of esophageal adenocarcinoma.
  • The natural history of Barrett's esophagus is not well known, but the annual incidence of invasive adenocarcinoma is estimated to be 0.5% (reported range, 0.2%-2.0%).
  • This represents an increased risk for esophageal cancer of 30 to 60 times higher than normal subjects.
  • As for colorectal cancer, malignant degeneration is Barrett's esophagus is thought to occur through a continuum of histologic stages: metaplasia, dysplasia and neoplasia.
  • Barrett's high-grade dysplasia (formerly referred to as carcinoma in situ) is the histologic stage of disease that immediately precedes the development of invasive carcinoma.
  • CONCLUSIONS: Previously, Barrett's high-grade dysplasia patients were routinely referred for esophageal resection surgery based upon the assumption of inevitable progression to cancer, the high rate of undiagnosed synchronous cancers, and few treatment alternatives.
  • [MeSH-major] Barrett Esophagus / drug therapy. Barrett Esophagus / pathology. Photochemotherapy

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  • (PMID = 15718860.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mesoporphyrins; 0 / Photosensitizing Agents; 97067-70-4 / Dihematoporphyrin Ether; FU21S769PF / temoporfin
  • [Number-of-references] 166
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22. Pohl H, Koch M, Khalifa A, Papanikolaou IS, Scheiner K, Wiedenmann B, Rösch T: Evaluation of endocytoscopy in the surveillance of patients with Barrett's esophagus. Endoscopy; 2007 Jun;39(6):492-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of endocytoscopy in the surveillance of patients with Barrett's esophagus.
  • BACKGROUND AND STUDY AIMS: Surveillance for patients with Barrett's esophagus is time consuming and subject to sampling error.
  • RESULTS: Adenocarcinoma was histologically diagnosed in 4.2% of biopsy sites, high grade intraepithelial neoplasia (HGIN) in 16.9%, and low grade intraepithelial neoplasia (LGIN) in 12.1 %.
  • [MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagoscopy / methods. Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Biopsy. Carcinoma in Situ / etiology. Carcinoma in Situ / pathology. Female. Humans. Male. Mass Screening. Microscopy / methods. Middle Aged. Single-Blind Method

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  • [CommentIn] Endoscopy. 2007 Jun;39(6):540-1 [17554651.001]
  • (PMID = 17554642.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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23. Maltby EL, Dyson MJ, Wheeler MR, Thomson M, Sethuraman C, Cohen MC: Molecular abnormalities in pediatric barrett esophagus: can we test for potential of neoplastic progression? Pediatr Dev Pathol; 2010 Jul-Aug;13(4):310-7
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  • [Title] Molecular abnormalities in pediatric barrett esophagus: can we test for potential of neoplastic progression?
  • Barrett esophagus (BE) is a preneoplastic condition that predisposes to esophageal adenocarcinoma and is a consequence of prolonged gastroesophageal reflux disease.
  • We performed fluorescence in situ hybridization with probes from Abbott Vysis Corporation on 4-micron sections taken from 48 paraffin-embedded sequential biopsies of 10 cases of BE.
  • The probe sets were validated on 10 cases of adult Barrett adenocarcinoma.
  • The genetic markers informative in 50% of our cases were also identified in adult patients with Barrett adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Chromosome Aberrations. Esophageal Neoplasms / genetics. In Situ Hybridization, Fluorescence / methods. Precancerous Conditions / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease Progression. Esophagus / pathology. Female. Genetic Markers. Humans. Infant. Male. Predictive Value of Tests

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  • (PMID = 20053129.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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24. Shimizu Y, Yoshida T, Kato M, Hirota J, Ono S, Nakagawa M, Kobayashi T, Kubota K, Asaka M: Low-grade dysplasia component in early invasive squamous cell carcinoma of the esophagus. J Gastroenterol Hepatol; 2010 Feb;25(2):314-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-grade dysplasia component in early invasive squamous cell carcinoma of the esophagus.
  • BACKGROUND AND AIMS: It has not been determined whether low-grade squamous dysplasia (LGD) of the esophagus is a precancerous lesion or not.
  • However, the concept of 'basal cell layer type carcinoma in situ' may be suitable for squamous cell lesions with a high degree of cytological abnormalities confined to the lower half of the epithelium.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma in Situ / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Precancerous Conditions / pathology

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  • (PMID = 19968747.001).
  • [ISSN] 1440-1746
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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25. Van Den Eynde M, Jouret-Mourin A, Sempoux C, Piessevaux H, Deprez PH: Endoscopic mucosal or submucosal resection of early neoplasia in Barrett's esophagus after antireflux surgery. Gastrointest Endosc; 2010 Oct;72(4):855-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic mucosal or submucosal resection of early neoplasia in Barrett's esophagus after antireflux surgery.
  • BACKGROUND: Endoscopic resection and radiofrequency ablation are now established therapies for high-grade intraepithelial neoplasia and mucosal cancer complicating Barrett's esophagus.
  • OBJECTIVE: To assess the results of endoscopic resection for early neoplasia complicating Barrett's esophagus after antireflux surgery.
  • Pathology examination disclosed invasive adenocarcinoma in 3 patients and high-grade intraepithelial neoplasia in 4 patients.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / complications. Carcinoma in Situ / surgery. Esophageal Neoplasms / surgery. Fundoplication. Gastroesophageal Reflux / surgery

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  • [Copyright] Copyright © 2010 American Society for Gastrointestinal Endoscopy. Published by Mosby, Inc. All rights reserved.
  • (PMID = 20883865.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Chang LC, Oelschlager BK, Quiroga E, Parra JD, Mulligan M, Wood DE, Pellegrini CA: Long-term outcome of esophagectomy for high-grade dysplasia or cancer found during surveillance for Barrett's esophagus. J Gastrointest Surg; 2006 Mar;10(3):341-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome of esophagectomy for high-grade dysplasia or cancer found during surveillance for Barrett's esophagus.
  • Endoscopic surveillance is recommended for patients with Barrett's esophagus to detect high-grade dysplasia (HGD) or cancer.
  • Preoperative diagnosis was HGD in 9 patients (26.5%), carcinoma in situ in 16 (47%), and adenocarcinoma in 9 (26.5%).
  • Twenty-nine patients (85%) have no clinical, radiographic, or endoscopic evidence of recurrent esophageal cancer or metastasis.
  • Endoscopic surveillance in Barrett's patients yields malignant lesions at an early, generally curable, stage.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Carcinoma in Situ / surgery. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagectomy / methods. Precancerous Conditions / surgery

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  • (PMID = 16504878.001).
  • [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] Journal Article
  • [Publication-country] United States
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27. Woodall CE, Li Y, Liu QH, Wo J, Martin RC: Chemoprevention of metaplasia initiation and carcinogenic progression to esophageal adenocarcinoma by resveratrol supplementation. Anticancer Drugs; 2009 Jul;20(6):437-43
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  • [Title] Chemoprevention of metaplasia initiation and carcinogenic progression to esophageal adenocarcinoma by resveratrol supplementation.
  • The effects of resveratrol on the initiation of Barrett's metaplasia and the carcinogenic progression to esophageal adenocarcinoma have not been evaluated.
  • The aim of this study was to evaluate the effects of resveratrol on the transition from reflux esophagitis to Barrett's metaplasia to dysplasia to esophageal adenocarcinoma in an established rat model.
  • The distal esophagus was preserved for blinded histopathological examination at the time of harvest.
  • In conclusion, morphological characteristics consistent with decreased esophagitis and incidences of metaplasia and esophageal adenocarcinoma were seen on histopathology in the resveratrol group.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Esophageal Neoplasms / prevention & control. Esophagus / drug effects. Stilbenes / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Catalase / metabolism. Disease Models, Animal. Disease Progression. Glutathione / metabolism. Immunohistochemistry. In Situ Nick-End Labeling. Male. Metaplasia. Oxidative Stress / drug effects. Rats. Rats, Sprague-Dawley. Superoxide Dismutase / metabolism. Thiobarbituric Acid Reactive Substances / metabolism

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  • (PMID = 19398904.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Stilbenes; 0 / Thiobarbituric Acid Reactive Substances; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione; Q369O8926L / resveratrol
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28. Pohl H, Welch HG: The role of overdiagnosis and reclassification in the marked increase of esophageal adenocarcinoma incidence. J Natl Cancer Inst; 2005 Jan 19;97(2):142-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of overdiagnosis and reclassification in the marked increase of esophageal adenocarcinoma incidence.
  • BACKGROUND: The incidence of esophageal adenocarcinoma is rising dramatically.
  • This increase may reflect increased disease burden, reclassification of related cancers, or overdiagnosis resulting from increased diagnostic intensity, particularly upper endoscopy for patients with gastroesophageal reflux disease or Barrett esophagus.
  • METHODS: We used the National Cancer Institute's Surveillance, Epidemiology, and End Results database to extract information on incidence, stage distribution, and disease-specific mortality for esophageal adenocarcinoma as well as information on related cancers.
  • RESULTS: From 1975 to 2001, the incidence of esophageal adenocarcinoma rose approximately sixfold in the United States (from 4 to 23 cases per million), a relative increase greater than that for melanoma, breast, or prostate cancer.
  • Reclassification of squamous cell carcinoma is an unlikely explanation for the rise in incidence, because the anatomic distribution of esophageal cancer in general has changed.
  • The only location with increased incidence is the lower third of the esophagus-the site where adenocarcinoma typically arises.
  • Because there has been little change in the proportion of patients found with in situ or localized disease at diagnosis since 1975 (from 25% to 31%) and because esophageal adenocarcinoma mortality has increased more than sevenfold (from 2 to 15 deaths per million), overdiagnosis can be excluded as an explanation for the rise in incidence.
  • CONCLUSION: The rising incidence of esophageal adenocarcinoma represents a real increase in disease burden.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / epidemiology. Esophageal Neoplasms / classification. Esophageal Neoplasms / epidemiology
  • [MeSH-minor] Adult. Aged. Classification / methods. Confounding Factors (Epidemiology). Cost of Illness. Cross-Sectional Studies. Diagnosis, Differential. Diagnostic Errors. Female. Humans. Incidence. Male. Middle Aged. Risk Factors. SEER Program. United States / epidemiology

