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1. Somerville M, Pitt M: Surveillance of Barrett's oesophagus: do we yet know whether it is worthwhile? Frontline Gastroenterol; 2010 Jul;1(2):88-93

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  • [Title] Surveillance of Barrett's oesophagus: do we yet know whether it is worthwhile?
  • In 2004, the Peninsula Technology Assessment Group developed an economic model to assess the effectiveness and cost effectiveness of surveillance of Barrett's oesophagus in preventing morbidity and mortality from oesophageal adenocarcinoma.
  • At present, there seems little reason to change our original conclusion that surveillance of Barrett's oesophagus is unlikely to be cost effective and a definitive answer may only be possible from clinical trials now in progress.
  • As newer endoscopic techniques for treating Barrett's oesophagus and adenocarcinoma become more widely used, however, conventional surveillance programmes may no longer be undertaken, and revised economic models will be needed to assess the cost effectiveness of the new clinical pathways.

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  • (PMID = 28839554.001).
  • [ISSN] 2041-4137
  • [Journal-full-title] Frontline gastroenterology
  • [ISO-abbreviation] Frontline Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
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2. Langer R, Specht K, Becker K, Ewald P, Bekesch M, Sarbia M, Busch R, Feith M, Stein HJ, Siewert JR, Höfler H: Association of pretherapeutic expression of chemotherapy-related genes with response to neoadjuvant chemotherapy in Barrett carcinoma. Clin Cancer Res; 2005 Oct 15;11(20):7462-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of pretherapeutic expression of chemotherapy-related genes with response to neoadjuvant chemotherapy in Barrett carcinoma.
  • EXPERIMENTAL DESIGN: Pretherapeutic, paraffin-embedded, formalin-fixed endoscopic esophageal tumor biopsies of 38 patients with locally advanced esophageal adenocarcinomas (Barrett adenocarcinoma) were included.
  • Additionally, investigation of intratumoral heterogeneity of gene expression of relevant genes (MTHFR, caldesmon, HER-2/neu, ERCC4, and MRP1), verified in nine untreated Barrett adenocarcinomas by examination of five distinct tumor areas, revealed no significant heterogeneity in gene expression indicating that expression profiles obtained from biopsy material may yield a representative genetic expression profile of total tumor tissue.
  • CONCLUSIONS: Our results indicate that determination of mRNA levels of few genes may be useful for the prediction of the success of neoadjuvant chemotherapy in individual cancer patients with locally advanced Barrett adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Gene Expression Regulation, Neoplastic

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  • (PMID = 16243820.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calmodulin-Binding Proteins; 0 / DNA-Binding Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / RNA, Messenger; 0 / multidrug resistance-associated protein 1; 0 / xeroderma pigmentosum group F protein; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); EC 2.7.10.1 / Receptor, ErbB-2; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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3. Rastogi A, Sharma P: Short-Segment Barrett's Esophagus and Adenocarcinoma. Gastroenterol Hepatol (N Y); 2006 Feb;2(2):134-139

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

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  • (PMID = 28286441.001).
  • [ISSN] 1554-7914
  • [Journal-full-title] Gastroenterology & hepatology
  • [ISO-abbreviation] Gastroenterol Hepatol (N Y)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Barrett’s esophagus / adenocarcinoma / high-grade dysplasia / long-segment Barrett’s esophagus / low-grade dysplasia / short-segment Barrett’s esophagus
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4. Ectors N, Driessen A, De Hertog G, Lerut T, Geboes K: Is adenocarcinoma of the esophagogastric junction or cardia different from Barrett adenocarcinoma? Arch Pathol Lab Med; 2005 Feb;129(2):183-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is adenocarcinoma of the esophagogastric junction or cardia different from Barrett adenocarcinoma?
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cardia / pathology. Esophageal Neoplasms / pathology. Esophagogastric Junction / pathology

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  • (PMID = 15679417.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 17
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5. Burnat G, Majka J, Konturek PC: Bile acids are multifunctional modulators of the Barrett's carcinogenesis. J Physiol Pharmacol; 2010 Apr;61(2):185-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bile acids are multifunctional modulators of the Barrett's carcinogenesis.
  • Bile salts play an important pathogenic role in the development of Barrett adenocarcinoma (BA).
  • The aim of the present study was to compare the effects of two different bile salts, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) on the expression of COX-2, CDX-2 and DNA repair enzymes (MUTYH, OGG-1) in the Barrett epithelial cancer cells (OE-19).
  • We conclude that bile salts are involved in the carcinogenesis of Barrett adenocarcinoma via inhibition of DNA repair enzymes and induction of COX-2 and this last effect is, at least partly, mediated by NF kappaB.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Barrett Esophagus / genetics. Barrett Esophagus / pathology. Cell Line, Tumor. Cyclooxygenase 2 / genetics. DNA Glycosylases / genetics. Down-Regulation. Homeodomain Proteins / genetics. Humans. NF-kappa B / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • (PMID = 20436219.001).
  • [ISSN] 1899-1505
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / NF-kappa B; 0 / RNA, Messenger; 005990WHZZ / Deoxycholic Acid; 724L30Y2QR / Ursodeoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase; EC 3.2.2.- / oxoguanine glycosylase 1, human
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6. DeMeester SR: Re: Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma. Hum Pathol; 2009 Aug;40(8):1208-9; author reply 1209-10
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  • [Title] Re: Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Cardia / pathology. Esophageal Neoplasms / diagnosis. Intestines / pathology

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  • [CommentOn] Hum Pathol. 2009 Jan;40(1):65-74 [18755496.001]
  • (PMID = 19616700.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
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7. Williams LJ, Guernsey DL, Casson AG: Biomarkers in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma. Curr Oncol; 2006 Feb;13(1):33-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biomarkers in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma.
  • Primary esophageal adenocarcinomas are thought to arise from Barrett esophagus, an acquired condition in which the normal esophageal squamous epithelium is replaced by a specialized metaplastic columnar-cell-lined epithelium.Today, gerd is recognized as an important risk factor in Barrett esophagus.
  • Progression of Barrett esophagus to invasive adenocarcinoma is reflected histologically by the metaplasia-dysplasia-carcinoma sequence.
  • Although several molecular alterations associated with progression of Barrett esophagus to invasive adenocarcinoma have been identified, relatively few will ultimately have clinical application.
  • Currently, the histologic finding of high-grade dysplasia remains the most reliable predictor of progression to invasive esophageal adenocarcinoma.
  • It is anticipated that models incorporating combinations of objective scores of sociodemographic and lifestyle risk factors (that is, age, sex, body mass index), severity of gerd, endoscopic and histologic findings, and a panel of biomarkers will be developed to better identify patients with Barrett esophagus at increased risk for malignant progression, leading to more rational endoscopic surveillance and screening programs.

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  • (PMID = 17576439.001).
  • [ISSN] 1198-0052
  • [Journal-full-title] Current oncology (Toronto, Ont.)
  • [ISO-abbreviation] Curr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC1891165
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8. Casson AG, Zheng Z, Evans SC, Veugelers PJ, Porter GA, Guernsey DL: Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma. Carcinogenesis; 2005 Sep;26(9):1536-41
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  • [Title] Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma.
  • To test the hypothesis that aberrations of DNA repair contribute to susceptibility for the progression of gastroesophageal reflux disease (GERD) into Barrett esophagus (BE) and esophageal adenocarcinoma (EADC), we studied the frequency of polymorphisms of selected DNA repair genes in patients with GERD (n = 126), BE (n = 125) and EADC (n = 56) enrolled in a 2-year prospective case-control study.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. DNA Repair / genetics. Esophageal Neoplasms / genetics. Polymorphism, Genetic

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  • (PMID = 15878910.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; 0 / X-ray repair cross complementing protein 3
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9. Takubo K, Aida J, Naomoto Y, Sawabe M, Arai T, Shiraishi H, Matsuura M, Ell C, May A, Pech O, Stolte M, Vieth M: Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma. Hum Pathol; 2009 Jan;40(1):65-74
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  • [Title] Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma.
  • Many publications focusing on the background or original mucosa of Barrett adenocarcinoma have maintained that adenocarcinoma arises in intestinal-type mucosa with goblet cells in the columnar-lined esophagus, and this has become a central dogma.
  • The mucosa on each side of a series of 141 minute esophageal adenocarcinomas (almost all of which were mucosal carcinomas) resected by endoscopic mucosal resection was recorded as the background mucosa.
  • The present joint pathologic examination of the background mucosa of Barrett adenocarcinoma conducted by Japanese and German pathologists and gastroenterologists found that more than 70% of primary small adenocarcinomas (<2 cm) of the esophagus were adjacent to cardiac/fundic-type rather than intestinal-type mucosa.
  • In other words, there was no evidence to support the previously held view that Barrett adenocarcinoma is nearly always accompanied and preceded by intestinal-type mucosa.
  • Our study has demonstrated a close relationship between esophageal adenocarcinoma and cardiac-type mucosa.
  • Therefore, it is not proven histogenetically that the background mucosa of esophageal adenocarcinoma is the intestinal type.
  • Also, it seems better to define Barrett esophagus as metaplastic columnar-lined esophagus alone, without requiring the presence of goblet cells, in accordance with histogenetic and practical standpoints.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cardia / pathology. Esophageal Neoplasms / pathology. Intestines / pathology

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  • [CommentIn] Hum Pathol. 2009 Dec;40(12):1820 [19913679.001]
  • [CommentIn] Hum Pathol. 2009 Aug;40(8):1208-9; author reply 1209-10 [19616700.001]
  • [CommentIn] Hum Pathol. 2009 Aug;40(8):1206-7; author reply 1207-8 [19616698.001]
  • (PMID = 18755496.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. 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.
  • 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

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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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11. Konturek PC, Burnat G, Rau T, Hahn EG, Konturek S: Effect of adiponectin and ghrelin on apoptosis of Barrett adenocarcinoma cell line. Dig Dis Sci; 2008 Mar;53(3):597-605
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  • [Title] Effect of adiponectin and ghrelin on apoptosis of Barrett adenocarcinoma cell line.
  • BACKGROUND: Obesity is an important risk factor for Barrett adenocarcinoma.
  • However, the role of adiponectin (anti-inflammatory adipokine from adipose tissue) and ghrelin (orexigenic peptide gastric origin) on the progression of Barrett's carcinogenesis has not been investigated so far.
  • (1) to compare the expression of adiponectin and ghrelin receptors in Barrett's esophagus and in normal squamous epithelium;.
  • (2) to assess the effect of adiponectin and ghrelin on apoptosis in Barrett's adenocarcinoma cells in vitro; and (3) to investigate the effect of ghrelin on IL-1beta and COX-2 expression in OE-19 cells incubated with TNFalpha.
  • METHODS: The expression of ghrelin and adiponectin receptors (GHS-R1a, Adipo-R1, Adipo R-2) in biopsies from Barrett's esophagus and in Barrett's adenocarcinoma cell line OE-19 was assessed by quantitative RT-PCR (qRT-PCR).
  • At the mRNA level, the expression of adiponectin receptors (Adipo-R1, Adipo-R2) was decreased, and the expression of ghrelin receptor (GHS-R1a) was increased in Barrett's mucosa.
  • CONCLUSION: Adiponectin and ghrelin have an inhibitory effect on Barrett's carcinogenesis by two different mechanisms:.
  • The decrease in levels of these two peptides in obesity may explain the progression of Barrett's carcinoma in obese individuals.
  • [MeSH-major] Adenocarcinoma / metabolism. Apoptosis / physiology. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Receptors, Adiponectin / metabolism. Receptors, Ghrelin / metabolism

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  • (PMID = 17763959.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Culture Media; 0 / Ghrelin; 0 / Interleukin-1beta; 0 / Receptors, Adiponectin; 0 / Receptors, Ghrelin; 0 / Tumor Necrosis Factor-alpha; 005990WHZZ / Deoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2
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12. Rotimi O: Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma. Hum Pathol; 2009 Dec;40(12):1820

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cardiac rather than intestinal-type background in endoscopic resection specimens of minute Barrett adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cardia / pathology. Intestines / pathology

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  • [CommentOn] Hum Pathol. 2009 Jan;40(1):65-74 [18755496.001]
  • (PMID = 19913679.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
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13. Qazi A, Pal J, Maitah M, Fulciniti M, Pelluru D, Nanjappa P, Lee S, Batchu RB, Prasad M, Bryant CS, Rajput S, Gryaznov S, Beer DG, Weaver DW, Munshi NC, Goyal RK, Shammas MA: Anticancer activity of a broccoli derivative, sulforaphane, in barrett adenocarcinoma: potential use in chemoprevention and as adjuvant in chemotherapy. Transl Oncol; 2010 Dec 01;3(6):389-99
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  • [Title] Anticancer activity of a broccoli derivative, sulforaphane, in barrett adenocarcinoma: potential use in chemoprevention and as adjuvant in chemotherapy.
  • INTRODUCTION: The incidence of Barrett esophageal adenocarcinoma (BEAC) has been increasing at an alarming rate in western countries.