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  • [CommentIn] J Natl Cancer Inst. 2005 Jul 6;97(13):1013-4; author reply 1014 [15998956.001]
  • (PMID = 15657344.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
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29. Peters FP, Krishnadath KK, Rygiel AM, Curvers WL, Rosmolen WD, Fockens P, Ten Kate FJ, van Baal JW, Bergman JJ: Stepwise radical endoscopic resection of the complete Barrett's esophagus with early neoplasia successfully eradicates pre-existing genetic abnormalities. Am J Gastroenterol; 2007 Sep;102(9):1853-61
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  • [Title] Stepwise radical endoscopic resection of the complete Barrett's esophagus with early neoplasia successfully eradicates pre-existing genetic abnormalities.
  • Stepwise radical endoscopic resection of the Barrett's segment with early neoplasia is a promising new treatment resulting in complete re-epithelialization of the esophagus with neosquamous epithelium.
  • DNA fluorescent in-situ hybridization was (DNA-FISH) performed for evaluation of numerical abnormalities of chromosomes 1 and 9, and losses of p16 and p53.
  • CONCLUSIONS: Radical resection of Barrett's esophagus with early neoplasia successfully eradicates pre-existing genetic abnormalities and results in neosquamous epithelium without these genetic abnormalities.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / genetics. Barrett Esophagus / surgery. Esophageal Neoplasms / genetics. Esophageal Neoplasms / surgery. Esophagoscopy
  • [MeSH-minor] Chromosome Aberrations. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 9 / genetics. Genes, p16. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Precancerous Conditions / genetics. Precancerous Conditions / surgery. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 17509033.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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30. Wallace MB, Sharma P, Lightdale C, Wolfsen H, Coron E, Buchner A, Bajbouj M, Bansal A, Rastogi A, Abrams J, Crook JE, Meining A: Preliminary accuracy and interobserver agreement for the detection of intraepithelial neoplasia in Barrett's esophagus with probe-based confocal laser endomicroscopy. Gastrointest Endosc; 2010 Jul;72(1):19-24
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  • [Title] Preliminary accuracy and interobserver agreement for the detection of intraepithelial neoplasia in Barrett's esophagus with probe-based confocal laser endomicroscopy.
  • OBJECTIVE: To determine the preliminary evaluation accuracy and interobserver agreement of probe-based CLE (pCLE) in Barrett's esophagus (BE).
  • PATIENTS: This study involved nonconsecutive patients undergoing BE surveillance or evaluation of high-grade intraepithelial neoplasia or early adenocarcinoma.
  • INTERVENTION: Intravenous fluorescein pCLE imaging of each site within the BE segment, followed by matching biopsy.
  • MAIN OUTCOME MEASUREMENTS: Sensitivity, specificity, and agreement for the pCLE diagnosis of high-grade intraepithelial neoplasia or carcinoma.
  • The sensitivity for the diagnosis of neoplasia for the 11 endoscopists was 88% (range 6 of 11 to 11 of 11), and the specificity was 96% (range 7 of 9 to 9 of 9).
  • There was substantial agreement on the pCLE diagnosis (86%, kappa 0.72; 95% confidence interval, 0.58-0.86).
  • CONCLUSION: Results suggest that pCLE for the diagnosis of neoplasia in BE has very high accuracy and reliability.

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  • [Copyright] Copyright 2010 American Society for Gastrointestinal Endoscopy. Published by Mosby, Inc. All rights reserved.
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  • (PMID = 20381042.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA132892-04; United States / NCI NIH HHS / CA / K07 CA132892; United States / NCI NIH HHS / CA / K07 CA132892-04
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS307179; NLM/ PMC3144146
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31. Barbour AP, Rizk NP, Gonen M, Tang L, Bains MS, Rusch VW, Coit DG, Brennan MF: Adenocarcinoma of the gastroesophageal junction: influence of esophageal resection margin and operative approach on outcome. Ann Surg; 2007 Jul;246(1):1-8
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  • [Title] Adenocarcinoma of the gastroesophageal junction: influence of esophageal resection margin and operative approach on outcome.
  • OBJECTIVE: To determine whether the length of esophageal resection or the operative approach influences outcome for patients with adenocarcinoma of the gastroesophageal junction (GEJ).
  • SUMMARY BACKGROUND DATA: While R0 resection remains the mainstay of curative treatment of patients with GEJ cancer, the optimal length of esophageal resection remains controversial.
  • METHODS: Patients with Siewert I, II, or III adenocarcinoma who underwent complete gross resection without neoadjuvant therapy were identified from a prospectively maintained database.
  • Proximal margin lengths were recorded ex vivo as the distance from the gross tumor edge to the esophageal transection line.
  • Univariate analysis found >3.8 cm to be the ex vivo proximal margin length (approximately 5 cm in situ) most predictive of improved survival.
  • Multivariable analysis in patients who underwent R0 resection with >or=15 lymph nodes examined (n = 275) found the number of positive lymph nodes, T stage, tumor grade, and ex vivo proximal margin length >3.8 cm to be independent prognostic factors.
  • CONCLUSIONS: In patients not receiving neoadjuvant therapy, the goal for patients with adenocarcinoma of the GEJ should be R0 resection including at least 15 lymph nodes, preferably with 5 cm of grossly normal in situ proximal esophagus for those with <or=6 positive lymph nodes.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagectomy / methods. Esophagogastric Junction

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  • (PMID = 17592282.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1899203
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32. Madisch A, Miehlke S, Bayerdorffer E, Wiedemann B, Antos D, Sievert A, Vieth M, Stolte M, Schulz H: Long-term follow-up after complete ablation of Barrett's esophagus with argon plasma coagulation. World J Gastroenterol; 2005 Feb 28;11(8):1182-6
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  • [Title] Long-term follow-up after complete ablation of Barrett's esophagus with argon plasma coagulation.
  • AIM: To report the long-term outcome of patients after complete ablation of non-neoplastic Barrett's esophagus (BE) with respect to BE relapse and development of intraepithelial neoplasia or esophageal adenocarcinoma.
  • METHODS: In 70 patients with histologically proven non-neoplastic BE, complete BE ablation was achieved by argon plasma coagulation (APC) and high-dose proton pump inhibitor therapy (120 mg omeprazole daily).
  • In 8 of these patients (12.1%) non-neoplastic BE relapse was confirmed histologically giving a histological relapse rate of 3% per year.
  • In none of the patients, intraepithelial neoplasia nor an esophageal adenocarcinoma was detected.
  • CONCLUSION: The long-term relapse rate of non-neoplastic BE following complete ablation with high-power APC is low (3% per year).
  • [MeSH-major] Barrett Esophagus / therapy. Laser Coagulation
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adult. Aged. Argon. Carcinoma in Situ / epidemiology. Cohort Studies. Esophageal Neoplasms / epidemiology. Female. Follow-Up Studies. Humans. Male. Middle Aged. Recurrence. Risk Factors. Treatment Outcome

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  • (PMID = 15754401.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 67XQY1V3KH / Argon
  • [Other-IDs] NLM/ PMC4250710
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33. Wiech T, Nikolopoulos E, Weis R, Langer R, Bartholomé K, Timmer J, Walch AK, Höfler H, Werner M: Genome-wide analysis of genetic alterations in Barrett's adenocarcinoma using single nucleotide polymorphism arrays. Lab Invest; 2009 Apr;89(4):385-97
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  • [Title] Genome-wide analysis of genetic alterations in Barrett's adenocarcinoma using single nucleotide polymorphism arrays.
  • We performed genome-wide analysis of copy-number changes and loss of heterozygosity (LOH) in Barrett's esophageal adenocarcinoma by single nucleotide polymorphism (SNP) microarrays to identify associated genomic alterations.
  • DNA from 27 esophageal adenocarcinomas and 14 matching normal tissues was subjected to SNP microarrays.
  • As a validation, fluorescence in situ hybridization (FISH) of 8q24.21 (CMYC) and 8p23.1 (SOX7) was performed.
  • Previously described genomic alterations in esophageal adenocarcinomas could be confirmed by SNP microarrays, such as amplification on 8q (CMYC, confirmed by FISH) and 20q13 or deletion/LOH on 3p (FHIT) and 9p (CDKN2A).
  • Using this technique, we identified several novel genes and DNA regions associated with esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Polymorphism, Single Nucleotide

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  • (PMID = 18663352.001).
  • [ISSN] 1530-0307
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Tischoff I, Hengge UR, Vieth M, Ell C, Stolte M, Weber A, Schmidt WE, Tannapfel A: Methylation of SOCS-3 and SOCS-1 in the carcinogenesis of Barrett's adenocarcinoma. Gut; 2007 Aug;56(8):1047-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methylation of SOCS-3 and SOCS-1 in the carcinogenesis of Barrett's adenocarcinoma.
  • AIMS: This study was performed to elucidate the role of SOCS-1 and SOCS-3 in Barrett's adenocarcinoma and its precursor lesions.
  • CONCLUSIONS: These data indicate that promoter methylation and subsequent transcript downregulation of SOCS-3 transcripts and, to a much lesser extent, SOCS-1 are involved in the multistep carcinogenesis of Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Suppressor of Cytokine Signaling Proteins / genetics
  • [MeSH-minor] Carcinoma in Situ / genetics. Carcinoma, Squamous Cell / genetics. Cell Line, Tumor. CpG Islands / genetics. DNA, Neoplasm / genetics. Humans. Methylation. Neoplasm Proteins / genetics. Promoter Regions, Genetic / genetics. Transcription, Genetic / genetics

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  • (PMID = 17376806.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / SOCS1 protein, human; 0 / SOCS3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins
  • [Other-IDs] NLM/ PMC1955493
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35. Rossi E, Villanacci V, Bassotti G, Donato F, Festa A, Cengia G, Grisanti S, Cestari R: TOPOIIalpha and HER-2/neu overexpression/amplification in Barrett's oesophagus, dysplasia and adenocarcinoma. Histopathology; 2010 Jul;57(1):81-9
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  • [Title] TOPOIIalpha and HER-2/neu overexpression/amplification in Barrett's oesophagus, dysplasia and adenocarcinoma.
  • AIMS: Topoisomerase IIalpha (TOPOIIalpha) and HER-2/neu are chromosome 17q genes coamplified in various cancers; no data exist for Barrett's oesophagus (BO) and BO adenocarcinoma (ADC).
  • The aim was to investigate gene amplification and protein overexpression of TopoIIalpha and Her-2/neu in non-dysplastic BO, dysplastic BO, Barrett ADC, and chromosome 17 aneusomy.
  • METHODS AND RESULTS: Forty-four patients [18 BO, 13 BO with dysplasia (five low-grade dysplasia, eight high-grade dysplasia) and 13 ADC in BO] were evaluated by immunohistochemistry and fluorescence in situ hybridization (FISH).
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Antigens, Neoplasm / genetics. Barrett Esophagus / genetics. Barrett Esophagus / pathology. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Esophageal Neoplasms / genetics. Esophageal Neoplasms / pathology. Genes, erbB-2
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Aneuploidy. Chromosomes, Human, Pair 17 / genetics. Diagnosis, Differential. Female. Gene Amplification. Gene Expression. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Receptor, ErbB-2 / metabolism. Retrospective Studies

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  • (PMID = 20557373.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ PMC2916224
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36. Bajbouj M, Vieth M, Rösch T, Miehlke S, Becker V, Anders M, Pohl H, Madisch A, Schuster T, Schmid RM, Meining A: Probe-based confocal laser endomicroscopy compared with standard four-quadrant biopsy for evaluation of neoplasia in Barrett's esophagus. Endoscopy; 2010 Jun;42(6):435-40
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  • [Title] Probe-based confocal laser endomicroscopy compared with standard four-quadrant biopsy for evaluation of neoplasia in Barrett's esophagus.
  • BACKGROUND AND STUDY AIMS: Surveillance of Barrett's esophagus includes endoscopic inspection with biopsy of suspicious lesions followed by four-quadrant biopsy of the remaining mucosa.
  • We assessed the ability of probe-based confocal laser endomicroscopy (pCLE) to replace biopsy in the endoscopic evaluation of patients with Barrett's esophagus in a prospective and controlled setting.
  • PATIENTS AND METHODS: A total of 68 patients who were referred for endoscopic assessment of Barrett's esophagus were included across three centers. pCLE recordings were interpreted live during the examination as well as in a blinded manner at least 3 months after endoscopy. pCLE diagnosis of neoplasia based on pre-defined criteria was compared with histopathology from suspicious as well as four-quadrant biopsies.
  • Specificity and negative predictive value of pCLE in excluding neoplasia was 0.97 (90 %CI 0.95 - 0.98) and 0.93 (0.91 - 0.95) for the blinded evaluation, and 0.95 (0.90 - 0.98) and 0.92 (0.90 - 0.94) for the on-site assessment.
  • Positive predictive values (PPVs) and sensitivity were rather poor for both settings (46 %/28 % [blinded] and 18 %/12 % [on-site], respectively).
  • CONCLUSIONS: pCLE can be regarded as non-inferior to endoscopic biopsy in excluding neoplasia of Barrett's esophagus mucosa.
  • However, due to its low PPV and sensitivity, pCLE may currently not replace standard biopsy techniques for the diagnosis of Barrett's esophagus and associated neoplasia.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / complications. Esophageal Neoplasms / diagnosis. Esophagoscopy. Esophagus / pathology. Microscopy, Confocal
  • [MeSH-minor] Aged. Biopsy. Carcinoma in Situ / diagnosis. Carcinoma in Situ / etiology. Female. Humans. Male. Middle Aged. Prospective Studies. Single-Blind Method

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  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • [CommentIn] Endoscopy. 2010 Jun;42(6):487-9 [20506066.001]
  • (PMID = 20506064.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Comparative Study; Controlled Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] Germany
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37. Lai LA, Kostadinov R, Barrett MT, Peiffer DA, Pokholok D, Odze R, Sanchez CA, Maley CC, Reid BJ, Gunderson KL, Rabinovitch PS: Deletion at fragile sites is a common and early event in Barrett's esophagus. Mol Cancer Res; 2010 Aug;8(8):1084-94
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  • [Title] Deletion at fragile sites is a common and early event in Barrett's esophagus.
  • Barrett's esophagus (BE) is a premalignant intermediate to esophageal adenocarcinoma, which develops in the context of chronic inflammation and exposure to bile and acid.
  • Due to the consistency of the region of copy number loss, we were able to verify these results by quantitative PCR, which detected the loss of FRA3B and FRA16D, in 83% and 40% of early molecular stage BE patients, respectively.

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  • (PMID = 20647332.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R44 CA103406-02; United States / NCI NIH HHS / CA / CA103406-02; United States / NCI NIH HHS / CA / P01 CA091955-01; United States / NIA NIH HHS / AG / T32 AG00057; United States / NCI NIH HHS / CA / P01 CA091955; United States / NCI NIH HHS / CA / 2 R44 CA103406-02; United States / NCI NIH HHS / CA / CA091955-01; United States / NCI NIH HHS / CA / R44 CA103406; United States / NIA NIH HHS / AG / T32 AG000057-21; United States / NIA NIH HHS / AG / T32 AG000057; United States / NIA NIH HHS / AG / AG000057-21; United States / NCI NIH HHS / CA / P01 CA91955
  • [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 / Neoplasm Proteins; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS291718; NLM/ PMC3100793
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38. Shen KR, Cassivi SD, Deschamps C, Allen MS, Nichols FC 3rd, Harmsen WS, Pairolero PC: Surgical treatment of tumors of the proximal stomach with involvement of the distal esophagus: a 26-year experience with Siewert type III tumors. J Thorac Cardiovasc Surg; 2006 Oct;132(4):755-62
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  • [Title] Surgical treatment of tumors of the proximal stomach with involvement of the distal esophagus: a 26-year experience with Siewert type III tumors.
  • OBJECTIVE: A paucity of outcome data exists regarding patients with proximal stomach cancer involving the distal esophagus (Siewert type III tumors).
  • METHODS: Medical records were reviewed of all patients who underwent total gastrectomy and distal esophagectomy with Roux-en-Y esophagojejunostomy for Siewert type III tumors from January 1975 through December 2000.
  • Pathologic stage was 0 (carcinoma in situ) in 1 patient, IB in 13 patients, II in 17 patients, IIIA in 34 patients, IIIB in 10 patients, and IV in 41 patients.
  • Incomplete resection, increased tumor stage and grade, and splenic involvement significantly worsened long-term survival.
  • Although often palliative, surgical intervention can provide long-term survival, especially in patients with completely resected, early-stage, low-grade tumors.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagectomy. Gastrectomy. Stomach Neoplasms / surgery

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  • (PMID = 17000284.001).
  • [ISSN] 1097-685X
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Schoppmann SF, Jesch B, Friedrich J, Wrba F, Schultheis A, Pluschnig U, Maresch J, Zacherl J, Hejna M, Birner P: Expression of Her-2 in carcinomas of the esophagus. Am J Surg Pathol; 2010 Dec;34(12):1868-73
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  • [Title] Expression of Her-2 in carcinomas of the esophagus.
  • Her-2 protein expression was investigated in 341 esophageal carcinomas [152 squamous cell carcinomas (SCC), 189 adenocarcinomas (AC)], 39 cases of Barrett mucosa, and 11 cases of squamous cell dysplasia.
  • HER-2 gene amplification was assessed by colorimetric in-situ hybridization.
  • Although Her-2-overexpression in esophageal cancer seems to have no influence on patients' survival, these subtypes of esophageal ACs have to be considered as targets for an anti-Her-2 therapy.
  • [MeSH-major] Adenocarcinoma / secondary. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Esophagogastric Junction / metabolism. Esophagogastric Junction / pathology. Esophagogastric Junction / surgery. Gene Amplification. Gene Expression. Humans. In Situ Hybridization. Prognosis. Survival Rate

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  • (PMID = 21107094.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
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40. Su M, Chin SF, Li XY, Edwards P, Caldas C, Fitzgerald RC: Comparative genomic hybridization of esophageal adenocarcinoma and squamous cell carcinoma cell lines. Dis Esophagus; 2006;19(1):10-4
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  • [Title] Comparative genomic hybridization of esophageal adenocarcinoma and squamous cell carcinoma cell lines.
  • We compared whole genomic changes in cell lines generated from esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC).

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  • [ErratumIn] Dis Esophagus. 2006;19(2):135. Edwards, P [added]; Caldas, C [added]
  • (PMID = 16364037.001).
  • [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
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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41. Savoy AD, Wolfsen HC, Raimondo M, Woodward TA, Noh K, Pungpapong S, Hemminger LL, Wallace MB: The role of surveillance endoscopy and endosonography after endoscopic ablation of high-grade dysplasia and carcinoma of the esophagus. Dis Esophagus; 2008;21(2):108-13
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  • [Title] The role of surveillance endoscopy and endosonography after endoscopic ablation of high-grade dysplasia and carcinoma of the esophagus.
  • Barrett's esophagus (BE) with high-grade dysplasia (HGD) or early carcinoma treated with surgery or photodynamic therapy (PDT) is at risk of recurrence.
  • Consecutive patients with BE with HGD or carcinoma in situ treated with PDT were followed with EUS, CT scan and EGD with jumbo biopsies every 1 cm at 3, 4, or 6-month intervals.
  • Recurrent or residual adenocarcinoma (ACA) was detected in four patients during follow-up.
  • In the fourth patient, CT scan revealed perigastric lymphadenopathy and EUS-FNA (fine needle aspiration) confirmed adenocarcinoma.
  • Limitations of this study include non-blinding of results and preferential status of non-invasive imaging (CT) over EUS.

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  • (PMID = 18269644.001).
  • [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
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42. Shiraishi H, Mikami T, Aida J, Nakamura K, Izumiyama-Shimomura N, Arai T, Watanabe M, Okayasu I, Takubo K: Telomere shortening in Barrett's mucosa and esophageal adenocarcinoma and its association with loss of heterozygosity. Scand J Gastroenterol; 2009;44(5):538-44
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  • [Title] Telomere shortening in Barrett's mucosa and esophageal adenocarcinoma and its association with loss of heterozygosity.
  • The purpose of this study was to measure telomere length in a series of Barrett's adenocarcinomas (BAs), focusing on the telomere/centromere fluorescent intensity ratio (TCR) with tissue quantitative fluorescent in situ hybridization (Q-FISH).
  • MATERIAL AND METHODS: A total of 11 cases of BA were evaluated for upper esophagus (UE), lower esophagus (LE), Barrett's mucosa (BM), BA, and gastric cardiac mucosa (GC).
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Loss of Heterozygosity. Microsatellite Instability. Telomere / metabolism
  • [MeSH-minor] Analysis of Variance. Female. Gastric Mucosa / pathology. Genetic Markers. Humans. In Situ Hybridization, Fluorescence. Male. Mucous Membrane / pathology. Neoplasm Staging. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Probability. Sampling Studies. Sensitivity and Specificity. Statistics, Nonparametric. Tissue Culture Techniques

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  • (PMID = 19221928.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Genetic Markers
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43. Rossi E, Grisanti S, Villanacci V, Della Casa D, Cengia P, Missale G, Minelli L, Buglione M, Cestari R, Bassotti G: HER-2 overexpression/amplification in Barrett's oesophagus predicts early transition from dysplasia to adenocarcinoma: a clinico-pathologic study. J Cell Mol Med; 2009 Sep;13(9B):3826-33
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  • [Title] HER-2 overexpression/amplification in Barrett's oesophagus predicts early transition from dysplasia to adenocarcinoma: a clinico-pathologic study.
  • Barrett's oesophagus (BO) is the primary precursor lesion for oesophageal adenocarcinoma (ADC).
  • We retrospectively evaluated by univariate analysis of single variables clinical records and histological specimens of 21 patients with a confirmed diagnosis of BO and/or oesophageal dysplasia.
  • HER2 status was studied by immunohistochemistry and fluorescence in situ hybridization (FISH) on paraffin-embedded tissue.
  • Median age at diagnosis was 63 years (range 37-84).
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Gene Expression Regulation, Neoplastic. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Genes, erbB-2. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Retrospective Studies. Treatment Outcome