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  • (PMID = 21151478.001).
  • [ISSN] 1936-5233
  • [Journal-full-title] Translational oncology
  • [ISO-abbreviation] Transl Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA125711-04; United States / NCI NIH HHS / CA / R01 CA124929; United States / NCI NIH HHS / CA / R01 CA125711; United States / NCI NIH HHS / CA / R01 CA125711-04
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3000464
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14. Casson AG, Zheng Z, Porter GA, Guernsey DL: Genetic polymorphisms of microsomal epoxide hydroxylase and glutathione S-transferases M1, T1 and P1, interactions with smoking, and risk for esophageal (Barrett) adenocarcinoma. Cancer Detect Prev; 2006;30(5):423-31
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  • [Title] Genetic polymorphisms of microsomal epoxide hydroxylase and glutathione S-transferases M1, T1 and P1, interactions with smoking, and risk for esophageal (Barrett) adenocarcinoma.
  • BACKGROUND: The aim of this case-control study was to test the hypothesis that polymorphisms of the microsomal epoxide hydroxylase (mEH) and glutathione S-transferase (GST) genes modulate the susceptibility to esophageal adenocarcinoma (EADC) associated with smoking.
  • METHODS: Cases included patients with gastroesophageal reflux disease (GERD) (n=126), Barrett esophagus (BE) (n=125), and EADC (n=56); controls comprised 95 strictly asymptomatic individuals.
  • [MeSH-minor] Adenocarcinoma / genetics. Alleles. Barrett Esophagus / genetics. Case-Control Studies. Female. Gastroesophageal Reflux / genetics. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Risk Factors

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  • (PMID = 17064856.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1; EC 3.3.2.- / Epoxide Hydrolases
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15. Mafune K: [Barrett's adenocarcinoma]. Nihon Rinsho; 2005 Aug;63(8):1463-9
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  • [Title] [Barrett's adenocarcinoma].
  • Esophageal adenocarcinoma has seen a rapid increase in incidence throughout the Western world.
  • Gastroesophageal reflux disease is an important risk factor for this cancer that develops in patients with Barrett's esophagus, but infection with Helicobacter pylori may reduce the risk.
  • The diagnosis of Barrett's adenocarcinoma is often at an advanced stage and is generally associated with a poor prognosis.
  • Further evaluation is warranted to define the optimal method and standardize the procedures for diagnosis and management of Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control

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  • (PMID = 16101241.001).
  • [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 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 0 / Enzyme Inhibitors; 0 / Proton Pump Inhibitors
  • [Number-of-references] 44
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16. Andreu Garcia M: [Esophageal adenoma-carcinoma and Barrett's esophagus. Gastric adenocarcinoma and Helicobacter pylori]. Gastroenterol Hepatol; 2008 Oct;31 Suppl 4:66-9
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  • [Title] [Esophageal adenoma-carcinoma and Barrett's esophagus. Gastric adenocarcinoma and Helicobacter pylori].
  • [Transliterated title] Adenocarcinoma esfágico y esófago de Barrett. Adenocarcinoma gástrico y Helicobacter pylori.
  • In the meeting of the American Gastroenterological Association, notable among all the studies presented on the prevention and treatment of esophageal and gastric cancer were the following contributions: the use of clinical practice guidelines for the prevention and surveillance of Barrett's esophagus (BE) should be improved; treatment with proton pump inhibitors does not seem to reduce the risk of esophageal cancer; endoscopic therapy of intramucosal cancer through complete mucosal resection is effective; Helicobacter pylori eradication prevents the development of metachronous gastric cancer in patients treated for a first intramucosal adenocarcinoma through endoscopic resection; the risk of developing gastric cancer is 6 times higher in patients with mucosa-associated lymphoid tissue (MALT) lymphoma than in the general population; and photodynamic therapy may be an alternative for the treatment of "invisible" gastric adenocarcinoma, which should be followed-up endoscopically.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Helicobacter Infections / complications. Helicobacter pylori. Stomach Neoplasms / etiology


17. Jovanović I, Todorović V, Milosavljević T, Micev M, Pesko P, Bjelović M, Mouzas Y, Tzardi M: Expression of p53 protein in Barrett's adenocarcinoma and adenocarcinoma of the gastric cardia and antrum. Vojnosanit Pregl; 2005 Dec;62(12):879-85
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  • [Title] Expression of p53 protein in Barrett's adenocarcinoma and adenocarcinoma of the gastric cardia and antrum.
  • METHODS: The material comprised 66 surgical specimens; 10 were Barrett's carcinomas, 25 adenocarcinomas of the gastric cardia (type II adenocarcinoma of the esophagogastric junction - EGJ), and 31 adenocarcinomas of the antrum.
  • There was, however, a significant difference observed in the depth of tumour invasion between Barrett's adenocarcinoma and adenocarcinoma of the cardia compared with the adenocarcinoma of the antrum.
  • Namely, at the time of surgery, both Barrett's adenocarcinomas and adenocarcinomas of the cardia, were significantly more advanced comparing with the adenocarcinomas of the antrum.
  • Overexpression of p53 was found in 40% (4/10) of Barrett's adenocarcinomas, 72% (18/25) of adenocarcinoma of the cardia and 65% (20/31) of adenocarcinoma of the antrum.
  • Patients with more advanced Barrett's adenocarcinoma and in the cases of lymph node invasion revealed tendency for the greater p53 positivity compared with the early forms and lymph node-negative cases; however, this difference was not significant according to the statistical analysis.
  • With regard to adenocarcinoma of the cardia, higher rates of p53 positivity were recorded in poorly differentiated, more advanced cases with lymph node invasion.
  • On the contrary, in the patients with adenocarcinoma of the antrum, greater p53 positivity was revealed in early forms without lymph node involvement, but the observed difference was not statistically significant.
  • CONCLUSION: No significant differences in p53 protein expression in terms of sex, type (Lauren) of tumour, depth of invasion, lymph node involvement, or tumour differentiation were observed in any of the analyzed groups of tumours (Barrett's adenocarcinoma, adenocarcinoma of the cardia and adenocarcinoma of the antrum).
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / complications. Cardia. Esophageal Neoplasms / metabolism. Pyloric Antrum. Stomach Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • [CommentIn] Vojnosanit Pregl. 2006 Jan;63(1):87-8; author reply 88-9 [16471255.001]
  • (PMID = 16375215.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Serbia and Montenegro
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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18. Konturek PC, Kania J, Burnat G, Hahn EG: NO-releasing aspirin exerts stronger growth inhibitory effect on Barrett's adenocarcinoma cells than traditional aspirin. J Physiol Pharmacol; 2006 Dec;57 Suppl 12:15-24
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  • [Title] NO-releasing aspirin exerts stronger growth inhibitory effect on Barrett's adenocarcinoma cells than traditional aspirin.
  • Expression of cyclooxygenase-2 (COX-2) is involved in the chronic inflammation-related development of Barrett's adenocarcinoma and the use of selective COX-2 inhibitors (coxibs) might provide new chemoprevention strategy for Barrett's adenocarcinoma (BA).
  • The role of NO-ASA in the prevention of Barrett's adenocarcinoma (BA) has not been studied so far.
  • 2) to compare the effect of NO-ASA with that of ASA on proliferation rate in Barrett''s adenocarcinoma cell line (OE-33 cells);.
  • The expression of COX-2 was assessed in biopsies obtained from the Barrett's mucosa and normal squamous epithelial esophageal mucosa from 20 BE patients by RT-PCR and Western blot analysis, respectively.
  • In Barrett's mucosa a significant up-regulation of COX-2 was observed.
  • These results indicate that this compound may represent a promising chemopreventive agent for Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Aspirin / pharmacology. Cyclooxygenase 2 Inhibitors / pharmacology. Nitric Oxide / metabolism. Nitric Oxide Donors / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Barrett Esophagus / drug therapy. Barrett Esophagus / enzymology. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Dose-Response Relationship, Drug. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / enzymology. Gene Expression. Humans. In Vitro Techniques

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  • (PMID = 17244951.001).
  • [ISSN] 1899-1505
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Nitric Oxide Donors; 31C4KY9ESH / Nitric Oxide; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.22.- / Caspase 3; R16CO5Y76E / Aspirin
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19. Appelman HD: Adenocarcinoma in Barrett mucosa treated by endoscopic mucosal resection. Arch Pathol Lab Med; 2009 Nov;133(11):1793-7
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  • [Title] Adenocarcinoma in Barrett mucosa treated by endoscopic mucosal resection.
  • Adenocarcinoma and dysplasias are recognized complications of Barrett mucosa.
  • Also, Barrett mucosa has duplicated stromal layers beneath the mucosa that include a new lamina propria and a new muscularis mucosae.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophagoscopy / methods. Precancerous Conditions / surgery

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  • (PMID = 19886713.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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20. Pera M, Grande L, Iglesias M, Ramón JM, Conio M: [New advances in the diagnosis and treatment of early onset dysplasia and adenocarcinoma in Barrett's oesophagus]. Cir Esp; 2009 Jun;85(6):331-40
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  • [Title] [New advances in the diagnosis and treatment of early onset dysplasia and adenocarcinoma in Barrett's oesophagus].
  • [Transliterated title] Nuevos avances en el diagnóstico y el tratamiento de la displasia y el adenocarcinoma precoz en el esófago de Barrett.
  • Periodic endoscopic follow-up is recommended after the diagnosis of Barrett's oesophagus, particularly in patients with dysplasia.
  • The new endoscopic techniques show promising results in identifying areas suspected of housing high grade dysplasia and adenocarcinoma.
  • Endoscopic resection of the mucosa has become a fundamental technique for the complete histological assessment of these lesions and is able to establish appropriate therapeutic decisions.
  • Likewise, this technique may be the therapeutic option in patients with high grade dysplasia and adenocarcinoma, although its application must be complemented with ablation techniques such as radiofrequency to eliminate the residual Barrett's metaplasia.
  • Oesophagectomy associated with lymphadenectomy is the option of choice in patients with submucosal adenocarcinoma.
  • The diagnosis and treatment of patients with early onset high grade dysplasia and adenocarcinoma must be carried out with multidisciplinary teams who can evaluate each case individually.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / surgery. Esophagus / pathology

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  • (PMID = 19463990.001).
  • [ISSN] 0009-739X
  • [Journal-full-title] Cirugía española
  • [ISO-abbreviation] Cir Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Number-of-references] 71
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21. Vallböhmer D, Peters JH, Oh D, Kuramochi H, Shimizu D, Demeester SR, Hagen JA, Chandrasoma PT, Danenberg KD, DeMeester TR, Danenberg P: Survivin, a potential biomarker in the development of Barrett's adenocarcinoma. Surgery; 2005 Oct;138(4):701-6; discussion 706-7
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  • [Title] Survivin, a potential biomarker in the development of Barrett's adenocarcinoma.
  • The aim of this study was to measure survivin gene expression in normal squamous/columnar epithelium and in the various stages of development of Barrett's adenocarcinoma.
  • (2) antral tissue from patients with no evidence of Barrett's, dysplasia, or cancer (n = 29, antral control);.
  • (3) specialized intestinal metaplasia from patients with Barrett's esophagus (n = 16; Barrett's group);.
  • (4) low- or high-grade dysplasia (n = 12, dysplasia group), and (5) adenocarcinoma (n = 45 cancer group).
  • Expression in quiescent Barrett's epithelium was similar to both control tissues.
  • Expression levels in dysplastic epithelium were greater than in squamous control (P = .01) and Barrett's tissues (P = .04), but not higher than columnar control tissues, whereas expression in adenocarcinoma was greater than all tissues except dysplasia (P < .001).
  • CONCLUSIONS: Survivin expression may be a biomarker in the development of Barrett's adenocarcinoma that is able to distinguish between quiescent Barrett's, dysplastic Barrett's, and Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Barrett Esophagus / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / etiology. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism

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  • (PMID = 16269299.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA84424-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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22. 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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  • [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.
  • METHODS: DNA of specimens from 19 Barrett's adenocarcinomas, 56 Barrett's intraepithelial neoplasias (n = 29 low grade and n = 27 high grade), 30 Barrett's mucosa without neoplasia, 20 samples of normal squamous and gastric epithelium and four cell lines were studied using methylation specific PCR for the SOCS-1 and SOCS-3 promoter following microdissection.
  • RESULTS: In normal squamous epithelium and normal gastric mucosa, neither SOCS-3 nor SOCS-1 methylation was observed.
  • In Barrett's mucosa without intraepithelial neoplasia, SOCS-3 methylation occurred in 4/30 cases (13%) whereas SOCS-1 was unmethylated.
  • A hypermethylated SOCS-3 promoter was found in 14/19 Barrett's adenocarcinomas (74%) and in 20/29 high and 6/27 low grade intraepithelial neoplasias (69% and 22%, respectively).
  • 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

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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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23. Vona-Davis L, Frankenberry K, Cunningham C, Riggs DR, Jackson BJ, Szwerc MF, McFadden DW: MAPK and PI3K inhibition reduces proliferation of Barrett's adenocarcinoma in vitro. J Surg Res; 2005 Jul 1;127(1):53-8
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  • [Title] MAPK and PI3K inhibition reduces proliferation of Barrett's adenocarcinoma in vitro.
  • BACKGROUND: Esophageal adenocarcinoma often arises from Barrett's esophagus.
  • We hypothesized that inhibition of these pathways in Barrett's adenocarcinoma would decrease cell proliferation and alter apoptosis in vitro.
  • MATERIALS AND METHODS: Two Barrett's-associated adenocarcinoma cell lines, SEG-1 (wild-type p53) and BIC-1 (mutant p53), were treated with MAPK (U0126) and PI3K (LY294002) inhibitors at 20 microm concentrations.
  • CONCLUSIONS: Herein, we report significant antiproliferative effects against Barrett's adenocarcinoma by MAPK and PI3K inhibition in vitro.
  • [MeSH-major] Barrett Esophagus / pathology. Butadienes / pharmacology. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Morpholines / pharmacology. Nitriles / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma. Apoptosis / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Esophageal Neoplasms. Humans. Necrosis