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  • (PMID = 19292734.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC4516530
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44. Rygiel AM, Milano F, Ten Kate FJ, de Groot JG, Peppelenbosch MP, Bergman JJ, Krishnadath KK: Assessment of chromosomal gains as compared to DNA content changes is more useful to detect dysplasia in Barrett's esophagus brush cytology specimens. Genes Chromosomes Cancer; 2008 May;47(5):396-404
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  • [Title] Assessment of chromosomal gains as compared to DNA content changes is more useful to detect dysplasia in Barrett's esophagus brush cytology specimens.
  • Abnormal DNA ploidy status has been suggested as a prognostic factor for Barrett's esophagus progression into esophageal adenocarcinoma (EAC).
  • The aim of the study was to compare image cytometry DNA analysis (ICDA) and fluorescent in situ hybridization (FISH) in the assessment of DNA ploidy status in Barrett's esophagus (BE), and to determine the value of these abnormalities as an adjunct to conventional cytology in detection of dysplasia and EAC.
  • Gains of chromosome 7 and/or 17 were present in 13% of nondysplasia cases, which further increased with dysplasia stage, while overall DNA content aneuploidy was detected predominantly in high grade dysplasia (HGD) and EAC.
  • [MeSH-major] Barrett Esophagus / genetics. DNA / analysis
  • [MeSH-minor] Humans. In Situ Hybridization, Fluorescence. Ploidies

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18265409.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-49-2 / DNA
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45. Safran H, Dipetrillo T, Akerman P, Ng T, Evans D, Steinhoff M, Benton D, Purviance J, Goldstein L, Tantravahi U, Kennedy T: Phase I/II study of trastuzumab, paclitaxel, cisplatin and radiation for locally advanced, HER2 overexpressing, esophageal adenocarcinoma. Int J Radiat Oncol Biol Phys; 2007 Feb 1;67(2):405-9
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  • [Title] Phase I/II study of trastuzumab, paclitaxel, cisplatin and radiation for locally advanced, HER2 overexpressing, esophageal adenocarcinoma.
  • PURPOSE: To determine the overall survival for patients with locally advanced, HER2 overexpressing, esophageal adenocarcinoma receiving trastuzumab, paclitaxel, cisplatin, and radiation on a Phase I-II study.
  • METHODS AND MATERIALS: Patients with adenocarcinoma of the esophagus without distant organ metastases and 2+/3+ HER2 overexpression by immunohistochemistry (IHC) were eligible.
  • Fourteen of 19 patients (74%) had either 3+ HER2 expression by immunohistochemistry, or an increase in HER2 gene copy number by HER2 gene amplification or high polysomy by fluorescence in situ hybridization.
  • CONCLUSIONS: Assessment of the effect of trastuzumab in the treatment of patients with esophageal adenocarcinoma overexpressing HER2 is limited by the small number of patients in this study.
  • Evaluation of HER2 status should be performed in future trials for patients with adenocarcinoma of the esophagus that investigate therapies targeting the HER family.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / radiotherapy

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  • (PMID = 17097832.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Neoplasm Proteins; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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46. Cooper GS, Kou TD, Chak A: Receipt of previous diagnoses and endoscopy and outcome from esophageal adenocarcinoma: a population-based study with temporal trends. Am J Gastroenterol; 2009 Jun;104(6):1356-62
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  • [Title] Receipt of previous diagnoses and endoscopy and outcome from esophageal adenocarcinoma: a population-based study with temporal trends.
  • OBJECTIVES: Endoscopic screening of the at-risk population with chronic gastroesophageal reflux disease (GERD) for the presence of intestinal metaplasia or Barrett's esophagus has been suggested as a method to reduce mortality from esophageal adenocarcinoma.
  • METHODS: All patients aged 68 years and older with a new diagnosis of adenocarcinoma of the esophagus from 1994 to 2002 were identified from a linked tumor registry health claims database.
  • Using claims from 1991 to 2002, the use of endoscopy as well as a diagnosis of GERD or Barrett's esophagus during the time interval from 3 years through 6 months prior to diagnosis were measured.
  • The association of these measures with early-stage cancer (in situ, local) and long-term survival was determined, as well as changes over time.
  • RESULTS: We identified 2,754 patients, including 30.8% at early stage.
  • Previous endoscopy had been performed in 11.5% of patients, and GERD and Barrett's esophagus diagnoses were recorded in 22.4 and 8.1% of patients, respectively.
  • Barrett's esophagus diagnosis was strongly associated with both early-stage cancer (odds ratio 3.68, confidence interval (CI) 1.30-10.40) and survival (hazard ratio 0.45, CI 0.25-0.80).
  • A GERD diagnosis was associated only with early stage, and endoscopy was associated only with survival.
  • There was no association of year of diagnosis with stage or survival.
  • [MeSH-major] Adenocarcinoma / diagnosis. Endoscopy, Gastrointestinal / methods. Esophageal Neoplasms / diagnosis. SEER Program / trends
  • [MeSH-minor] Aged. Aged, 80 and over. Combined Modality Therapy. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Incidence. Male. Neoplasm Staging / methods. Prognosis. Retrospective Studies. Risk Factors. Survival Rate / trends. United States / epidemiology

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  • [CommentIn] Am J Gastroenterol. 2009 Dec;104(12):3106-7; author reply 3107-8 [19956133.001]
  • [CommentIn] Am J Gastroenterol. 2009 Oct;104(10):2632-3; author reply 2633 [19806097.001]
  • [CommentIn] Am J Gastroenterol. 2009 Jun;104(6):1363-5 [19436281.001]
  • (PMID = 19491849.001).
  • [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 / K05 CA 90677; United States / NIDDK NIH HHS / DK / K24 DK 02800
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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47. Nicolás Pérez D, Quintero E, Parra Blanco A: [Screening the at-risk population for squamous cell carcinoma of the esophagus]. Gastroenterol Hepatol; 2005 Jun-Jul;28(6):337-46
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  • [Title] [Screening the at-risk population for squamous cell carcinoma of the esophagus].
  • [Transliterated title] Cribado del carcinoma escamoso de esófago en población de riesgo.
  • Together with adenocarcinoma, epidermoid esophageal carcinoma is the most clinically important neoplasm of the esophagus.
  • Because of the low incidence of epidermoid esophageal carcinoma in the general population, strategies for its early diagnosis are not a priority compared with other neoplasms.
  • However, because survival is low when the disease is diagnosed in symptomatic patients (less than 20% at 5 years), methods for its early diagnosis should be investigated.
  • The use of cytology or Lugol chromoendoscopy in countries with a high incidence of epidermoid carcinoma or in individuals at increased risk (mainly alcoholics and smokers) has allowed early diagnosis and potentially curative treatment, substantially increasing life expectancy in this group of patients.
  • These results should stimulate the evaluation and eventual implementation of programs to achieve early diagnosis and therefore greater survival in patients with epidermoid esophageal carcinoma in Western countries.
  • [MeSH-major] Carcinoma, Squamous Cell / diagnosis. Esophageal Neoplasms / diagnosis. Mass Screening
  • [MeSH-minor] Alcohol Drinking / adverse effects. Carcinoma in Situ / diagnosis. Carcinoma in Situ / surgery. Coloring Agents. Cytological Techniques. Disease Susceptibility. Early Diagnosis. Esophagoscopy. Female. Gastrointestinal Hemorrhage / etiology. Humans. Incidence. Iodides. Male. Mucous Membrane / pathology. Occult Blood. Precancerous Conditions / diagnosis. Precancerous Conditions / surgery. Prevalence. Risk. Smoking / adverse effects. Survival Rate. Tolonium Chloride

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  • (PMID = 15989816.001).
  • [ISSN] 0210-5705
  • [Journal-full-title] Gastroenterología y hepatología
  • [ISO-abbreviation] Gastroenterol Hepatol
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Iodides; 15XUH0X66N / Tolonium Chloride; T66M6Y3KSA / Lugol's solution
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48. Pech O, Behrens A, May A, Nachbar L, Gossner L, Rabenstein T, Manner H, Guenter E, Huijsmans J, Vieth M, Stolte M, Ell C: Long-term results and risk factor analysis for recurrence after curative endoscopic therapy in 349 patients with high-grade intraepithelial neoplasia and mucosal adenocarcinoma in Barrett's oesophagus. Gut; 2008 Sep;57(9):1200-6
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  • [Title] Long-term results and risk factor analysis for recurrence after curative endoscopic therapy in 349 patients with high-grade intraepithelial neoplasia and mucosal adenocarcinoma in Barrett's oesophagus.
  • OBJECTIVE: Endoscopic therapy is increasingly being used in the treatment of high-grade intraepithelial neoplasia (HGIN) and mucosal adenocarcinoma (BC) in patients with Barrett's oesophagus.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Carcinoma in Situ / surgery. Esophageal Neoplasms / surgery. Precancerous Conditions / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Epidemiologic Methods. Esophagoscopy. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Treatment Outcome

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  • [CommentIn] Endoscopy. 2010 Jan;42(1):42-5 [19967633.001]
  • (PMID = 18460553.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
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49. Levy MJ, Clain JE, Clayton A, Halling KC, Kipp BR, Rajan E, Roberts LR, Root RM, Sebo TJ, Topazian MD, Wang KK, Wiersema MJ, Gores GJ: Preliminary experience comparing routine cytology results with the composite results of digital image analysis and fluorescence in situ hybridization in patients undergoing EUS-guided FNA. Gastrointest Endosc; 2007 Sep;66(3):483-90
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  • [Title] Preliminary experience comparing routine cytology results with the composite results of digital image analysis and fluorescence in situ hybridization in patients undergoing EUS-guided FNA.
  • BACKGROUND: Studies indicate enhanced diagnostic accuracy for digital image analysis (DIA) and fluorescence in situ hybridization (FISH) versus routine cytology examination (RC) when biliary strictures are evaluated.
  • The final diagnosis was based on strict cytopathologic and imaging criteria and 12-month follow-up.
  • PATIENTS: A total of 39 patients were enrolled in whom each diagnostic test was performed on samples from 42 sites to evaluate lymphadenopathy (n=19), pancreatic mass (n=19), esophageal or gastric wall mass (n=3), and thyroid mass (n=1).
  • RESULTS: Malignancy was diagnosed in 30 of 42 patients, including esophageal squamous cell carcinoma, esophageal adenocarcinoma, gastric adenocarcinoma, pancreatic adenocarcinoma, pancreatic mucinous cystic neoplasia, intraductal papillary mucinous neoplasia, metastatic forearm sarcoma, small cell and non-small cell lung cancer, thyroid carcinoma, malignant GI stromal tumor, melanoma, adenocarcinoma of unknown primary, and lymphoma.
  • [MeSH-major] Biopsy, Fine-Needle. Endosonography. Esophageal Neoplasms / pathology. Image Processing, Computer-Assisted. In Situ Hybridization, Fluorescence. Lymphatic Metastasis / pathology. Pancreatic Neoplasms / pathology. Stomach Neoplasms / pathology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cohort Studies. Esophagus / pathology. Female. Humans. Lymph Nodes / pathology. Male. Middle Aged. Neoplasm Invasiveness / pathology. Neoplasm Staging. Pancreas / pathology. Pilot Projects. Sensitivity and Specificity. Stomach / pathology