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  • (PMID = 15964304.001).
  • [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] 0 / Butadienes; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Nitriles; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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24. de Faria PC Jr, Andreollo NA, Trevisan MA, Lopes LR: [Relationship of the sialomucins (Tn and Stn antigens) with adenocarcinoma in Barrett's esophagus]. Rev Assoc Med Bras (1992); 2007 Jul-Aug;53(4):360-4
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  • [Title] [Relationship of the sialomucins (Tn and Stn antigens) with adenocarcinoma in Barrett's esophagus].
  • [Transliterated title] A inter-relação das sialomucinas (antígenos Tn e Stn) com o adenocarcinoma no esôfago de Barrett.
  • OBJECTIVE: Barrett's esophagus (BE) is a consequence of chronic gastroesophageal reflux and is considered a risk factor for adenocarcinoma.
  • This research aimed to analyze these antigens in patients with BE and in adenocarcinoma associated with BE.
  • METHODS: Utilizing immunohistochemistry tests, Tn and Stn antigens were studied in the endoscopic biopsies of 29 patients with BE and seven with adenocarcinoma in BE, as well as eight individuals with normal esophageal epithelium at upper digestive endoscopy.
  • However, in adenocarcinoma in BE, both antigens were 100% positive.
  • CONCLUSION: It is probable that the BE group in which the Tn antigens in the goblet cells are positive, similarly to the same antigen in the adenocarcinoma group, might indicate a higher susceptibility for potential occurrence of cancer.
  • In the future, trials with sialomucins could be used routinely, thereby contributing as a prognostic factor of adenocarcinoma in BE.
  • [MeSH-major] Adenocarcinoma / immunology. Barrett Esophagus / immunology. Esophageal Neoplasms / immunology. Sialomucins / analysis

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  • (PMID = 17823742.001).
  • [ISSN] 0104-4230
  • [Journal-full-title] Revista da Associação Médica Brasileira (1992)
  • [ISO-abbreviation] Rev Assoc Med Bras (1992)
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Biomarkers, Tumor; 0 / Sialomucins; 0 / Tn antigen; 0 / sialosyl-Tn antigen
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25. Yamamoto S, Kijima H, Hara T, Chino O, Shimada H, Tanaka M, Inokuchi S, Makuuchi H: Mucin expression and proliferating cell index of esophageal Barrett's adenocarcinoma. Int J Mol Med; 2005 Sep;16(3):375-80
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  • [Title] Mucin expression and proliferating cell index of esophageal Barrett's adenocarcinoma.
  • Barrett's esophagus is a premalignant condition associated with gastroesophageal reflux disease, and consists of mucosa with a metaplastic columnar epithelium (specialized columnar epithelium).
  • In this study, we examined the expression of mucin and the Ki-67 labeling index (LI) in 15 cases of esophageal Barrett's adenocarcinoma, and clarified the significance of incomplete intestinal metaplasia of Barrett's mucosa as a premalignant lesion.
  • The Ki-67 LI was 34.1% in Barrett's adenocarcinoma.
  • In all cases, gastric mucin was found in the non-neoplastic Barrett's mucosa around the adenocarcinoma.
  • MUC2 was detected in 86.7% of proximal non-neoplastic mucosa and 100% of distal non-neoplastic mucosa, while CD10 was found in 20.0% of proximal non-neoplastic mucosa and 40.0% of distal non-neoplastic mucosa of Barrett's adenocarcinoma.
  • In conclusion, Barrett's esophageal mucosa with intestinal metaplasia and a high Ki-67 LI is suggested to be more important as a premalignant lesion, and predominantly found in the proximal rather than distal region of Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Ki-67 Antigen / analysis. Mucins / analysis

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  • (PMID = 16077942.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Gastric Mucins; 0 / Ki-67 Antigen; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / MUC6 protein, human; 0 / Mucin 5AC; 0 / Mucin-2; 0 / Mucin-6; 0 / Mucins; EC 3.4.24.11 / Neprilysin
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26. Islam A, Banerjee S, Kambhampati S, Baranda J, Banerjee S, Weston AP, Saxena NK, Banerjee SK: Angiogenic switch in Barrett's adenocarcinoma: the role of vascular endothelial growth factor. Front Biosci; 2006;11:2336-48
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  • [Title] Angiogenic switch in Barrett's adenocarcinoma: the role of vascular endothelial growth factor.
  • In this article, we reviewed the role this troupe in the development of Barrett's adenocarcinoma and also discussed the possible remedies, which have the impact on blocking the function of this troupe.
  • [MeSH-major] Adenocarcinoma / physiopathology. Barrett Esophagus / physiopathology. Esophageal Neoplasms / physiopathology. Neovascularization, Pathologic / physiopathology. Vascular Endothelial Growth Factor A / physiology

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  • (PMID = 16720317.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 87680; United States / NCRR NIH HHS / RR / P20 RR015563
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 123
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27. Kiss J: [Surgical management of Barrett's esophagus]. Magy Seb; 2005 Dec;58(6):368-72
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  • [Title] [Surgical management of Barrett's esophagus].
  • [Transliterated title] Barrett-oesophagus sebészi kezelése.
  • Barrett's esophagus is a complication of gastroesophageal reflux disease in which metaplastic, intestinal-type epithelium containing mucin-producing goblet cells with characteristic staining on histology replaces the squamous epithelium normally found in the esophagus.
  • This condition is named after the British thoracic surgeon, N. R. Barrett.
  • Different surgical procedures are suggested in dysplasia free patients, in low grade dysplasia, high grade dysplasia and adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / pathology. Barrett Esophagus / surgery
  • [MeSH-minor] Adenocarcinoma / etiology. Australia. Esophageal Neoplasms / etiology. Esophagectomy / methods. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / surgery. History, 20th Century. Humans. Intensive Care Units / history. Journalism, Medical. London. Societies, Medical. Surgery Department, Hospital / history. Thoracic Surgical Procedures / history

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  • (PMID = 16550796.001).
  • [ISSN] 0025-0295
  • [Journal-full-title] Magyar sebészet
  • [ISO-abbreviation] Magy Seb
  • [Language] hun
  • [Publication-type] Biography; English Abstract; Historical Article; Journal Article; Portraits; Review
  • [Publication-country] Hungary
  • [Number-of-references] 22
  • [Personal-name-as-subject] Barrett N
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28. Goda K, Tajiri H, Ikegami M, Urashima M, Nakayoshi T, Kaise M: Usefulness of magnifying endoscopy with narrow band imaging for the detection of specialized intestinal metaplasia in columnar-lined esophagus and Barrett's adenocarcinoma. Gastrointest Endosc; 2007 Jan;65(1):36-46
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  • [Title] Usefulness of magnifying endoscopy with narrow band imaging for the detection of specialized intestinal metaplasia in columnar-lined esophagus and Barrett's adenocarcinoma.
  • BACKGROUND: Barrett's esophagus with specialized intestinal metaplasia (SIM) from columnar-lined esophagus is difficult to distinguish with routine endoscopy.
  • OBJECTIVE: To examine the values of fine mucosal patterns and the capillary patterns observed by magnifying endoscopy with narrow band imaging (MENBI) for the detection of SIM in columnar-lined esophagus and superficial Barrett's adenocarcinoma.
  • PATIENTS: Fifty-eight patients, including 4 with superficial Barrett's adenocarcinoma.
  • RESULTS: Upon observation, all 6 adenocarcinoma sites were classified as irregular patterns in both the fine mucosal patterns and capillary patterns.
  • The addition of capillary patterns to fine mucosal patterns appeared to improve the diagnostic value for detecting SIM and superficial Barrett's adenocarcinoma upon observation by MENBI.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal / methods. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Intestinal Mucosa / pathology

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  • [CommentIn] Gastrointest Endosc. 2007 Jan;65(1):47-9 [17185079.001]
  • (PMID = 17185078.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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29. Takubo K, Vieth M, Aida J, Sawabe M, Kumagai Y, Hoshihara Y, Arai T: Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia. Digestion; 2009;80(4):248-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia.
  • METHODS: Here we discuss four such important differences: the definition of the esophagogastric junction (EGJ), the possible precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus (BE), and the histologic criteria for mucosal adenocarcinoma.
  • Our research on German subjects has indicated that many small Barrett's adenocarcinomas may arise not in the intestinal-type but in the cardiac-type mucosa.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Gastroenterology / standards. Precancerous Conditions / diagnosis. Terminology as Topic

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  • [Copyright] 2009 S. Karger AG, Basel.
  • (PMID = 19828957.001).
  • [ISSN] 1421-9867
  • [Journal-full-title] Digestion
  • [ISO-abbreviation] Digestion
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 59
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30. McFadden DW, Riggs DR, Jackson BJ, Cunningham C: Corn-derived carbohydrate inositol hexaphosphate inhibits Barrett's adenocarcinoma growth by pro-apoptotic mechanisms. Oncol Rep; 2008 Feb;19(2):563-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corn-derived carbohydrate inositol hexaphosphate inhibits Barrett's adenocarcinoma growth by pro-apoptotic mechanisms.
  • We hypothesized that IP6 would inhibit the cell growth rate of Barrett's adenocarcinoma in vitro.
  • Two Barrett's-associated adenocarcinoma cell lines, SEG-1 and BIC-1, were treated with IP6 at 0.5, 1.0 and 5.0 mM concentrations.
  • Our findings suggest that IP6 has the potential to become an effective adjunct for Barrett's adenocarcinoma.
  • Further studies are needed to evaluate safety and clinical utility of this agent in patients with Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Barrett Esophagus / pathology. Cell Proliferation / drug effects. Esophageal Neoplasms / pathology. Phytic Acid / pharmacology

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  • (PMID = 18202808.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbohydrates; 7IGF0S7R8I / Phytic Acid
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31. Peyre CG, DeMeester SR, Rizzetto C, Bansal N, Tang AL, Ayazi S, Leers JM, Lipham JC, Hagen JA, DeMeester TR: Vagal-sparing esophagectomy: the ideal operation for intramucosal adenocarcinoma and barrett with high-grade dysplasia. Ann Surg; 2007 Oct;246(4):665-71; discussion 671-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vagal-sparing esophagectomy: the ideal operation for intramucosal adenocarcinoma and barrett with high-grade dysplasia.
  • OBJECTIVE: Our aim was to compare outcome of vagal-sparing esophagectomy with transhiatal and en bloc esophagectomy in patients with intramucosal adenocarcinoma or high-grade dysplasia.
  • SUMMARY BACKGROUND DATA: Intramucosal adenocarcinoma and high grade dysplasia have a low likelihood of lymphatic or systemic metastases and esophagectomy is curative in most patients.
  • METHOD: Retrospective review of outcome in patients with intramucosal adenocarcinoma or high grade dysplasia that had a vagal-sparing (n=49), transhiatal (n=39) or en bloc (n=21) esophagectomy.
  • CONCLUSION: Survival with intramucosal adenocarcinoma or Barrett's with high-grade dysplasia is independent of the type of resection.
  • Consequently a vagal-sparing esophagectomy is the preferred procedure for patients with intramucosal adenocarcinoma or high grade dysplasia.
  • [MeSH-minor] Adenocarcinoma / surgery. Aged. Barrett Esophagus / surgery. Body Weight / physiology. Diarrhea / prevention & control. Dumping Syndrome / prevention & control. Esophageal Neoplasms / surgery. Esophagus / physiopathology. Female. Follow-Up Studies. Hospitalization. Humans. Length of Stay. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Postoperative Complications / prevention & control. Retrospective Studies. Survival Rate. Treatment Outcome

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  • [CommentIn] Nat Clin Pract Gastroenterol Hepatol. 2008 Jun;5(6):302-3 [18431373.001]
  • (PMID = 17893503.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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32. Abraham SC, Krasinskas AM, Correa AM, Hofstetter WL, Ajani JA, Swisher SG, Wu TT: Duplication of the muscularis mucosae in Barrett esophagus: an underrecognized feature and its implication for staging of adenocarcinoma. Am J Surg Pathol; 2007 Nov;31(11):1719-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Duplication of the muscularis mucosae in Barrett esophagus: an underrecognized feature and its implication for staging of adenocarcinoma.
  • Depth of invasion is one of the most important prognostic indicators in esophageal adenocarcinoma.
  • Unlike other regions of the gastrointestinal tract, the esophagus in Barrett metaplasia frequently develops duplication of the muscularis mucosae (MM), but this feature is underrecognized, and its effect on appropriate staging of superficially invasive adenocarcinoma is unclear.
  • We first randomly selected 50 esophageal resections for high-grade dysplasia or T1 adenocarcinoma in Barrett esophagus (BE) to evaluate the sensitivity and specificity of MM duplication for BE and its histologic characteristics, including percentage of the Barrett segment involved by MM duplication, origin of the duplicated muscle layer, and appearance of the tissue between duplicated MM.
  • Next, to study the clinical significance of MM duplication, we evaluated 30 resections for BE that had superficial adenocarcinoma confined to regions of duplicated MM.
  • We observed MM duplication in 46 of 50 (92%) BE resections, involving 5% to >90% of the Barrett segment, in contrast to none in 20 (0%) resected squamous cell carcinoma, P<0.0001.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology

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  • [CommentIn] Am J Surg Pathol. 2008 Dec;32(12):1913; author reply 1913-4 [18824891.001]
  • (PMID = 18059229.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Gatenby PA, Ramus JR, Caygill CP, Winslet MC, Watson A: Aspirin is not chemoprotective for Barrett's adenocarcinoma of the oesophagus in multicentre cohort. Eur J Cancer Prev; 2009 Sep;18(5):381-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aspirin is not chemoprotective for Barrett's adenocarcinoma of the oesophagus in multicentre cohort.
  • Barrett's columnar-lined oesophagus is the precursor lesion for oesophageal adenocarcinoma.
  • The overall rate of progression to adenocarcinoma is 0.59% per annum.
  • A large prospective multicentre trial is recruiting to assess the role of aspirin as a chemoprotective agent in prevention of development of cancer as well as cardiovascular protection in patients with Barrett's oesophagus.
  • This retrospective analysis of the large UK National Barrett's Oesophagus Registry database seeks to analyse this question from within its large natural history study cohort.
  • End point was development of dysplasia or oesophageal adenocarcinoma.
  • Numbers of patients developing all grades of dysplasia and adenocarcinoma were: 13 aspirin (15.1%) and 97 no aspirin (14.9%) (hazard ratio 0.723, 95% confidence interval 0.410-1.310, P = 0.294), high-grade dysplasia and adenocarcinoma: five aspirin (5.8%) and 25 no aspirin (3.8%) (hazard ratio 0.898, 95% confidence interval 0.340-2.368, P = 0.827) and adenocarcinoma: four aspirin (4.7%) and 16 no aspirin (2.5%) (hazard ratio 1.092, 95% confidence interval 0.358-3.335, P = 0.877).
  • No significant difference was observed in hazard of developing dysplasia or adenocarcinoma between patients taking aspirin and those not taking aspirin during the course of follow-up of surveillance for columnar-lined oesophagus.
  • In conclusion, no difference in risk of development of dysplasia or adenocarcinoma was observed between patients taking aspirin and those not taking aspirin in this large cohort.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anticarcinogenic Agents / therapeutic use. Aspirin / therapeutic use. Barrett Esophagus / drug therapy. Esophageal Neoplasms / prevention & control. Precancerous Conditions / drug therapy

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  • (PMID = 19620873.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; R16CO5Y76E / Aspirin
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34. Portale G, Peters JH, Hagen JA, Demeester SR, Gandamihardja TA, Tharavej C, Hsieh CC, Demeester TR: Comparison of the clinical and histological characteristics and survival of distal esophageal-gastroesophageal junction adenocarcinoma in patients with and without barrett mucosa. Arch Surg; 2005 Jun;140(6):570-4; discussion 574-5
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  • [Title] Comparison of the clinical and histological characteristics and survival of distal esophageal-gastroesophageal junction adenocarcinoma in patients with and without barrett mucosa.
  • BACKGROUND: The incidence of adenocarcinoma in the distal esophagus and at the gastroesophageal junction (GEJ) has been increasing in the last decades.
  • It has been suggested that patients in whom Barrett mucosa can be identified in the surgical specimen have a better prognosis compared with those without.
  • This has led to the belief that patients with and without Barrett mucosa may represent 2 distinct cancer types.
  • HYPOTHESIS: Distal esophageal-GEJ adenocarcinoma with and without Barrett mucosa share the same origin, but differ only in clinical presentation and outcome.
  • PATIENTS AND METHODS: Between 1992 and 2002, 215 patients (173 men and 42 women; median age, 66 years; age range, 26-91 years) had esophagogastrectomy for adenocarcinoma of the distal esophagus-GEJ.
  • MAIN OUTCOME MEASURES: Clinical presentation, tumor characteristics, and survival were compared in patients with Barrett mucosa (n = 140) and those without (n = 75).
  • RESULTS: Patients with Barrett mucosa in the specimen had tumors that were diagnosed earlier; were smaller in size; earlier in stage, with fewer node metastases; and had a better 5-year survival.
  • CONCLUSIONS: Observed differences in survival between patients with distal esophageal-GEJ adenocarcinoma with and without Barrett mucosa can be explained by earlier diagnosis.
  • Patients without Barrett mucosa have their tumors detected later, when the disease is more advanced.
  • This suggests the possibility that tumors without Barrett mucosa are not of a different origin, but rather are larger tumors that may have overgrown areas of Barrett mucosa.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / mortality. Esophageal Neoplasms / pathology. Esophagogastric Junction

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  • (PMID = 15967904.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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35. 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.
  • 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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36. Ferguson HR, Wild CP, Anderson LA, Murphy SJ, Johnston BT, Murray LJ, Watson RG, McGuigan J, Reynolds JV, Hardie LJ: No association between hOGG1, XRCC1, and XPD polymorphisms and risk of reflux esophagitis, Barrett's esophagus, or esophageal adenocarcinoma: results from the factors influencing the Barrett's adenocarcinoma relationship case-control study. Cancer Epidemiol Biomarkers Prev; 2008 Mar;17(3):736-9
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  • [Title] No association between hOGG1, XRCC1, and XPD polymorphisms and risk of reflux esophagitis, Barrett's esophagus, or esophageal adenocarcinoma: results from the factors influencing the Barrett's adenocarcinoma relationship case-control study.
  • Reflux of gastric contents can lead to development of reflux esophagitis and Barrett's esophagus.
  • Barrett's esophagus is a risk factor for esophageal adenocarcinoma.
  • Small studies have reported associations with XPD Lys 751 Gln and esophageal adenocarcinoma.
  • XRCC1 Arg 399 Gln has been linked to Barrett's esophagus and reflux esophagitis.
  • In a population-based case-control study, we examined associations of the hOGG1 Ser 326 Cys, XRCC1 Arg 399 Gln, and XPD Lys 751 Gln polymorphisms with risk of esophageal adenocarcinoma, Barrett's esophagus, and reflux esophagitis.
  • Genomic DNA was extracted from blood samples collected from cases of esophageal adenocarcinoma (n = 210), Barrett's esophagus (n = 212), reflux esophagitis (n = 230), and normal population controls frequency matched for age and sex (n = 248).
  • There were no statistically significant associations between these polymorphisms and risk of esophageal adenocarcinoma, Barrett's esophagus, or reflux esophagitis.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Esophagitis, Peptic / genetics. Polymorphism, Genetic

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  • (PMID = 18349297.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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37. Horváth OP: [Surgical treatment for early Barrett cancer]. Magy Seb; 2009 Apr;62(2):51-8
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  • [Title] [Surgical treatment for early Barrett cancer].
  • [Transliterated title] A korai Barrett-carcinomák sebészi kezelése.
  • Adenocarcinomas in Barrett's oesophagus are more commonly diagnosed at an early stage due to effective surveillance programmes.
  • Subtotal oesophagectomy with extended lymphadenectomy is considered the best curative treatment for patients with early adenocarcinoma of the oesophagus.
  • An individualized strategy should be employed based on staging (tumour penetration into the mucosa/submucosa, presence of lymph node metastasis), multicentricity, length of the underlying Barrett mucosa and risk factors of the patient.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / surgery. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / surgery. Esophagectomy / methods. Lymph Node Excision
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / surgery. Early Detection of Cancer. Esophagoscopy. Humans. Lymphatic Metastasis. Neoplasm Invasiveness. Neoplasm Recurrence, Local / prevention & control. Quality of Life. Sentinel Lymph Node Biopsy. Survival Rate. Vagus Nerve / surgery

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  • (PMID = 19386564.001).
  • [ISSN] 0025-0295
  • [Journal-full-title] Magyar sebészet
  • [ISO-abbreviation] Magy Seb
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Number-of-references] 56
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38. Odze RD: Barrett esophagus: histology and pathology for the clinician. Nat Rev Gastroenterol Hepatol; 2009 Aug;6(8):478-90
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  • [Title] Barrett esophagus: histology and pathology for the clinician.
  • The incidence of adenocarcinoma of the esophagus and gastroesophageal junction has increased dramatically over the past 30 years.
  • The major precursor to this type of adenocarcinoma is Barrett esophagus, which is defined as the conversion of normal squamous epithelium into metaplastic columnar epithelium.
  • Abundant evidence suggests that adenocarcinoma in the setting of Barrett esophagus develops via a progressive sequence of histological and molecular events.
  • Consequently, patients with Barrett esophagus routinely undergo endoscopic surveillance for early detection of neoplasia.
  • This Review provides physicians with a summary of the pertinent, clinically relevant histological features of Barrett esophagus and its neoplastic complications.
  • The histology of Barrett esophagus and the gastroesophageal junction is summarized, and an overview of information necessary to interpret pathology reports from patients either with or without endoscopic evidence of Barrett esophagus is provided to appropriately guide management of patients.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology

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  • (PMID = 19581906.001).
  • [ISSN] 1759-5053
  • [Journal-full-title] Nature reviews. Gastroenterology & hepatology
  • [ISO-abbreviation] Nat Rev Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 99
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39. Yoon HY, Kim HI, Kim CB: [Clinicopathologic characteristics of adenocarcinoma in cardia according to Siewert classification]. Korean J Gastroenterol; 2008 Nov;52(5):293-7
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  • [Title] [Clinicopathologic characteristics of adenocarcinoma in cardia according to Siewert classification].
  • RESULTS: Barrett's adenocarcinoma was recognized in two patients so called type I.
  • [MeSH-major] Adenocarcinoma / pathology. Cardia. Stomach Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Esophageal Neoplasms / classification. Esophageal Neoplasms / mortality. Esophageal Neoplasms / pathology. Female. Humans. Kaplan-Meier Estimate. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Analysis

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  • (PMID = 19077475.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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40. von Rahden BH, Stein HJ, Feith M, Pühringer F, Theisen J, Siewert JR, Sarbia M: Overexpression of TGF-beta1 in esophageal (Barrett's) adenocarcinoma is associated with advanced stage of disease and poor prognosis. Mol Carcinog; 2006 Oct;45(10):786-94
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  • [Title] Overexpression of TGF-beta1 in esophageal (Barrett's) adenocarcinoma is associated with advanced stage of disease and poor prognosis.
  • Expression of TGF-beta1, a major member of the TGF-beta superfamily and important promoter of tumor growth, was investigated in a series of primary resected esophageal (Barrett's) adenocarcinomas to establish its potential clinical significance and prognostic relevance in this entity.
  • A series of 123 primary resected adenocarcinomas of the distal esophagus, arising in association with Barrett's esophagus, and corresponding normal squamous epithelium (n = 12) and non-malignant Barrett's mucosa (n = 11), were investigated by means of quantitative RT-PCR for expression of TGF-beta1, using paraffin embedded tissue samples.
  • The relative gene expression was significantly higher in tumor tissue compared to squamous epithelium (P = 0.005) and Barrett's mucosa (P=0.002), expressing only low amounts of TGF-beta1.
  • Our data show that TGF-beta1 overexpression is associated with advanced stage of esophageal adenocarcinoma and implies a negative impact on survival.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Esophageal Neoplasms / genetics. Esophageal Neoplasms / pathology. Gene Expression Regulation, Neoplastic / genetics. Transforming Growth Factor beta / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / genetics. Barrett Esophagus / pathology. Humans. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate. Transforming Growth Factor beta1

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  • (PMID = 16921482.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TGFB1 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1
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41. Schmassmann A, Gebbers JO: [Barrett's esophagus: diagnosis and therapy]. Praxis (Bern 1994); 2005 May 25;94(21):861-8
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  • [Title] [Barrett's esophagus: diagnosis and therapy].
  • [Transliterated title] Barrett-Osophagus: Diagnostik und Therapie.
  • Barrett's esophagus is usually diagnosed by the endoscopic and histological finding of columnar epithelium with intestinal metaplasia in the distal esophagus.
  • The prevalence of Barrett's esophagus (long segment) is <2% in the general population and 3-5% in patients with chronic reflux symptoms.
  • Barrett mucosa predisposes patients to adenocarcinoma that develops in approximately 0.5% of these patients per year (Barrett mucosa --> dysplasia --> cancer sequence).
  • The incidence of esophageal adenocarcinoma over the past few decades; the present incidence, however, is still rather low and is reported to be approximately 4 and approximately 0.5 per 100,000 in males and females, respectively.
  • The malignant potential of the Barrett mucosa increases with dysplastic changes.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Precancerous Conditions / diagnosis
  • [MeSH-minor] Adult. Biopsy. Cell Transformation, Neoplastic / pathology. Esophagitis, Peptic / complications. Esophagitis, Peptic / pathology. Esophagitis, Peptic / therapy. Esophagoscopy. Esophagus / pathology. Female. Follow-Up Studies. Humans. Intestinal Mucosa / pathology. Male. Metaplasia. Middle Aged. Practice Guidelines as Topic

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  • (PMID = 15966485.001).
  • [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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42. Lozoya-González D, Farca-Belsaguy A, Peláez-Luna M, Vázquez-Ballesteros E, González-Galeote E, Salceda-Otero JC: [Endoscopic mucosal resection due to adenocarcinoma of the esophagus caused by Barrett's esophagus.]. Rev Gastroenterol Mex; 2009 Oct-Dec;74(4):383-6
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  • [Title] [Endoscopic mucosal resection due to adenocarcinoma of the esophagus caused by Barrett's esophagus.].
  • [Transliterated title] Resección endoscópica de la mucosa debido a adenocarcinoma de esófago originado en un esófago de Barrett.
  • We present a case of a patient with high surgical risk, who underwent an upper endoscopy because of long history of gastroesophageal reflux disease and uncontrollable hiccup with successful endoscopic mucosal resection with plastic cap and polipectomy loop of an early stage esophageal adenocarcinoma derived of Barrett s esophagus.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / surgery. Esophageal Neoplasms / etiology. Esophageal Neoplasms / surgery. Esophagoscopy. Esophagus / surgery
  • [MeSH-minor] Aged. Barrett Esophagus / complications. Endosonography. Humans. Male. Mucous Membrane / surgery