50. Rice TW, Rusch VW, Ishwaran H, Blackstone EH, Worldwide Esophageal Cancer Collaboration: Cancer of the esophagus and esophagogastric junction: data-driven staging for the seventh edition of the American Joint Committee on Cancer/International Union Against Cancer Cancer Staging Manuals. Cancer; 2010 Aug 15;116(16):3763-73
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  • [Title] Cancer of the esophagus and esophagogastric junction: data-driven staging for the seventh edition of the American Joint Committee on Cancer/International Union Against Cancer Cancer Staging Manuals.
  • BACKGROUND: Previous American Joint Committee on Cancer/International Union Against Cancer (AJCC/UICC) stage groupings for esophageal cancer have not been data driven or harmonized with stomach cancer.
  • At the request of the AJCC, worldwide data from 3 continents were assembled to develop data-driven, harmonized esophageal staging for the seventh edition of the AJCC/UICC cancer staging manuals.
  • METHODS: All-cause mortality among 4627 patients with esophageal and esophagogastric junction cancer who underwent surgery alone (no preoperative or postoperative adjuvant therapy) was analyzed by using novel random forest methodology to produce stage groups for which survival was monotonically decreasing, distinctive, and homogeneous.
  • Resulting stage groupings departed from a simple, logical arrangement of TNM.
  • Stage groupings for stage I and II adenocarcinoma were based on pT, pN, and histologic grade; and groupings for squamous cell carcinoma were based on pT, pN, histologic grade, and location.
  • Stage III was similar for histopathologic cell types and was based only on pT and pN.
  • Stage 0 and stage IV, by definition, were categorized as tumor in situ (Tis) (high-grade dysplasia) and pM1, respectively.
  • CONCLUSIONS: The prognosis for patients with esophageal and esophagogastric junction cancer depends on the complex interplay of TNM classifications as well as nonanatomic factors, including histopathologic cell type, histologic grade, and cancer location.
  • These features were incorporated into a data-driven staging of these cancers for the seventh edition of the AJCC/UICC cancer staging manuals.
  • [MeSH-major] Esophageal Neoplasms / pathology. Esophagogastric Junction. Neoplasm Staging / methods

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  • [Copyright] Copyright (c) 2010 American Cancer Society.
  • (PMID = 20564099.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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51. Sonoda R, Naomoto Y, Shirakawa Y, Fujiwara Y, Yamatsuji T, Noma K, Tanabe S, Takaoka M, Gunduz M, Tsujigiwa H, Nagatsuka H, Ohara N, Yoshino T, Takubo K, Vieth M, Tanaka N: Preferential up-regulation of heparanase and cyclooxygenase-2 in carcinogenesis of Barrett's oesophagus and intestinal-type gastric carcinoma. Histopathology; 2010 Jul;57(1):90-100
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  • AIMS: Metaplastic changes secondary to chronic inflammation at the gastro-oesophageal junction and at the pyloric antrum are recognized as the premalignant conditions of Barrett's oesophageal adenocarcinoma and intestinal-type gastric carcinoma (GC), respectively.
  • METHODS AND RESULTS: First, expression of HPSE and COX-2 in 78 clinical tissues of Barrett's oesophagus was examined by immunohistochemistry and in situ hybridization.
  • These molecules may play an important role during the development of inflammation-related adenocarcinoma of the upper gastrointestinal tract.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Cyclooxygenase 2 / metabolism. Esophageal Neoplasms / enzymology. Glucuronidase / metabolism. Stomach Neoplasms / enzymology
  • [MeSH-minor] Base Sequence. Carcinoma in Situ / enzymology. Carcinoma in Situ / genetics. Carcinoma in Situ / pathology. Cell Line, Tumor. DNA Primers / genetics. Humans. Microvessels / pathology. Neovascularization, Pathologic. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Up-Regulation

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  • (PMID = 20653782.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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52. Rugge M, Fassan M, Zaninotto G, Pizzi M, Giacomelli L, Battaglia G, Rizzetto C, Parente P, Ancona E: Aurora kinase A in Barrett's carcinogenesis. Hum Pathol; 2010 Oct;41(10):1380-6
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  • In Barrett's mucosa, both aneuploidy and TP53 mutations are consistently recognized as markers of an increased risk of Barrett's adenocarcinoma.
  • Eighty-seven esophageal biopsy samples representative of all the phenotypic lesions occurring in the multistep process of Barrett's carcinogenesis (gastric metaplasia in 25, intestinal metaplasia in 25, low-grade intraepithelial neoplasia in 16, high-grade intraepithelial neoplasia in 11, and Barrett's adenocarcinoma in 10) were obtained from long segments of Barrett's mucosa.
  • Twenty-five additional biopsy samples of native esophageal mucosa were used for control purposes.
  • AURKA overexpression is significantly associated with Barrett's mucosa progressing to Barrett's adenocarcinoma and contributes to esophageal carcinogenesis via chromosome instability.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Cell Transformation, Neoplastic / metabolism. Esophageal Neoplasms / enzymology. Esophagus / enzymology. Protein-Serine-Threonine Kinases / biosynthesis
  • [MeSH-minor] Aurora Kinase A. Aurora Kinases. Carcinoma in Situ / enzymology. Carcinoma in Situ / pathology. Cell Nucleus Size. Gastric Mucosa / enzymology. Gastric Mucosa / pathology. Humans. Immunohistochemistry. Intestinal Mucosa / enzymology. Intestinal Mucosa / pathology. Metaplasia. Mucous Membrane / enzymology. Mucous Membrane / pathology. Oligonucleotide Array Sequence Analysis. Retrospective Studies. Tumor Suppressor Protein p53 / biosynthesis

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20656315.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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53. Maqani N, Belkhiri A, Moskaluk C, Knuutila S, Dar AA, El-Rifai W: Molecular dissection of 17q12 amplicon in upper gastrointestinal adenocarcinomas. Mol Cancer Res; 2006 Jul;4(7):449-55
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  • DNA amplification at 17q is frequently detected in upper gastrointestinal adenocarcinomas (UGC; stomach and esophagus).
  • In this study, we did fluorescence in situ hybridization on a tissue microarray that contained 304 UGCs and 89 normal stomach samples using a approximately 168-kb BAC clone (CTD-2019C10) that maps to 17q12-q21.1.
  • Adenocarcinomas of gastroesophageal junction and lower esophagus had the highest frequency of amplification (45%) compared with stomach tumors (27%; P = 0.04).
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 17 / genetics. Esophageal Neoplasms / genetics. Stomach Neoplasms / genetics
  • [MeSH-minor] Female. Gene Amplification. Gene Dosage. Humans. In Situ Hybridization, Fluorescence / methods. Male. Neoplasm Staging. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods


54. Thomas T, Singh R, Ragunath K: Trimodal imaging-assisted endoscopic mucosal resection of early Barrett's neoplasia. Surg Endosc; 2009 Jul;23(7):1609-13
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  • Trimodal imaging endoscopy is useful in identifying early neoplasia in Barrett's esophagus.
  • RESULTS: Sixteen patients were included: 13 patients had high-grade intraepithelial neoplasia (HGIN); 3 patients had intramucosal carcinoma (IMC); (8 males, median age, 69.5 (range, 50-77) years with Barrett's esophagus (interquartile range (IQR), 2-5 cm; median length, 3 cm).
  • CONCLUSIONS: Trimodal imaging endoscopy is a feasible alternative to chromoendoscopy to identify inconspicuous neoplasia and assist EMR of early neoplasia in Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / pathology. Carcinoma in Situ / surgery. Esophageal Neoplasms / surgery. Esophagoscopy / methods. Fluorometry / methods. Video-Assisted Surgery / methods

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  • (PMID = 19296171.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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55. Gossner L: The role of endoscopic resection and ablation therapy for early lesions. Best Pract Res Clin Gastroenterol; 2006;20(5):867-76
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  • The choice of the different available techniques depends on the site, the macroscopic type of the tumour and the personal experience of the endoscopist.
  • A recently described method of EMR comprises the circumferential mucosal incision with a special type of needle-knife and subsequent en-bloc resection following prior injection under the lesions, but only a few patients with early Barrett's cancer were treated so far.
  • EMR should be considered as the treatment of choice for high-grade intraepithelial neoplasia (HGIN) and mucosal adenocarcinoma in Barrett's oesophagus.
  • Photodynamic therapy and other ablation therapies, although they are comparably effective, have a decisive disadvantage in comparison with ER: they lack the opportunity for histological processing of the resected specimen and therefore, provide no information regarding the depth of invasion of the individual layers of the oesophageal wall, and regarding radicality of the resection.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Catheter Ablation. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagoscopy
  • [MeSH-minor] Barrett Esophagus / complications. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Carcinoma in Situ / etiology. Carcinoma in Situ / pathology. Carcinoma in Situ / surgery. Humans. Neoplasm Staging

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  • (PMID = 16997166.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 33
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56. van Duin M, van Marion R, Vissers KJ, Hop WC, Dinjens WN, Tilanus HW, Siersema PD, van Dekken H: High-resolution array comparative genomic hybridization of chromosome 8q: evaluation of putative progression markers for gastroesophageal junction adenocarcinomas. Cytogenet Genome Res; 2007;118(2-4):130-7
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  • It is usually detected in high-grade, high-stage GEJ adenocarcinomas.
  • Of the 37 specimens, 21 originated from the esophagus and 16 were derived from the gastric cardia.
  • Significant overexpression was found for MYC and EXT1 in GEJ adenocarcinoma cell lines and xenografts compared to normal controls.
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 8. Esophageal Neoplasms / genetics. Esophagogastric Junction / pathology. Nucleic Acid Conformation. Stomach Neoplasms / genetics
  • [MeSH-minor] Disease Progression. Humans. In Situ Hybridization, Fluorescence. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 18000363.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / RNA, Messenger
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57. Izzo JG, Luthra R, Wu TT, Correa AM, Luthra M, Anandasabapathy S, Chao KS, Hung MC, Aggarwal B, Hittelman WN, Ajani JA: Molecular mechanisms in Barrett's metaplasia and its progression. Semin Oncol; 2007 Apr;34(2 Suppl 1):S2-6
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  • The dramatic increase in the incidence and poor overall survival rates of esophageal/gastroesophageal junction adenocarcinoma underscore the necessity to discover molecular markers that can be used for risk assessment, early diagnosis, and targeted therapeutic intervention.
  • Barrett's esophagus (BE) is proposed to represent a precursor of esophageal/gastroesophageal junction adenocarcinoma.
  • Using a combination of in situ tissue-based and high-throughput analyses, we investigated alterations of cell-cycle regulators and inflammation-associated molecular effectors.
  • [MeSH-major] Barrett Esophagus / pathology. Biomarkers, Tumor / analysis. Esophageal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Cell Transformation, Neoplastic / pathology. Chemoprevention. Cyclin D1 / physiology. Disease Progression. Early Diagnosis. Humans. Metaplasia. NF-kappa B / physiology. Risk Assessment. Signal Transduction / physiology. Treatment Outcome