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  • (PMID = 20423774.001).
  • [ISSN] 0375-0906
  • [Journal-full-title] Revista de gastroenterología de México
  • [ISO-abbreviation] Rev Gastroenterol Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] Adenocarcinoma Of Esophagus
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43. Jiménez P, Piazuelo E, Cebrian C, Ortego J, Strunk M, García-Gonzalez MA, Santander S, Alcedo J, Lanas A: Prostaglandin EP2 receptor expression is increased in Barrett's oesophagus and oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2010 Feb 1;31(3):440-51
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  • [Title] Prostaglandin EP2 receptor expression is increased in Barrett's oesophagus and oesophageal adenocarcinoma.
  • AIM: To investigate which PGE2 receptor subtypes regulate PGE2 signals in the oesophageal adenocarcinoma sequence.
  • METHODS: Expression was determined in oesophageal biopsies from 85 patients with oesophagitis, Barrett's metaplasia, intraepithelial neoplasia, oesophageal adenocarcinoma and normal oesophagus.
  • Expression of EP receptors was also determined in response to acid and bile exposure in the Barrett's adenocarcinoma cell line OE33.
  • COX-2 and, especially, EP2 were increased in the Barrett's metaplasia-intraepithelial neoplasia-adenocarcinoma sequence.
  • Expression of the EP4 receptor protein was increased in oesophageal adenocarcinoma.
  • CONCLUSIONS: Our data suggest that in addition to COX-2, EP2 and EP4 receptors could be a selective target in the prevention and/or treatment of the Barrett's-associated adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cyclooxygenase 1 / metabolism. Esophageal Neoplasms / pathology. RNA, Messenger / metabolism. Receptors, Prostaglandin E / metabolism

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  • (PMID = 19843025.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / PTGER2 protein, human; 0 / RNA, Messenger; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP2 Subtype; EC 1.14.99.1 / Cyclooxygenase 1
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44. Sappati Biyyani RS, Chessler L, McCain E, Nelson K, Fahmy N, King J: Familial trends of inheritance in gastro esophageal reflux disease, Barrett's esophagus and Barrett's adenocarcinoma: 20 families. Dis Esophagus; 2007;20(1):53-7
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  • [Title] Familial trends of inheritance in gastro esophageal reflux disease, Barrett's esophagus and Barrett's adenocarcinoma: 20 families.
  • We reported four families with familial Barrett's esophagus (FBE) in 1993.
  • This follow-up study includes an additional 16 families with FBE, gastroesophageal reflux disease (GERD) and BE-related adenocarcinoma (BEAC) highlighting the familial trends of inheritance.

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  • (PMID = 17227311.001).
  • [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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45. Peng DF, Razvi M, Chen H, Washington K, Roessner A, Schneider-Stock R, El-Rifai W: DNA hypermethylation regulates the expression of members of the Mu-class glutathione S-transferases and glutathione peroxidases in Barrett's adenocarcinoma. Gut; 2009 Jan;58(1):5-15
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  • [Title] DNA hypermethylation regulates the expression of members of the Mu-class glutathione S-transferases and glutathione peroxidases in Barrett's adenocarcinoma.
  • BACKGROUND: The accumulation of reactive oxygen species and subsequent oxidative DNA damage underlie the development of Barrett's oesophagus (BO) and its progression to Barrett's dysplasia (BD) and adenocarcinoma (BAC).
  • CONCLUSION: Epigenetic inactivation of members of the glutathione pathway can be an important mechanism in Barrett's tumourigenesis.

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  • (PMID = 18664505.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA106176-06; United States / NCI NIH HHS / CA / R01 CA106176-06; United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / CA106176-07A1; United States / NCI NIH HHS / CA / R01 CA106176-07A1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / Hydroxamic Acids; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 1.11.1.9 / Glutathione Peroxidase; EC 2.5.1.18 / Glutathione Transferase; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS186959; NLM/ PMC2845391
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46. Szachnowicz S, Cecconello I, Iriya K, Marson AG, Takeda FR, Gama-Rodrigues JJ: Origin of adenocarcinoma in Barrett's esophagus: p53 and Ki67 expression and histopathologic background. Clinics (Sao Paulo); 2005 Apr;60(2):103-12
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  • [Title] Origin of adenocarcinoma in Barrett's esophagus: p53 and Ki67 expression and histopathologic background.
  • Barrett's esophagus is the substitution of squamous epithelium of the distal esophagus by columnar epithelium.
  • Intestinal metaplasia in Barrett's esophagus is considered to be the main risk factor for the development of adenocarcinoma.
  • Diffuse adenocarcinoma and Barrett's esophagus without intestinal metaplasia are rare, and reports on the subject are scarce.
  • PURPOSE AND METHOD: To estimate the prevalence of adenocarcinoma in 297 patients with Barrett's esophagus, during the period of 1990 to 2002, and in 13 patients undergoing surgery, to conduct detailed macroscopic and microscopic analysis, with performance of immunohistochemical tests for p53 and Ki67, correlating the type of tumor with its adjacent epithelium.
  • RESULTS: In our patients with Barrett's esophagus, there was a prevalence of 5.7% of adenocarcinoma.
  • The tumors developed only when the Barrett's esophagus segment was long (>3.0 cm).
  • The histological study revealed 2 patients (15.4%) with Barrett's esophagus adjacent to a tumor with gastric metaplasia without the presence of intestinal metaplasia.
  • CONCLUSION: Adenocarcinoma develops from mixed columnar epithelium, either intestinal or gastric, showing both the gastric and the intestinal patterns; thus, tumors can also grow in columnar epithelium without intestinal metaplasia.
  • Barrett's esophagus should be followed up for the possibility of progression to malignancy, especially when the segment is longer than 3 cm.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Ki-67 Antigen / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 15880245.001).
  • [ISSN] 1807-5932
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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47. Kubo A, Corley DA, Jensen CD, Kaur R: Dietary factors and the risks of oesophageal adenocarcinoma and Barrett's oesophagus. Nutr Res Rev; 2010 Dec;23(2):230-46
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  • [Title] Dietary factors and the risks of oesophageal adenocarcinoma and Barrett's oesophagus.
  • Incidence rates for oesophageal adenocarcinoma have increased by over 500% during the past few decades without clear reasons.
  • Gastro-oesophageal reflux disease, obesity and smoking have been identified as risk factors, although the demographic distribution of these risk factors is not consistent with the demographic distribution of oesophageal adenocarcinoma, which is substantially more common among whites and males than any other demographic groups.
  • Numerous epidemiological studies have suggested associations between dietary factors and the risks of oesophageal adenocarcinoma and its precursor, Barrett's oesophagus, though a comprehensive review is lacking.
  • The main aim of the present review is to consider the evidence linking dietary factors with the risks of oesophageal adenocarcinoma, Barrett's oesophagus, and the progression from Barrett's oesophagus to oesophageal adenocarcinoma.
  • The existing epidemiological evidence is strongest for an inverse relationship between intake of vitamin C, β-carotene, fruits and vegetables, particularly raw fruits and vegetables and dark green, leafy and cruciferous vegetables, carbohydrates, fibre and Fe and the risk of oesophageal adenocarcinoma and Barrett's oesophagus.
  • Patients at higher risk for Barrett's oesophagus and oesophageal adenocarcinoma may benefit from increasing their consumption of fruits and vegetables and reducing their intake of red meat and other processed food items.
  • Further research is needed to evaluate the relationship between diet and the progression of Barrett's oesophagus to oesophageal adenocarcinoma.
  • Evidence from cohort studies will help determine whether randomised chemoprevention trials are warranted for the primary prevention of Barrett's oesophagus or its progression to cancer.

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  • (PMID = 20624335.001).
  • [ISSN] 1475-2700
  • [Journal-full-title] Nutrition research reviews
  • [ISO-abbreviation] Nutr Res Rev
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK081271-02; United States / NIDDK NIH HHS / DK / F32 DK081271; United States / NIDDK NIH HHS / DK / 5F32DK81271-2; United States / NIDDK NIH HHS / DK / F32 DK081271-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Micronutrients
  • [Other-IDs] NLM/ NIHMS223558; NLM/ PMC3062915
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48. 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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  • [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.
  • 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.
  • 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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49. Peitz U, Malfertheiner P: [Barrett carcinoma--diagnosis, screening, surveillance, endoscopic treatment, prevention]. Z Gastroenterol; 2007 Dec;45(12):1264-72
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  • [Title] [Barrett carcinoma--diagnosis, screening, surveillance, endoscopic treatment, prevention].
  • [Transliterated title] Barrett-Karzinom--Diagnose, Screening, Surveillance, endoskopische Therapie, Prävention.
  • An adenocarcinoma of the distal esophagus may also be designated as Barrett's carcinoma as it evolves from Barrett's esophagus.
  • Barrett's esophagus currently is defined as a columnar metaplasia of the distal esophagus, as identified by endoscopy, that, upon histopathology, is confirmed to contain intestinal metaplasia.
  • A different histological entity of columnar metaplasia of the distal esophagus is cardia-type mucosa which probably precedes intestinal metaplasia, but lacks goblet cells typical for the latter.
  • The conversion rate from Barrett's esophagus to Barrett's carcinoma amounts to 0.5 to 1 % per year.
  • Patients with reflux symptoms should undergo early endoscopy in order to search for Barrett's esophagus (screening).
  • In those cases where Barrett's esophagus is identified, regular endoscopic controls should be scheduled (surveillance).
  • The rapid increase of the incidence of Barrett's carcinoma in Western countries suggests that life style factors, in particular overweight, having a causal role.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Esophagoscopy. Mass Screening

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  • (PMID = 18080229.001).
  • [ISSN] 0044-2771
  • [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] 127
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50. Trakál E, Guidi A, Butti AL, Trakál JJ, Sambuelli R, Zárate FE: Detection of the risk of adenocarcinoma in Barrett's esophagus by means of tumor markers (p53 and Ki67). Acta Gastroenterol Latinoam; 2010 Sep;40(3):211-5
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  • [Title] Detection of the risk of adenocarcinoma in Barrett's esophagus by means of tumor markers (p53 and Ki67).
  • The rising incidence of adenocarcinoma in Barrett's esophagus has intensified the research into methods of early recognition of cancer risk, detecting cytological and architectural changes (dysplasia) or using biomarkers as predictive tests.
  • The aim of this paper is to evaluate the involvement of two tumor markers: p53 (tumor suppressor gene) and Ki67 (proliferation marker), by means of immunohistochemical analysis with monoclonal antibodies designed for the specific localization of p53 and Ki67 antigens, in esophageal biopsies with columnar metaplasia of patients with and without dysplasia and adenocarcinoma, and to anticipate which ones are liable to suffer it in the future.
  • Both markers were positive in all intestinal metaplasia patients with high-grade dysplasia and adenocarcinoma, and even in some cases with low grade or without dysplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Biomarkers, Tumor / analysis. Esophageal Neoplasms / pathology. Ki-67 Antigen / analysis. Precancerous Conditions / pathology. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 21049770.001).
  • [ISSN] 0300-9033
  • [Journal-full-title] Acta gastroenterologica Latinoamericana
  • [ISO-abbreviation] Acta Gastroenterol. Latinoam.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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51. Zhang HY, Spechler SJ, Souza RF: Esophageal adenocarcinoma arising in Barrett esophagus. Cancer Lett; 2009 Mar 18;275(2):170-7
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  • [Title] Esophageal adenocarcinoma arising in Barrett esophagus.
  • The major risk factors for esophageal adenocarcinoma are gastroesophageal reflux disease (GERD) and Barrett esophagus, a squamous-to-columnar cell metaplasia that predisposes to malignancy.
  • Adenocarcinomas in Barrett esophagus are thought to arise through a sequence of growth-promoting, genetic alterations that accumulate until the cells have acquired the physiologic hallmarks of cancer proposed by Hanahan and Weinberg.
  • Moreover, GERD and Barrett esophagus are associated with chronic esophagitis, and inflammation is a well known risk factor for cancer formation.
  • The cell that gives rise to Barrett metaplasia is not known.
  • Alternatively, it is possible that Barrett metaplasia develops through the conversion of one differentiated cell type into another.
  • Regardless of the cell of origin, Barrett metaplasia ultimately must be sustained by stem cells, which might be identified by intestinal stem cell markers.
  • If Barrett cancers develop from Barrett stem cells, then a therapy targeted at those stem cells might prevent esophageal adenocarcinoma.
  • This report reviews the risk factors for Barrett esophagus and esophageal adenocarcinoma, the mechanisms by which genetic alterations might contribute to carcinogenesis in Barrett esophagus, and the role of stem cells in the development of Barrett metaplasia and adenocarcinoma.

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  • (PMID = 18703277.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK063621-06A2; United States / NIDDK NIH HHS / DK / R01 DK063621; United States / NIDDK NIH HHS / DK / DK 63621; United States / NIDDK NIH HHS / DK / R01 DK063621-06A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Ireland
  • [Number-of-references] 71
  • [Other-IDs] NLM/ NIHMS98405; NLM/ PMC2673195
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52. Song S, Krishnan K, Liu K, Bresalier RS: Polyphenon E inhibits the growth of human Barrett's and aerodigestive adenocarcinoma cells by suppressing cyclin D1 expression. Clin Cancer Res; 2009 Jan 15;15(2):622-31
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  • [Title] Polyphenon E inhibits the growth of human Barrett's and aerodigestive adenocarcinoma cells by suppressing cyclin D1 expression.
  • This study was designed to determine the effects of Poly E on the growth of human Barrett's and aerodigestive adenocarcinoma cells and the mechanisms involved in growth regulation by this agent.
  • EXPERIMENTAL DESIGN: Human adenocarcinoma cells and immortalized Barrett's epithelial cells were used as model systems.
  • RESULTS: Poly E inhibited the proliferation of immortalized Barrett's cells as well as various adenocarcinoma cells, and this was associated with the down-regulation of cyclin D1 protein expression.
  • These results provide insight into the mechanisms by which Poly E inhibits growth of Barrett's and adenocarcinoma cells, and provides a rationale for using this agent as a potential chemopreventive and therapeutic strategy for esophageal adenocarcinoma and its precursor, Barrett's esophagus.

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  • (PMID = 19147768.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA069480-13; United States / NCI NIH HHS / CA / CA069480-13; United States / NIDDK NIH HHS / DK / P30 DK056338; United States / NCI NIH HHS / CA / R01CA69480; United States / NIDDK NIH HHS / DK / DK56338; United States / NCI NIH HHS / CA / R01 CA069480
  • [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 / Antineoplastic Agents; 0 / Tea; 0 / polyphenon E; 136601-57-5 / Cyclin D1; 8R1V1STN48 / Catechin; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.4.99.- / ATP dependent 26S protease
  • [Other-IDs] NLM/ NIHMS220918; NLM/ PMC2925407
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53. Sabo E, Beck AH, Montgomery EA, Bhattacharya B, Meitner P, Wang JY, Resnick MB: Computerized morphometry as an aid in determining the grade of dysplasia and progression to adenocarcinoma in Barrett's esophagus. Lab Invest; 2006 Dec;86(12):1261-71
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  • [Title] Computerized morphometry as an aid in determining the grade of dysplasia and progression to adenocarcinoma in Barrett's esophagus.
  • The aims of this study were to use computerized morphometry in order to differentiate between the degree of dysplasia and to predict progression to invasive adenocarcinoma in Barrett's esophagus (BE).
  • Moreover, histomorphometric quantification of nuclear texture is a powerful tool for predicting progression to invasive adenocarcinoma in patients with HGD.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / pathology. Esophageal Neoplasms / etiology. Image Interpretation, Computer-Assisted / methods. Precancerous Conditions / pathology

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  • (PMID = 17075582.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR17695
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
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54. Lanas A, Alcedo González J: [Chemoprevention in adenocarcinoma of the esophagus]. Acta Gastroenterol Latinoam; 2007 Mar;37(1):37-48
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  • [Title] [Chemoprevention in adenocarcinoma of the esophagus].
  • [Transliterated title] Quimioprevención en adenocarcinoma de esófago.
  • The incidence of the adenocarcinoma of the esophagus (ACE) has dramatically for the last decades in western countries, which has been associated with a parallel increase in the incidence and prevalence of symptoms associated with gastroesophageal reflux diseases (GERD) and Barrett's esophagus (BE).
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / drug therapy. Esophageal Neoplasms / prevention & control. Gastroesophageal Reflux / drug therapy

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  • (PMID = 17486744.001).
  • [ISSN] 0300-9033
  • [Journal-full-title] Acta gastroenterologica Latinoamericana
  • [ISO-abbreviation] Acta Gastroenterol. Latinoam.
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Argentina
  • [Number-of-references] 93
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55. Matono S, Fujita H, Sueyoshi S, Tanaka T, Yamana H, Shirouzu K: Long-term survival after three-field lymph-adenectomy for an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node. Jpn J Thorac Cardiovasc Surg; 2006 Jan;54(1):11-5
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  • [Title] Long-term survival after three-field lymph-adenectomy for an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node.
  • Here, we report a case of long-term survival after resection of an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node.
  • They were pathologically found to be an adenocarcinoma in the esophagus which had metastasised to the lymph node.
  • The pathological diagnosis was adenocarcinoma in Barrett's esophagus with the UICC stage classification of pT1, pN1, pM1-LYM, Stage IVB.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / surgery. Lymph Node Excision / methods

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  • (PMID = 16482930.001).
  • [ISSN] 1344-4964
  • [Journal-full-title] The Japanese journal of thoracic and cardiovascular surgery : official publication of the Japanese Association for Thoracic Surgery = Nihon Kyobu Geka Gakkai zasshi
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  • [Language] eng
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56. Sayana H, Wani S, Sharma P: Esophageal adenocarcinoma and Barrett's esophagus. Minerva Gastroenterol Dietol; 2007 Jun;53(2):157-69
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  • [Title] Esophageal adenocarcinoma and Barrett's esophagus.
  • Esophageal adenocarcinoma (EAC) is the most rapidly rising incidence cancer associated with a poor 5-year survival rate.
  • Barrett's esophagus (BE) is a well established premalignant condition for the development of EAC and hence it is imperative that patients with BE or at risk for developing BE should be identified and managed appropriately.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / etiology

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  • (PMID = 17557044.001).
  • [ISSN] 1121-421X
  • [Journal-full-title] Minerva gastroenterologica e dietologica
  • [ISO-abbreviation] Minerva Gastroenterol Dietol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 95
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57. Konturek PC, Burnat G, Hahn EG: Inhibition of Barret's adenocarcinoma cell growth by simvastatin: involvement of COX-2 and apoptosis-related proteins. J Physiol Pharmacol; 2007 Aug;58 Suppl 3:141-8
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  • [Title] Inhibition of Barret's adenocarcinoma cell growth by simvastatin: involvement of COX-2 and apoptosis-related proteins.
  • The role of statins in the prevention and therapy of Barrett's adenocarcinoma (BA) has not been investigated so far.
  • Clinical trial are necessary to prove the beneficial effects of statins on cancerogenesis in Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cyclooxygenase 2 / metabolism. Esophageal Neoplasms / drug therapy. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. Simvastatin / pharmacology
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Barrett Esophagus / complications. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Gene Expression Regulation / drug effects. Humans. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. bcl-2-Associated X Protein / drug effects. bcl-2-Associated X Protein / metabolism

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  • (PMID = 17901590.001).
  • [ISSN] 0867-5910
  • [Journal-full-title] Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
  • [ISO-abbreviation] J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; AGG2FN16EV / Simvastatin; EC 1.14.99.1 / Cyclooxygenase 2
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58. Shammas MA, Koley H, Batchu RB, Bertheau RC, Protopopov A, Munshi NC, Goyal RK: Telomerase inhibition by siRNA causes senescence and apoptosis in Barrett's adenocarcinoma cells: mechanism and therapeutic potential. Mol Cancer; 2005 Jul 15;4:24
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  • [Title] Telomerase inhibition by siRNA causes senescence and apoptosis in Barrett's adenocarcinoma cells: mechanism and therapeutic potential.
  • RESULTS: We designed siRNAs against two different regions of telomerase gene and evaluated their effect on telomere length, proliferative potential, and gene expression in Barrett's adenocarcinoma SEG-1 cells.
  • Telomerase siRNAs may therefore be strong candidates for highly selective therapy for chemoprevention and treatment of Barrett's adenocarcinoma.

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  • (PMID = 16022731.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / PHS HHS / / P01-78378; United States / PHS HHS / / NIH-P50-100007; United States / NIDDK NIH HHS / DK / R01 DK031092; United States / PHS HHS / / P050-100007; United States / NIDDK NIH HHS / DK / DK031092
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC1187920
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59. Zhao J, Chang AC, Li C, Shedden KA, Thomas DG, Misek DE, Manoharan AP, Giordano TJ, Beer DG, Lubman DM: Comparative proteomics analysis of Barrett metaplasia and esophageal adenocarcinoma using two-dimensional liquid mass mapping. Mol Cell Proteomics; 2007 Jun;6(6):987-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparative proteomics analysis of Barrett metaplasia and esophageal adenocarcinoma using two-dimensional liquid mass mapping.
  • Esophageal adenocarcinoma, currently the seventh leading cause of cancer-related death, has been associated with the presence of Barrett metaplasia.
  • The malignant potential of Barrett metaplasia is evidenced by ultimate progression of this condition to invasive adenocarcinoma.
  • We utilized liquid phase separation of proteins with chromatofocusing in the first dimension and nonporous reverse phase HPLC in the second dimension followed by ESI-TOF mass spectrometry to identify proteins differentially expressed in six Barrett metaplasia samples as compared with six esophageal adenocarcinoma samples; all six Barrett samples were obtained from the identical six patients from whom we obtained the esophageal adenocarcinoma tissue.
  • Among the proteins that were identified, Rho GDP dissociation inhibitor 2, alpha-enolase, Lamin A/C, and nucleoside-diphosphate kinase A were demonstrated to be up-regulated in both mRNA and protein expression in esophageal adenocarcinomas relative to Barrett metaplasia.
  • The cellular expression patterns were verified in both esophageal adenocarcinomas and in Barrett metaplasia by immunohistochemistry.
  • These differentially expressed proteins may have utility as useful candidate markers of esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Proteomics. Spectrometry, Mass, Electrospray Ionization

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  • (PMID = 16829691.001).
  • [ISSN] 1535-9476
  • [Journal-full-title] Molecular & cellular proteomics : MCP
  • [ISO-abbreviation] Mol. Cell Proteomics
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA71606; United States / NCI NIH HHS / CA / R01CA10010; United States / NCI NIH HHS / CA / R01CA90503; United States / NIGMS NIH HHS / GM / R01GM49500
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger
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60. Goldblum JR: Controversies in the diagnosis of Barrett esophagus and Barrett-related dysplasia: one pathologist's perspective. Arch Pathol Lab Med; 2010 Oct;134(10):1479-84
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  • [Title] Controversies in the diagnosis of Barrett esophagus and Barrett-related dysplasia: one pathologist's perspective.
  • CONTEXT: athologists frequently assess esophageal biopsy specimens to “rule out Barrett esophagus,” as well as to assess for the presence or absence of dysplasia.
  • OBJECTIVE: To review some of the recent controversies in the diagnosis of Barrett esophagus and Barrett-related dysplasia.
  • CONCLUSIONS: Although goblet cells are required by the American College of Gastroenterology to confirm a diagnosis of Barrett esophagus, this definition might expand to include columnar-lined esophagus without goblet cells.
  • The recognition of dysplasia in Barrett esophagus remains a difficult task for the surgical pathologist, with difficulties in distinguishing reactive epithelium from dysplasia, low-grade dysplasia from high-grade dysplasia, and even high-grade dysplasia from intramucosal adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Biopsy. Diagnosis, Differential. Esophagus / pathology. Goblet Cells / pathology. Humans. Observer Variation. Selection Bias

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  • [ErratumIn] Arch Pathol Lab Med. 2010 Dec;134(12):1729
  • (PMID = 20923304.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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61. Tschanz ER: Do 40% of patients resected for barrett esophagus with high-grade dysplasia have unsuspected adenocarcinoma? Arch Pathol Lab Med; 2005 Feb;129(2):177-80
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  • [Title] Do 40% of patients resected for barrett esophagus with high-grade dysplasia have unsuspected adenocarcinoma?
  • Results of studies conducted in the last 2 decades suggest that the detection of high-grade dysplasia in patients with Barrett esophagus is the harbinger of a synchronous adenocarcinoma, which remains undetected even by rigorous biopsy protocols but is discovered during resection of the esophagus.
  • Future research should utilize the combination of new endoscopic technologies with the continuing search for validated biomarkers that help predict the biological behavior of Barrett epithelium in individual patients, with a particular focus on the possible development of preneoplastic and neoplastic lesions.
  • Pathologists who chose to shift their focus from the traditional morphological investigation of dysplasia to the search for usable biomarkers can position themselves at the center of innovative research projects that could radically modify the management of patients with Barrett esophagus.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / surgery. Esophageal Neoplasms / diagnosis. Esophagus / abnormalities. Esophagus / surgery