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  • (PMID = 17449347.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 86390; United States / NIDCR NIH HHS / DE / R01 DE 13157-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / NF-kappa B; 136601-57-5 / Cyclin D1
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58. Marx AH, Zielinski M, Kowitz CM, Dancau AM, Thieltges S, Simon R, Choschzick M, Yekebas E, Kaifi JT, Mirlacher M, Atanackovic D, Brümmendorf TH, Fiedler W, Bokemeyer C, Izbicki JR, Sauter G: Homogeneous EGFR amplification defines a subset of aggressive Barrett's adenocarcinomas with poor prognosis. Histopathology; 2010 Sep;57(3):418-26
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  • The aim of this study was performed to determine the potential impact of tumour heterogeneity on anti-EGFR therapy in Barrett's adenocarcinoma (BAC).
  • METHODS AND RESULTS: Tissue microarray (TMA) sections of 112 BAC and 45 lymph node metastases were analysed for EGFR amplification and expression using fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC).
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Gene Amplification. Receptor, Epidermal Growth Factor / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Lymph Nodes / pathology. Male. Middle Aged. Prognosis

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  • [Copyright] © 2010 Blackwell Publishing Limited.
  • (PMID = 20840671.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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59. Jaiswal K, Lopez-Guzman C, Souza RF, Spechler SJ, Sarosi GA Jr: Bile salt exposure increases proliferation through p38 and ERK MAPK pathways in a non-neoplastic Barrett's cell line. Am J Physiol Gastrointest Liver Physiol; 2006 Feb;290(2):G335-42
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  • [Title] Bile salt exposure increases proliferation through p38 and ERK MAPK pathways in a non-neoplastic Barrett's cell line.
  • Bile reflux has been implicated in the neoplastic progression of Barrett's esophagus (BE).
  • Bile salts increase proliferation in a Barrett's-associated adenocarcinoma cell line (SEG-1 cells) by activating ERK and p38 MAPK pathways.
  • However, it is not clear that these findings in cancer cells are applicable to non-neoplastic cells of benign BE.
  • We examined the effect of bile salts on three human cell lines: normal esophageal squamous (NES) cells, non-neoplastic Barrett's cells (BAR cells), and SEG-1 cells.
  • In conclusion, in a non-neoplastic Barrett's cell line, GCDA exposure induces proliferation by activation of both ERK and p38 MAPK pathways.
  • [MeSH-major] Barrett Esophagus / metabolism. Bile Acids and Salts / pharmacology. Mitogen-Activated Protein Kinases / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Annexin A5 / metabolism. Antimetabolites. Apoptosis / drug effects. Blotting, Western. Bromodeoxyuridine. Cell Count. Cell Line. Cell Line, Tumor. Cell Proliferation / drug effects. Esophageal Neoplasms / metabolism. Esophagus / cytology. Esophagus / drug effects. Esophagus / metabolism. Humans. In Situ Nick-End Labeling. Phosphorylation

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  • (PMID = 16239404.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-63621
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antimetabolites; 0 / Bile Acids and Salts; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; G34N38R2N1 / Bromodeoxyuridine
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60. Bonde P, Gao D, Chen L, Miyashita T, Montgomery E, Harmon JW, Wei C: Duodenal reflux leads to down regulation of DNA mismatch repair pathway in an animal model of esophageal cancer. Ann Thorac Surg; 2007 Feb;83(2):433-40; discussion 440
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  • [Title] Duodenal reflux leads to down regulation of DNA mismatch repair pathway in an animal model of esophageal cancer.
  • BACKGROUND: Gastroduodenal reflux is implicated in esophageal carcinogenesis.
  • We tested the effect of reflux, either alone or in combination with the human dietary mutagen methyl-n-amyl nitrosamine (MNAN), on DNA damage in adenocarcinoma and squamous cell cancer of the esophagus in a rat model.
  • RESULTS: Tumors (adenocarcinoma) developed in 15 (50%) of 30 animals with reflux alone; this increased to 26 (86.6%) of 30 when reflux was combined with MNAN treatment, with tumor histology consistent with adenosquamous and squamous cell cancer.
  • This pathway has an important role in esophageal carcinogenesis in rats.
  • [MeSH-major] Adenocarcinoma / etiology. Carcinoma, Squamous Cell / etiology. DNA Mismatch Repair. Down-Regulation. Duodenogastric Reflux / complications. Duodenogastric Reflux / genetics. Esophageal Neoplasms / etiology
  • [MeSH-minor] Animals. Apoptosis. Carcinogens. Caspases / metabolism. Cytochromes c / metabolism. DNA Damage. DNA Repair Enzymes / metabolism. Guanosine / analogs & derivatives. Guanosine / metabolism. In Situ Nick-End Labeling. Male. Nitrosamines. Rats. Rats, Sprague-Dawley. Staining and Labeling

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  • (PMID = 17257966.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 12133JR80S / Guanosine; 13256-07-0 / N-amyl-N-methylnitrosamine; 3868-31-3 / 8-hydroxyguanosine; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspases; EC 6.5.1.- / DNA Repair Enzymes
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61. Schiffman SC, Li Y, Dryden G, Li X, Martin RC: Positive correlation of image analysis by mini-endoscopy with micro-PET scan and histology in rats after esophagoduodenal anastomosis. Surg Endosc; 2010 Nov;24(11):2835-41

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  • In previous studies we have used micro-PET scan to analyze the esophageal adenocarcinoma (EAC) transformation in an intact rat model of esophagoduodenal anastomosis (EDA), in which intestinal metaplasia and EAC were reproduced successfully.
  • RESULTS: The endoscope provided visualization of the entire esophageal tract and upper stomach, with the smallest detectable lesion being 0.5 mm in diameter.
  • Mini-endoscopy was performed regularly and was tolerated without any significant procedure-related alterations in the esophageal tract.
  • The visualized esophageal lesion correlated well with the micro-PET image and the histological changes in the EDA rats.
  • CONCLUSIONS: The new mini-endoscope constitutes a practical and reliable tool for diagnosis and regular follow-up of the esophagus in rats.
  • Lesions identified by endoscopic observation were consistent with the changes found in the micro-PET scan, histopathology, and alteration of cellular and molecular events in esophageal mucosa.
  • [MeSH-major] Duodenum / pathology. Duodenum / surgery. Esophagoscopy. Esophagus / pathology. Esophagus / surgery. Positron-Emission Tomography
  • [MeSH-minor] Anastomosis, Surgical. Animals. Apoptosis. Cell Proliferation. Esophagoscopes. Fluorodeoxyglucose F18. In Situ Nick-End Labeling. Miniaturization. Radiopharmaceuticals. Rats. Rats, Sprague-Dawley

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  • (PMID = 20440518.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA127801-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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62. Kibria R, Akram S, Moezzi J, Ali S: Esophageal squamous papillomatosis with dysplasia. Is there a role of balloon-based radiofrequency ablation therapy? Acta Gastroenterol Belg; 2009 Jul-Sep;72(3):373-6
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  • [Title] Esophageal squamous papillomatosis with dysplasia. Is there a role of balloon-based radiofrequency ablation therapy?
  • Esophageal squamous papillomatosis (ESP) is a rare condition, occurring in an estimated 0.01-0.097% in data from upper gastrointestinal endoscopies and autopsy series.
  • Photodynamic therapy (PDT) has been successfully used to treat Barrett's esophagus as well as superficial adenocarcinoma.
  • In recent clinical trials, it has shown great promise in treating Barrett's esophagus with high-grade dysplasia.
  • Clinical symptoms resolved after the first therapy session, however, ablation therapy was terminated early because squamous cell carcinoma in-situ was detected on surveillance endoscopy prior to the fourth therapy session.
  • [MeSH-major] Catheter Ablation. Esophageal Neoplasms / surgery. Papilloma / surgery

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  • (PMID = 19902876.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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63. Jouret-Mourin A, Sempoux C, Duc KH, Geboes K: Usefulness of histopathological markers in diagnosing Barrett's intraepithelial neoplasia (dysplasia). Acta Gastroenterol Belg; 2009 Oct-Dec;72(4):425-32
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  • The incidence of oesophageal adenocarcinoma has significantly increased in Europe over the last 30 years.
  • The progression from normal mucosa to adenocarcinoma has been associated with genetic and morphological traits regrouped under the term "intraepithelial neoplasia" (IEN) according to the Vienna classification.
  • Discrepancies between high grade IEN and adenocarcinoma can be minimized by using the Vienna classification, which groups both of these lesions under the "stage IV".
  • Erroneous and overstated diagnosis of low grade IEN induces an unnecessary follow-up of patients with obvious psychological and economic consequences.
  • Because of these interpretation problems, scientists have looked for non-morphological criteria to confirm the pre-cancerous state.
  • [MeSH-major] Barrett Esophagus / pathology. Biomarkers, Tumor / analysis. Carcinoma in Situ / pathology. Esophageal Neoplasms / pathology

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  • (PMID = 20163037.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  • [Number-of-references] 42
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64. Yang Y, Fruehauf J, Xiang S, Li CJ: Genomic instability in precancerous lesions before inactivation of tumor suppressors p53 and APC in patients. Cell Cycle; 2006 Jul;5(13):1443-7
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  • Precancerous Barrett's esophagus (BE) provides a clinical model to investigate GIN in cancer progression.
  • We analyzed specimens from endoscopic biopsies or esophagectomies in patients with BE (ten cases, including five cases with multilayered epithelium (ME)), BE-associated esophageal adenocarcinoma (ten cases), or with normal gastro-esophageal junction (five cases).
  • Chromosomal enumeration probe Cep 7, 11, 12, 17 and 18 were detected by fluorescence in situ hybridization (FISH).
  • Increased p53 expression, a measurement of p53 mutations, was observed in BE with high grade dysplasia (HGD) and in BE-associated esophageal cancer (EC).
  • [MeSH-minor] Chromosomes, Human. Gene Expression. Humans. In Situ Hybridization, Fluorescence

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  • (PMID = 16855398.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Tumor Suppressor Protein p53
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65. Dreilich M, Wanders A, Brattström D, Bergström S, Hesselius P, Wagenius G, Bergqvist M: HER-2 overexpression (3+) in patients with squamous cell esophageal carcinoma correlates with poorer survival. Dis Esophagus; 2006;19(4):224-31
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  • [Title] HER-2 overexpression (3+) in patients with squamous cell esophageal carcinoma correlates with poorer survival.
  • The incidence of esophageal carcinoma is increasing worldwide.
  • The present study retrospectively investigates survival in 97 patients with esophageal carcinoma in regard to their HER-2 status as examined by immunohistochemistry (IHC) and chromogen in situ hybridization (CISH).
  • Eight (30%) of 27 adenocarcinoma patients overexpressed (3+) HER-2.
  • In squamous cell carcinoma patients, HER-2 overexpression (3+) correlated with poorer survival (P = 0.035), whereas in adenocarcinoma patients, HER-2 status (3+) did not.
  • In conclusion, HER-2 overexpression (3+) seems to be associated with poorer survival in esophageal carcinomas, especially in patients with squamous cell esophageal carcinoma.

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  • (PMID = 16866851.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, ErbB-2
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66. Li Y, Reuter NP, Li X, Liu Q, Zhang J, Martin RC: Colocalization of MnSOD expression in response to oxidative stress. Mol Carcinog; 2010 Jan;49(1):44-53
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  • The loss of manganese superoxide dismutase function has been associated with increased incidence of Barrett's esophagus and esophageal adenocarcinoma.
  • In previous studies, we have demonstrated that loss of MnSOD resulted in severe esophageal damage by both endogenous and exogenous bile.
  • However, the alterative manner of MnSOD in esophageal epithelium is largely unknown.
  • In this study, we investigated the expression and localization of MnSOD in response to the exposure to bile salts in an esophageal epithelial cell line.
  • Immunocytochemical staining demonstrated that esophageal epithelial cell underwent morphological alteration and MnSOD relocalization after bile salts treatment.
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Line. Cell Proliferation / drug effects. Cytosol / drug effects. Cytosol / enzymology. Esophagus / cytology. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Mitochondria / drug effects. Mitochondria / enzymology. Taurocholic Acid / pharmacology

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  • [Copyright] 2009 Wiley-Liss, Inc.
  • (PMID = 19623544.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 5E090O0G3Z / Taurocholic Acid; EC 1.15.1.1 / Superoxide Dismutase
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67. Zhang H, Jin Y, Chen X, Jin C, Law S, Tsao SW, Kwong YL: Papillomavirus type 16 E6/E7 and human telomerase reverse transcriptase in esophageal cell immortalization and early transformation. Cancer Lett; 2007 Jan 8;245(1-2):184-94
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  • [Title] Papillomavirus type 16 E6/E7 and human telomerase reverse transcriptase in esophageal cell immortalization and early transformation.
  • Infection with high-risk human papillomavirus (HPV) has been implicated in the pathogenesis of esophageal squamous cell carcinoma, and up-regulation of telomerase in esophageal adenocarcinoma.
  • We immortalized normal esophageal epithelial cells by over-expression of the HPV16 E6/E7 and human telomerase reverse transcriptase (hTERT) genes.
  • Fluorescence in situ hybridization showed that the Aurora-A gene locus was amplified in E6E7 immortalized cells, which might account in part for the Aurora-A over-expression.
  • E6E7 and hTERT immortalized esophageal cells recapitulated many of the molecular changes observed in esophageal carcinomas, where RB and p53 are frequently down-regulated.
  • However, down-regulation of p16 and p21 occurred frequently in esophageal cancer, owing to aberrant gene promoter methylation.
  • In addition to supporting the role of HPV and telomerase in esophageal carcinogenesis, our cell lines may also be useful in vitro models for further studies of esophageal carcinogenesis.
  • [MeSH-minor] Aurora Kinases. Blotting, Western. Cadherins / genetics. Cell Cycle / drug effects. Cells, Cultured. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. DNA Methylation. Esophagus / cytology. Esophagus / metabolism. Flow Cytometry. Gene Amplification. Gene Expression Regulation, Neoplastic. Humans. In Situ Hybridization, Fluorescence. Nocodazole / pharmacology. Papillomavirus E7 Proteins. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. Transfection. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / genetics

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  • (PMID = 16488074.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cadherins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / E6 protein, Human papillomavirus type 16; 0 / Oncogene Proteins, Viral; 0 / Papillomavirus E7 Proteins; 0 / RASSF1 protein, human; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / oncogene protein E7, Human papillomavirus type 16; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; SH1WY3R615 / Nocodazole
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68. Pohl H, Aschenbeck J, Drossel R, Schröder A, Mayr M, Koch M, Rothe K, Anders M, Voderholzer W, Hoffmann J, Schulz HJ, Liehr RM, Gottschalk U, Wiedenmann B, Rösch T: Endoscopy in Barrett's oesophagus: adherence to standards and neoplasia detection in the community practice versus hospital setting. J Intern Med; 2008 Oct;264(4):370-8
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  • Only 13% were found during surveillance, but 57% were diagnosed at an early stage.
  • Despite a generally poor adherence to guidelines, most neoplasias found were at an early and potentially curable stage.
  • [MeSH-major] Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Esophagoscopy / standards. Guideline Adherence / standards
  • [MeSH-minor] Adenocarcinoma / pathology. Age Factors. Aged. Berlin. Carcinoma in Situ / pathology. Community Health Services / standards. Family Practice / standards. Female. Hospitals. Humans. Logistic Models. Male. Middle Aged. Precancerous Conditions / diagnosis. Retrospective Studies

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  • (PMID = 18482289.001).
  • [ISSN] 1365-2796
  • [Journal-full-title] Journal of internal medicine
  • [ISO-abbreviation] J. Intern. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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69. Onwuegbusi BA, Aitchison A, Chin SF, Kranjac T, Mills I, Huang Y, Lao-Sirieix P, Caldas C, Fitzgerald RC: Impaired transforming growth factor beta signalling in Barrett's carcinogenesis due to frequent SMAD4 inactivation. Gut; 2006 Jun;55(6):764-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND AND AIMS: Transforming growth factor beta (TGF-beta) is frequently involved in gastrointestinal carcinogenesis although its contribution to oesophageal adenocarcinoma (AC) and its precursor Barrett's oesophageal epithelium (BE) metaplasia are unclear.
  • METHODS: Expression of TGF-beta signalling components was assessed by reverse transcription-polymerase chain reaction (PCR), western blot, and immunohistochemistry in oesophageal endoscopic biopsies and cell lines.
  • Genomic alterations in SMAD4 were characterised by fluorescence in situ hybridisation, methylation specific PCR, and sequencing.
  • RESULTS: smad4 mRNA expression was progressively reduced in the metaplasia-dysplasia-adenocarcinoma sequence (p<0.01).
  • In 6/8 oesophageal cell lines, chromosomal rearrangements affected the smad4 locus.
  • TGF-beta failed to inhibit proliferation in 5/8 oesophageal cell lines.
  • [MeSH-major] Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Precancerous Conditions / metabolism. Smad4 Protein / metabolism. Transforming Growth Factor beta / physiology
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Base Sequence. Cell Proliferation. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. DNA Methylation. Disease Progression. Gene Expression Regulation, Neoplastic. Genome. Humans. Molecular Sequence Data. Neoplasm Proteins / metabolism. Prospective Studies. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Signal Transduction. Transfection. Tumor Cells, Cultured

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  • (PMID = 16368780.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Smad4 Protein; 0 / Transforming Growth Factor beta
  • [Other-IDs] NLM/ PMC1856235
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70. Anandasabapathy S: Novel Endoscopic Techniques for the Detection of Barrett's Dysplasia. Gastrointest Cancer Res; 2008 Mar;2(2):81-4
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  • Barrett's esophagus is highly prevalent in the US population and is the only known precursor of esophageal adenocarcinoma, one of the most lethal and increasingly common cancers in the developed world.
  • Over the past 4 decades, the incidence of esophageal adenocarcinoma has increased some 300% to 500%.
  • This dramatic trend has sparked tremendous interest in the early diagnosis of Barrett's dysplasia.
  • The diagnosis of dysplasia and early cancer in Barrett's esophagus presents a number of challenges.
  • Emerging technologies in the field of endoscopic microscopy and spectroscopy offer the potential for visual biopsies-real-time, in-situ diagnoses that can be rendered without removing tissue.
  • Used as an adjunct to standard white-light endoscopy, these technologies may enhance the detection of dysplasia and early cancer, thus offering the potential for early diagnosis and improved survival.
  • This article reviews the current status of these novel, optical-based diagnostic technologies and their emerging role in the endoscopic detection of esophageal neoplasia.

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  • (PMID = 19259299.001).
  • [ISSN] 1934-7820
  • [Journal-full-title] Gastrointestinal cancer research : GCR
  • [ISO-abbreviation] Gastrointest Cancer Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2630821
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71. Bergman JJ, Tytgat GN: New developments in the endoscopic surveillance of Barrett's oesophagus. Gut; 2005 Mar;54 Suppl 1:i38-42
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patients with a Barrett's oesophagus are at risk for developing an adenocarcinoma of the distal oesophagus.
  • Therefore, many patients undergo endoscopic surveillance to detect dysplasia and/or cancer at an early and curable stage.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Esophagoscopy / methods. Precancerous Conditions / diagnosis
  • [MeSH-minor] Biomarkers / analysis. Esophagus / pathology. Humans. In Situ Hybridization, Fluorescence / methods

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  • (PMID = 15711007.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers
  • [Number-of-references] 27
  • [Other-IDs] NLM/ PMC1867795
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72. Haveri H, Westerholm-Ormio M, Lindfors K, Mäki M, Savilahti E, Andersson LC, Heikinheimo M: Transcription factors GATA-4 and GATA-6 in normal and neoplastic human gastrointestinal mucosa. BMC Gastroenterol; 2008;8:9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Samples of normal and neoplastic gastrointestinal tract from children and adults were subjected to RNA in situ hybridization with 33P labelled probes and immunohistochemistry, using an avidin-biotin immunoperoxidase system.
  • Both factors were also present in Barrett's esophagus and metaplasia of the stomach.
  • [MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. Colonic Neoplasms / genetics. GATA4 Transcription Factor / metabolism. GATA6 Transcription Factor / metabolism. Gastric Mucosa / metabolism. Rectal Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Barrett Esophagus / genetics. Barrett Esophagus / pathology. Biopsy. Child. Child, Preschool. Esophagus / metabolism. Esophagus / pathology. Gastritis / genetics. Gastritis / pathology. Gastritis, Atrophic / genetics. Gastritis, Atrophic / pathology. Humans. Immunohistochemistry. Infant. Middle Aged. RNA, Messenger / analysis