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  • (PMID = 15679415.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 29
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62. Inomata Y, Koike T, Ohara S, Abe Y, Sekine H, Iijima K, Ariizumi K, Yamagishi H, Kitagawa Y, Imatani A, Shimosegawa T: Preservation of gastric acid secretion may be important for the development of gastroesophageal junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status. Am J Gastroenterol; 2006 May;101(5):926-33
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  • [Title] Preservation of gastric acid secretion may be important for the development of gastroesophageal junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status.
  • BACKGROUND: We have previously reported that Helicobacter pylori infection prevents reflux esophagitis (RE) and Barrett's esophagus (BE) by decreasing gastric acid secretion.
  • Gastroesophageal (GE) junction adenocarcinoma, including Barrett's adenocarcinoma, has been thought to be a complication of gastroesophageal reflux disease (GERD).
  • However, the relationship between H. pylori infection, gastric acid secretion, and GE junction adenocarcinoma has not yet been investigated in Japan.
  • METHODS: A total of 168 Japanese patients (RE alone: 80, short-segment BE (SSBE): 16, long-segment BE (LSBE): 20, GE junction adenocarcinoma: 12, distal early gastric cancer (EGC): 40; male/female = 106/62; mean age 61.5 yr) and 80 Japanese control subjects who had no localized lesions in the upper gastrointestinal tract (male/female = 43/37, mean age 58.1 yr) were enrolled for this study.
  • On the other hand, while the prevalence of H. pylori infection in patients with GE junction adenocarcinoma (58.3%) was significantly lower than that in patients with EGC (87.5%), it tended to be higher than that in patients with RE alone or BE.
  • The mean EGT value in patients with GE junction adenocarcinoma (3.94) was significantly higher than that in control subjects and patients with EGC (0.67), but it was comparable to that independent of the H. pylori infection status in patients with RE alone or BE.
  • CONCLUSION: Preservation of gastric acid secretion may be important for the development of GE junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / physiopathology. Esophageal Neoplasms / complications. Esophageal Neoplasms / physiopathology. Esophagitis, Peptic / physiopathology. Esophagogastric Junction. Gastric Acid / secretion. Helicobacter Infections / complications. Helicobacter pylori
  • [MeSH-minor] Barrett Esophagus / complications. Barrett Esophagus / physiopathology. Female. Gastric Acidity Determination. Gastrins / analysis. Humans. Male. Middle Aged. Prevalence. Stomach Neoplasms / complications. Stomach Neoplasms / physiopathology

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  • [CommentIn] Am J Gastroenterol. 2006 May;101(5):934-6 [16696780.001]
  • (PMID = 16573782.001).
  • [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 / Gastrins
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63. Piessen G, Wacrenier A, Briez N, Triboulet JP, Van Seuningen I, Mariette C: Clinical impact of MUC1 and MUC4 expression in Barrett-associated oesophageal adenocarcinoma. J Clin Pathol; 2009 Dec;62(12):1144-6
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  • [Title] Clinical impact of MUC1 and MUC4 expression in Barrett-associated oesophageal adenocarcinoma.
  • AIMS: To study the expression of MUC1 and MUC4 mucins in Barrett-associated oesophageal adenocarcinoma and coexisting lesions of the carcinogenic sequence (normal mucosa, metaplasia, dysplasia) if present, and to investigate their prognostic significance.
  • METHODS: The expression profiles of MUC1 and MUC4 were investigated by immunohistochemistry in tissue samples obtained from consecutive patients with primary surgically resected lower third oesophageal adenocarcinoma (OA) between 1997 and 2002.
  • RESULTS: All 52 patients exhibited OA, with 25 patients (48.1%) having associated Barrett oesophagus lesions (metaplasia or/and dysplasia).
  • MUC1 and MUC4 were expressed in 52 and 41 of the 52 patients with adenocarcinoma (100% and 78%), respectively.
  • The prevalence of MUC4 staining was significantly decreased in metaplasia compared with normal mucosa (53% versus 92%, p<0.001).
  • The results do not support a role for these two membrane-bound mucins as either a phenotypic or a prognostic marker for the development of Barrett OA.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / metabolism. Mucin-1 / metabolism. Mucin-4 / metabolism

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  • (PMID = 19946103.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MUC1 protein, human; 0 / MUC4 protein, human; 0 / Mucin-1; 0 / Mucin-4; 0 / Neoplasm Proteins
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64. Ren CR, Dong L, Guo XY: [Expression of c-myb in reflux esophagitis, Barrett esophagus and esophageal adenocarcinoma]. Nan Fang Yi Ke Da Xue Xue Bao; 2010 Dec;30(12):2693-5
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  • [Title] [Expression of c-myb in reflux esophagitis, Barrett esophagus and esophageal adenocarcinoma].
  • OBJECTIVE: To investigate the expression of c-myb in reflux esophagitis, Barrett esophagus and esophageal adenocarcinoma.
  • METHODS: The expression levels of c-myb in the esophageal mucosa tissue of patients with reflux esophagitis, Barrett esophagus and esophageal adenocarcinoma were detected by real-time fluorescent quantitative RT-PCR.
  • RESULTS: The expression levels of c-myb mRNA in Barrett esophagus and esophageal adenocarcinoma tissues was significantly higher than that in normal and reflux esophagitis esophageal tissue (P<0.05 or 0.01), and increased progressively with the development of reflux esophagitis into Barrett esophagus and esophageal adenocarcinoma.
  • CONCLUSIONS: The expression level of c-myb mRNA is closely related with the development of Barrett esophagus and esophageal adenocarcinoma, and may be used as a valuable index for monitoring the early onset and intervention of Barrett esophagus and esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Esophagitis, Peptic / metabolism. Proto-Oncogene Proteins c-myb / metabolism

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  • (PMID = 21177182.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb
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65. Huang Q, Yu C, Zhang X, Goyal RK: Comparison of DNA histograms by standard flow cytometry and image cytometry on sections in Barrett's adenocarcinoma. BMC Clin Pathol; 2008 May 30;8:5

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  • [Title] Comparison of DNA histograms by standard flow cytometry and image cytometry on sections in Barrett's adenocarcinoma.
  • BACKGROUND: The purpose of this study was to compare DNA histograms obtained by standard flow cytometry (FC) and high fidelity image cytometry on sections (ICS) in normal gastrointestinal mucosa and Barrett's adenocarcinoma (BAC).

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  • (PMID = 18513411.001).
  • [ISSN] 1472-6890
  • [Journal-full-title] BMC clinical pathology
  • [ISO-abbreviation] BMC Clin Pathol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062867
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2424056
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66. Oberg S, Wenner J, Johansson J, Walther B, Willén R: Barrett esophagus: risk factors for progression to dysplasia and adenocarcinoma. Ann Surg; 2005 Jul;242(1):49-54
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] Barrett esophagus: risk factors for progression to dysplasia and adenocarcinoma.
  • OBJECTIVE: To evaluate risk factors for dysplasia and adenocarcinoma development in nondysplastic Barrett mucosa.
  • SUMMARY BACKGROUND DATA: The risk for patients with Barrett esophagus to develop esophageal adenocarcinoma is low, and most patients undergoing surveillance will not develop malignancy.
  • Identification of risk factors may allow for more rational surveillance programs in which patients are stratified according to their individual risk of progressing to dysplasia and invasive adenocarcinoma.
  • METHODS: The development of dysplasia and esophageal adenocarcinoma was studied during long-term endoscopic and histologic surveillance in 140 patients with Barrett esophagus free from dysplasia.
  • Risk factors for progression to dysplasia and adenocarcinoma were evaluated.
  • Forty-four patients (31.4%) developed low-grade dysplasia and 7 patients (5%) developed high-grade dysplasia or esophageal adenocarcinoma.
  • Low-grade dysplasia (relative risk = 5.5; 95% confidence interval, 1.1-28.6) and long duration of reflux symptoms (relative risk = 1.3; 95% confidence interval, 1.2-1.7) were independently associated with an increased risk of developing high-grade dysplasia or esophageal adenocarcinoma.
  • CONCLUSIONS: Successful antireflux surgery protects the Barrett mucosa from developing high-grade dysplasia and esophageal adenocarcinoma, possibly by better control of reflux of gastric contents.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Precancerous Conditions / pathology

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  • (PMID = 15973101.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1357704
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67. Burnat G, Rau T, Elshimi E, Hahn EG, Konturek PC: Bile acids induce overexpression of homeobox gene CDX-2 and vascular endothelial growth factor (VEGF) in human Barrett's esophageal mucosa and adenocarcinoma cell line. Scand J Gastroenterol; 2007 Dec;42(12):1460-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bile acids induce overexpression of homeobox gene CDX-2 and vascular endothelial growth factor (VEGF) in human Barrett's esophageal mucosa and adenocarcinoma cell line.
  • OBJECTIVE: Barrett's esophagus (BE) is an acquired precancerous condition that develops from mucosal injury incurred after chronic gastroesophageal acid and bile reflux.
  • The aims of the present study were 1) to compare the mRNA and protein expression of CDX-2 in biopsies obtained from patients with BE and normal squamous epithelium and 2) to study the effect of two different bile salts, ursodeoxycholic acid (UDCA) and deoxycholic acid (DCA), on the mRNA expression of CDX-2 and vascular endothelial growth factor (VEGF) in Barrett's the adenocarcinoma cell line (OE-33).
  • MATERIAL AND METHODS: CDX-2 expression was measured in Barrett's mucosa and normal esophageal mucosa obtained from 15 patients with BE histologically diagnosed by immunohistochemistry, Western blot, and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR).
  • RESULTS: Both mRNA and protein expression of CDX-2 were significantly up-regulated in Barrett's mucosa as compared to normal esophageal mucosa.
  • DCA appears to be a stronger stimulant of the expression of VEGF than UDCA in the Barrett's carcinoma cell line, indicating a stronger carcinogenic potential of this bile salt.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Bile Acids and Salts / pharmacology. Esophageal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 17852856.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
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68. Mashimo H, Wagh MS, Goyal RK: Surveillance and screening for Barrett esophagus and adenocarcinoma. J Clin Gastroenterol; 2005 Apr;39(4 Suppl 2):S33-41
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  • [Title] Surveillance and screening for Barrett esophagus and adenocarcinoma.
  • Current recommendations for screening and surveillance of Barrett esophagus and related lesions are based on recent guidelines by the Practice Parameters Committee of the American College of Gastroenterology.
  • There is strong rationale for vigorous initial testing to document the baseline status and identify early adenocarcinoma, and for surveillance of high-grade dysplasia.
  • Recommendations for screening and surveillance are not evidence-based and unlikely to alter national mortality from esophageal adenocarcinoma.
  • Current recommendations are limited by inconsistent endoscopic findings and sampling errors, inconsistent histologic diagnoses of Barrett esophagus and dysplasia, and our poor understanding of the natural history of various histologic lesions.
  • Effective screening programs depend on development of simple, inexpensive, and reliable methods to identify the small group of patients truly at high risk for adenocarcinoma for endoscopic screening.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis

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  • (PMID = 15758657.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK031092; United States / NIDDK NIH HHS / DK / DK62867
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 52
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69. Murphy SJ, Hughes AE, Patterson CC, Anderson LA, Watson RG, Johnston BT, Comber H, McGuigan J, Reynolds JV, Murray LJ: A population-based association study of SNPs of GSTP1, MnSOD, GPX2 and Barrett's esophagus and esophageal adenocarcinoma. Carcinogenesis; 2007 Jun;28(6):1323-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A population-based association study of SNPs of GSTP1, MnSOD, GPX2 and Barrett's esophagus and esophageal adenocarcinoma.
  • Oxidative stress appears to be important in the pathogenesis of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC).
  • The Factors Influencing the Barrett's Adenocarcinoma Relationship (FINBAR) study is a population-based, case-control study of BE and EAC in Ireland.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Glutathione Peroxidase / genetics. Glutathione S-Transferase pi / genetics. Polymorphism, Single Nucleotide. Superoxide Dismutase / genetics

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  • (PMID = 17277236.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.11.1.- / GPX2 protein, human; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi
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70. Quaroni L, Casson AG: Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy. Analyst; 2009 Jun;134(6):1240-6
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  • [Title] Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy.
  • Matched histologically normal esophageal squamous epithelium (NS), premalignant Barrett esophagus (BE), and primary esophageal adenocarcinoma (EADC) tissues, each defined according to strict clinicopathologic criteria, were obtained from patients who underwent esophageal resection.
  • [MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Spectroscopy, Fourier Transform Infrared / methods
  • [MeSH-minor] Adenocarcinoma / pathology. Cluster Analysis. Goblet Cells / cytology. Goblet Cells / pathology. Humans. Intestines / pathology. Light. Metaplasia / pathology. Microscopy. Synchrotrons

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  • (PMID = 19475154.001).
  • [ISSN] 1364-5528
  • [Journal-full-title] The Analyst
  • [ISO-abbreviation] Analyst
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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71. Mino-Kenudson M, Ban S, Ohana M, Puricelli W, Deshpande V, Shimizu M, Nishioka NS, Lauwers GY: Buried dysplasia and early adenocarcinoma arising in barrett esophagus after porfimer-photodynamic therapy. Am J Surg Pathol; 2007 Mar;31(3):403-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Buried dysplasia and early adenocarcinoma arising in barrett esophagus after porfimer-photodynamic therapy.
  • The restoration of squamous epithelium after photodynamic therapy (PDT) for Barrett esophagus (BE) and its related neoplasms has been noted.
  • Fifty-two BE patients with high-grade dysplasia (n=19), intramucosal adenocarcinoma (n=28), and invasive adenocarcinoma (n=5) were treated with porfimer PDT.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus. Dihematoporphyrin Ether / therapeutic use. Esophageal Neoplasms / pathology. Photochemotherapy. Photosensitizing Agents / therapeutic use. Precancerous Conditions / pathology