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  • (PMID = 18405344.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GATA4 Transcription Factor; 0 / GATA6 Transcription Factor; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2323380
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73. Wehrmann T, Müller M, Arnold R, Sendler A: [Early Barrett's carcinoma/high grade intraepithelial neoplasia (HG-IEN): pro endoscopic treatment--pro surgical treatment]. Z Gastroenterol; 2009 Jun;47(6):583-91
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The incidence of adenocarcinoma of the oesophagus developing within Barrett's mucosa has substantially risen in the past few years.
  • Therefore, patients with HG-IEN or early Barrett's carcinoma of the esophagus should be recruited into controlled studies and be treated in specialised high-volume centres.
  • [MeSH-major] Barrett Esophagus / surgery. Carcinoma in Situ / surgery. Endoscopy / methods. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagectomy / methods

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  • (PMID = 19533549.001).
  • [ISSN] 1439-7803
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 62
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74. Javle MM, Nwogu CE, Donohue KA, Iyer RV, Brady WE, Khemka SV, Smith JL, Demmy TL, Yang GY, Nava HR: Management of locoregional stage esophageal cancer: a single center experience. Dis Esophagus; 2006;19(2):78-83
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of locoregional stage esophageal cancer: a single center experience.
  • Therapeutic options for locoregional esophageal cancer (EC) include primary surgery, neoadjuvant or definitive chemoradiation and systemic chemotherapy.
  • We conducted a retrospective analysis of 172 patients with locoregional (AJCC stages I-III) EC treated at RPCI between February 14, 1990 and September 20, 2002.
  • There were 100 regional (stages IIB-III), 69 local (stages I-IIA) and three in situ cases.
  • Median survival for all patients was 25.3 months and was better for local stage with surgery alone (75 months) than with neoadjuvant (35.7 months) or definitive chemoradiation (19.1 months, P < 0.001).
  • Patients with locoregional esophageal cancer who are eligible for surgical resection either alone or as a part of multimodal therapy may have better outcomes than those treated with non-surgical approaches.

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  • (PMID = 16643174.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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75. Huang Q, Hardie LJ: Biomarkers in Barrett's oesophagus. Biochem Soc Trans; 2010 Apr;38(2):343-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Biomarkers are needed to screen multiple stages in the clinical pathway of Barrett's oesophagus patients; from disease diagnosis to risk stratification and predicting response to therapy.
  • Biomarkers are also being developed to improve detection of high-grade dysplasia and oesophageal adenocarcinoma, utilizing brush cytology combined with FISH (fluorescence in situ hybridization), and to assess therapeutic success and risk of complication during photodynamic therapy.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / genetics. Biomarkers / analysis

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  • (PMID = 20298180.001).
  • [ISSN] 1470-8752
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / C11347
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Pharmacological
  • [Number-of-references] 50
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76. Hage M, Siersema PD, Vissers KJ, Steyerberg EW, Haringsma J, Kuipers EJ, van Dekken H: Molecular evaluation of ablative therapy of Barrett's oesophagus. J Pathol; 2005 Jan;205(1):57-64
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Barrett's oesophagus is a major risk factor for developing oesophageal adenocarcinoma.
  • The premalignant potential of residual or recurring Barrett's oesophagus was assessed by p53 immunohistochemistry, Ki67-related proliferative capacity, and DNA ploidy status (ie an abnormal chromosome 1 number) as measured by interphase in situ hybridization.
  • Persistent Barrett's oesophagus may still harbour molecular aberrations and must therefore be considered still to be at risk of progression to adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / therapy. Esophageal Neoplasms / therapy. Laser Coagulation. Photochemotherapy. Precancerous Conditions / therapy

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  • (PMID = 15586364.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53
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77. Yannopoulos P, Theodoridis P, Manes K: Esophagectomy without thoracotomy: 25 years of experience over 750 patients. Langenbecks Arch Surg; 2009 Jul;394(4):611-6
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PATIENTS AND METHODS: This is a retrospective analysis of all THE operations performed between January 1981 until May 2007 in 750 patients: 60 patients (8%) had benign lesions, while 690 (92%) had malignant ones (5.2% of malignancies were located in the upper esophagus, 7.4% in the middle esophagus, 19% in the lower esophagus, and 68.4% at the cardioesophageal junction).
  • THE and esophageal reconstruction were performed at the same operation in all patients.
  • The stomach was our esophageal substitute of first choice with the colon and jejunum being acceptable alternatives in patients with prior gastric surgery and those necessitating synchronous gastrectomy for cancer invasion.
  • A gastric tube was used as an esophageal substitute in 624 patients (83.2%), the whole stomach in 70 (9.4%), the colon in 43 (5.73%), and a jejunal loop in 13 (1.73%).
  • CONCLUSION: THE is a safe and effective method of esophageal resection with low morbidity and mortality rates and good functional results when performed by experienced surgeons.
  • We believe that our strategies concerning the way of dissecting the cervical esophagus, avoidance of performing pyloromyotomy, the delayed removal of the cervical drain and the delayed advance to oral feeding have reduced, noticeably, morbidity and mortality in our series.

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  • (PMID = 19350267.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2687514
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78. Li Y, Wo JM, Su RR, Ray MB, Jones W, Martin RC: Esophageal injury with external esophageal perfusion. J Surg Res; 2005 Nov;129(1):107-13
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Esophageal injury with external esophageal perfusion.
  • BACKGROUND: External esophageal perfusion (EEP) with the idea that esophageal perfusion can be controlled with a single ingredient at a constant rate and concentration, might be used to dissect the injurious role of gastro-duodenal secretions for the progression from esophagitis to Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC).
  • The apoptotic index, the proliferating index, and expression of 8-OH-dG were significantly increased in the esophageal mucosa compared to controls.
  • CONCLUSIONS: The external esophageal perfusion model enabled precise control of the injurious agent.
  • Further studies are needed to induce Barrett's esophagus and esophageal adenocarcinoma.
  • [MeSH-major] Bile. Esophagitis, Peptic / pathology. Esophagus / pathology. Perfusion
  • [MeSH-minor] Animals. Apoptosis. Cell Division. Deoxyguanosine / analogs & derivatives. Deoxyguanosine / analysis. Gastric Juice / chemistry. Hypertrophy. Immunohistochemistry. In Situ Nick-End Labeling. Mucous Membrane / pathology. Rats. Rats, Sprague-Dawley. Superoxide Dismutase / analysis. Time Factors

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  • (PMID = 15921698.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; EC 1.15.1.1 / Superoxide Dismutase; G9481N71RO / Deoxyguanosine
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79. Monnier P, Jaquet Y, Radu A, Pilloud R, Grosjean P, Escher A, Piotet E, Blant SA: Extensive (8 to 12 cm2) noncircumferential endoscopic mucosal resection for early esophageal cancer. Ann Thorac Surg; 2010 Jun;89(6):S2151-5
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extensive (8 to 12 cm2) noncircumferential endoscopic mucosal resection for early esophageal cancer.
  • BACKGROUND: Endoscopic mucosal resection (EMR) is an appealing method for treating intramucosal esophageal cancer but must comply with the following stringent requirements: proper preoperative staging, complete resection of the lesion, obtaining a resected specimen for histologic analysis of safety margins, and squamous reepithelialization without stricture formation.
  • METHODS: A rigid esophagoscope was created to resect up to 12 cm(2) of esophageal mucosa in a single specimen and at a constant depth through the submucosa.
  • Under visual control, the esophageal mucosa is sucked into a transparent window and resected with a thin diathermy wire loop in 10 seconds.
  • Deep safety margins were clear in 19 of 21 resected specimens (2 patients, unfit for operations, had submucosal invasion of squamous cell carcinoma and adenocarcinoma, respectively).
  • CONCLUSIONS: Large EMRs of 12 cm(2) can safely be performed at the submucosal level in the esophagus.
  • [MeSH-major] Carcinoma in Situ / surgery. Carcinoma, Squamous Cell / surgery. Esophageal Neoplasms / surgery. Esophagoscopy / methods

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  • [Copyright] 2010 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20494000.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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80. Barnett BP, Sheth S, Ali SZ: Cytopathologic analysis of paratracheal masses: a study of 737 cases with clinicoradiologic correlation. Acta Cytol; 2009 Nov-Dec;53(6):672-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Of the malignant cases, 45 (73%) were metastatic tumors: adenocarcinoma (ACA) 19, small cell carcinoma 12, squamous cell carcinoma (SQCC) 11 and other tumors, from lung 34, esophagus 4 and other sites.
  • Malignant neoplasms from local spread included lung non-small cell carcinoma 6, SQCC 3 and ACA 3, papillary thyroid carcinoma 3 and other 2.
  • The most common diagnosis is a malignant tumor (60%), with metastatic carcinoma (73%) the most common neoplasm (lung ACA the most common primary source).
  • Ancillary studies (immunoctyochemistry, fluorescence in situ hybridization and electron microscopy) were helpful and provided definitive diagnosis in 30% of the initially nondiagnostic FNA samples.

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  • (PMID = 20014557.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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81. Jasim ZF, Walsh MY, Armstrong DK: Subacute lupus erythematosus-like rash associated with oesophageal adenocarcinoma in situ. Clin Exp Dermatol; 2007 Jul;32(4):443-5
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subacute lupus erythematosus-like rash associated with oesophageal adenocarcinoma in situ.
  • [MeSH-major] Adenocarcinoma / complications. Esophageal Neoplasms / complications. Lupus Erythematosus, Cutaneous / complications

  • Genetic Alliance. consumer health - Lupus.
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  • (PMID = 17376201.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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82. Sträter J, Wiesmüller C, Perner S, Kuefer R, Möller P: Alpha-methylacyl-CoA racemase (AMACR) immunohistochemistry in Barrett's and colorectal mucosa: only significant overexpression favours a diagnosis of intraepithelial neoplasia. Histopathology; 2008 Feb;52(3):399-402
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-methylacyl-CoA racemase (AMACR) immunohistochemistry in Barrett's and colorectal mucosa: only significant overexpression favours a diagnosis of intraepithelial neoplasia.
  • [MeSH-major] Barrett Esophagus / enzymology. Carcinoma in Situ / enzymology. Colorectal Neoplasms / enzymology. Intestinal Mucosa / enzymology. Racemases and Epimerases / metabolism
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / enzymology. Adenoma / diagnosis. Adenoma / enzymology. Biomarkers, Tumor / metabolism. Colitis, Ulcerative / diagnosis. Colitis, Ulcerative / enzymology. Diagnosis, Differential. Humans. Immunohistochemistry

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  • (PMID = 18081815.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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