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  • (PMID = 17325482.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 97067-70-4 / Dihematoporphyrin Ether
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72. Murphy SJ, Anderson LA, Ferguson HR, Johnston BT, Watson PR, McGuigan J, Comber H, Reynolds JV, Murray LJ, Cantwell MM: Dietary antioxidant and mineral intake in humans is associated with reduced risk of esophageal adenocarcinoma but not reflux esophagitis or Barrett's esophagus. J Nutr; 2010 Oct;140(10):1757-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dietary antioxidant and mineral intake in humans is associated with reduced risk of esophageal adenocarcinoma but not reflux esophagitis or Barrett's esophagus.
  • The role of antioxidants in the pathogenesis of reflux esophagitis (RE), Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC) remains unknown.
  • We performed an assessment of dietary antioxidant intake in a case control study of RE (n = 219), BE (n = 220), EAC (n = 224), and matched population controls (n = 256) (the Factors Influencing the Barrett's Adenocarcinoma Relationship study) using a modification of a validated FFQ.
  • [MeSH-major] Adenocarcinoma / prevention & control. Antioxidants / administration & dosage. Barrett Esophagus / prevention & control. Diet. Gastroesophageal Reflux / prevention & control. Minerals / administration & dosage

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  • (PMID = 20702746.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Minerals; 1406-18-4 / Vitamin E; 36-88-4 / Carotenoids; 789U1901C5 / Copper; H6241UJ22B / Selenium; J41CSQ7QDS / Zinc; PQ6CK8PD0R / Ascorbic Acid
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73. Horváth OP, Kalmár K: Early-stage adenocarcinoma in Barrett's esophagus: aspects of surgical therapies. Dig Dis; 2009;27(1):45-53
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  • [Title] Early-stage adenocarcinoma in Barrett's esophagus: aspects of surgical therapies.
  • Adenocarcinomas in Barrett's esophagus are increasingly diagnosed at early stages thanks to effective surveillance programs.
  • Subtotal esophagectomy with extended lymphadenectomy is considered the best curative treatment for patients with early adenocarcinoma of the esophagus.
  • An individualized strategy should be employed based on staging (tumor penetration into the mucosa/submucosa, presence of lymph node metastasis), multicentricity of tumor, length of the underlying Barrett's mucosa and risk factors of the affected patient.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophagectomy. Esophagoscopy
  • [MeSH-minor] Ablation Techniques. Humans. Lymph Node Excision. Lymphatic Metastasis. Minimally Invasive Surgical Procedures. Neoplasm Recurrence, Local. Neoplasm Staging. Respiratory Mucosa / pathology. Respiratory Mucosa / surgery

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  • (PMID = 19439960.001).
  • [ISSN] 1421-9875
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 55
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74. Miller RC, Atherton PJ, Kabat BF, Fredericksen MB, Geno DM, Deschamps C, Jatoi A, Sloan JA, Romero Y: Marital status and quality of life in patients with esophageal cancer or Barrett's esophagus: the mayo clinic esophageal adenocarcinoma and Barrett's esophagus registry study. Dig Dis Sci; 2010 Oct;55(10):2860-8
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  • [Title] Marital status and quality of life in patients with esophageal cancer or Barrett's esophagus: the mayo clinic esophageal adenocarcinoma and Barrett's esophagus registry study.
  • AIMS: To quantify the association of marital status and changes in QOL over time in patients with EC and patients with Barrett's esophagus (BE).
  • METHODS: Eligible patients in the Mayo Clinic Esophageal Adenocarcinoma and Barrett's Esophagus Registry completed QOL assessments at baseline and approximately 1 year later.
  • [MeSH-major] Adenocarcinoma / epidemiology. Barrett Esophagus / epidemiology. Esophageal Neoplasms / epidemiology. Marital Status / statistics & numerical data. Quality of Life

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  • (PMID = 20094784.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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75. Byard RW: Barrett esophagus and unexpected death. Am J Forensic Med Pathol; 2007 Jun;28(2):147-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Barrett esophagus and unexpected death.
  • Barrett esophagus is characterized by the presence of columnar mucosa in the lower esophagus in continuity with gastric mucosa.
  • Complications include ulceration and adenocarcinoma.
  • Although sudden and unexpected death is not a usual outcome, the case of a 63-year-old man is presented who died unexpectedly following perforation of an ulcerated Barrett esophagus, with development of an esophagopleural fistula.
  • Sudden and/or unexpected death in individuals with Barrett esophagus may result from hemorrhage due to erosion into mural vessels, the aorta or heart, or from penetration into the pleural space, trachea, bronchi, and pericardial sac, with the development of tension pyopneumothorax, bronchial fistula, and mediastinitis.
  • Ulceration of the lower esophagus at autopsy should prompt consideration of the possibility of a Barrett esophagus and initiate careful dissection/examination of the surrounding mediastinal tissues and vessels.
  • [MeSH-major] Barrett Esophagus / complications. Death, Sudden / etiology

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  • (PMID = 17525567.001).
  • [ISSN] 0195-7910
  • [Journal-full-title] The American journal of forensic medicine and pathology
  • [ISO-abbreviation] Am J Forensic Med Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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76. 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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  • [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.
  • 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

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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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77. Casson AG, Williams L, Guernsey DL: Epidemiology and molecular biology of Barrett esophagus. Semin Thorac Cardiovasc Surg; 2005;17(4):284-91
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  • [Title] Epidemiology and molecular biology of Barrett esophagus.
  • Over the past three decades, there has been a marked change in the epidemiology of esophageal malignancy, with an increasing incidence of esophageal adenocarcinoma.
  • It is hypothesized that chronic GERD results in acute mucosal injury, promotes cellular proliferation, and induces specialized columnar metaplasia (Barrett esophagus).
  • Progression of Barrett esophagus to invasive adenocarcinoma is reflected histologically by the metaplasia-dysplasia-carcinoma sequence.
  • Dysplasia is widely regarded as the precursor of invasive cancer, and high-grade dysplasia in Barrett epithelium is frequently associated with esophageal adenocarcinoma.
  • Although several molecular alterations have been described in Barrett esophagus, it is anticipated that relatively few will prove to be clinically useful.
  • To date, biomarkers which currently appear to predict the progression of Barrett esophagus to invasive malignancy include aneuploidy, loss of heterozygosity of 17p (implicating the p53 tumor suppressor gene), and cyclin D1 protein overexpression, and with further validation, will most likely be incorporated into routine clinical practice.
  • It is anticipated that models incorporating objective scores of sociodemographic and lifestyle risk factors (ie, age, gender, body mass index), severity of reflux symptoms, endoscopic and histologic findings, and an assessment of a panel of biomarkers will be developed to further define subsets of patients with Barrett esophagus at increased risk for malignant progression, thereby permitting the development of more rational endoscopic surveillance and screening programs.
  • [MeSH-major] Barrett Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Chronic Disease. Cyclin D1 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Epithelium / pathology. Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Gastroesophageal Reflux / complications. Genes, p53 / genetics. Humans. Ploidies

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  • (PMID = 16428034.001).
  • [ISSN] 1043-0679
  • [Journal-full-title] Seminars in thoracic and cardiovascular surgery
  • [ISO-abbreviation] Semin. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 136601-57-5 / Cyclin D1
  • [Number-of-references] 112
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78. Anandasabapathy S, Jhamb J, Davila M, Wei C, Morris J, Bresalier R: Clinical and endoscopic factors predict higher pathologic grades of Barrett dysplasia. Cancer; 2007 Feb 15;109(4):668-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and endoscopic factors predict higher pathologic grades of Barrett dysplasia.
  • BACKGROUND: Barrett esophagus is highly prevalent in the Western world; however, only a minority of affected individuals progress to esophageal adenocarcinoma.
  • Whereas many studies have examined risk factors for development of Barrett metaplasia, few data are available on risk factors for progression to neoplasia.
  • Identifying simple, reliable, clinical, and endoscopic predictors of high-grade dysplasia and adenocarcinoma would be helpful for risk stratification in screening and surveillance programs.
  • METHODS: Clinical, endoscopic, and histologic data were reviewed for patients with a new Barrett diagnosis between 2002 and 2005.
  • Patients were classified, by an expert gastrointestinal pathologist, as having intestinal metaplasia, indefinite-for-dysplasia, low-grade dysplasia, high-grade dysplasia, and esophageal adenocarcinoma.
  • Gender, age, race, ethnicity, hiatal hernia presence and size, Barrett segment length, H. pylori status, alcohol, smoking, proton pump inhibitor (PPI) use and duration, and reflux symptom duration were evaluated by logistic regression analysis for their association with dysplasia severity.
  • RESULTS: In all, 109 patients (26 women, 83 men, mean age: 58.8) were newly diagnosed with Barrett metaplasia (n = 39), indefinite/low-grade dysplasia (n = 35), and high-grade dysplasia/esophageal adenocarcinoma (n = 35) over a 3-year period.
  • On logistic regression analysis, duration of reflux symptoms for >or=20 years (odds ratio [OR]: 5.66, P = .012), longer Barrett segment length (OR for 3-6 cm vs. <3 cm: 9.05, P < .0001; OR for >or=6 cm: 8.374, P < .0001), hernia size >or=4 cm (OR: 10.63, P = .014), and male gender (OR: 4.03, P = .0019) were associated with higher pathologic grade.
  • Duration of reflux symptoms and Barrett length were significant as both discrete and continuous variables.
  • In bivariate models, gender and Barrett length (continuous form) were significantly associated with grade when considered together (OR: 2.52, P = .0490 and OR: 1.30, P < .0001), as were gender and hernia size >4 cm (OR: 4.64, P = .0049 and OR: 12.18, P = .0197).
  • These factors along with H. pylori status warrant further prospective evaluation as predictors of risk for development of high-grade dysplasia and esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagoscopy. Hernia, Hiatal / pathology

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  • (PMID = 17211862.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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79. Younes M: What is the role of cytokeratins in Barrett/cardia differentiation? Arch Pathol Lab Med; 2005 Feb;129(2):181-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] What is the role of cytokeratins in Barrett/cardia differentiation?
  • The importance of distinguishing between Barrett metaplasia and intestinal metaplasia of the gastric cardia is now accepted, and the management of each entity is quite different.
  • Patients with Barrett metaplasia are enrolled in surveillance programs, consisting of periodic endoscopy and biopsy, because of the known risk of developing adenocarcinoma of the esophagus.
  • Patients with intestinal metaplasia of the gastric cardia, however, are not currently enrolled in such programs, because this condition carries a low risk of developing adenocarcinoma of the gastric cardia.
  • They concluded that the Barrett CK7/CK20 pattern was a highly sensitive and specific marker for Barrett metaplasia.
  • However, because it may be associated with premalignant lesions elsewhere in the gastric mucosa, we propose that intestinal metaplasia of the gastric cardia may have the same clinical implication as Barrett metaplasia.
  • [MeSH-major] Barrett Esophagus / etiology. Cardia / pathology. Keratins / physiology. Metaplasia / etiology. Stomach Diseases / etiology

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  • (PMID = 15679416.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 68238-35-7 / Keratins
  • [Number-of-references] 16
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80. Pruyt M, Devriendt D, Vanneste A: Malignant melanoma and adenocarcinoma of a Barrett oesophagus. Acta Chir Belg; 2006 Sep-Oct;106(5):616-8
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  • [Title] Malignant melanoma and adenocarcinoma of a Barrett oesophagus.
  • An adenocarcinoma with a malignant melanoma in a Barrett oesophagus is extremely rare.
  • In our case it was obvious that there were two different tumours because the MM was negative for cytokeratin, but the adenocarcinoma was positive for cytokeratin.
  • [MeSH-major] Adenocarcinoma / complications. Barrett Esophagus / complications. Esophageal Neoplasms / complications. Melanoma / complications. Neoplasms, Multiple Primary / complications

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  • (PMID = 17168284.001).
  • [ISSN] 0001-5458
  • [Journal-full-title] Acta chirurgica Belgica
  • [ISO-abbreviation] Acta Chir. Belg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / S100 Proteins; EC 4.2.1.11 / Phosphopyruvate Hydratase
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81. Punia RS, Arya S, Mohan H, Duseja A, Bal A: Spectrum of clinico-pathological changes in Barrett oesophagus. J Assoc Physicians India; 2006 Mar;54:187-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spectrum of clinico-pathological changes in Barrett oesophagus.
  • OBJECTIVES: Barrett oesophagus is replacement of squamous epithelium to specialised intestinal metaplasia.
  • It is associated with an increased risk for adenocarcinoma which develops through dysplasia.
  • METHODS: Between January 1999 and June 2002 we diagnosed 13 cases of Barrett oesophagus.
  • RESULTS: Out of 55 patients with symptoms of gastro-oesophageal reflux disease, 13 cases were diagnosed as Barrett oesophagus.
  • At endoscopy, in 84.6% patients, lesions were in the form of islands of red mucosa.
  • Associated dysplasia was not seen in any of the case, while one case showed associated adenocarcinoma.
  • CONCLUSION: Barrett oesophagus is seen in a younger population amongst Indians.
  • There is a paucity of patients with pure dysplasia in Barrett metaplasia.
  • Despite the fact that there are a number of patients presenting with Barrett esophagus and carcinoma, very few patients present with dysplasia, indicating that Barrett oesophagus is a silent disease presenting later as a carcinoma.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / pathology. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology

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  • (PMID = 16800342.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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82. Shaheen NJ: Advances in Barrett's esophagus and esophageal adenocarcinoma. Gastroenterology; 2005 May;128(6):1554-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in Barrett's esophagus and esophageal adenocarcinoma.
  • Despite advances in diagnosis and therapy, esophageal adenocarcinoma remains an aggressive and usually lethal tumor.
  • This review focuses on the epidemiology of esophageal adenocarcinoma and its presumed precursor lesion, Barrett's esophagus; the pathogenesis of the cancer; advances in treatment of adenocarcinoma and Barrett's esophagus; and strategies for cancer prevention.
  • Although the absolute number of cases of adenocarcinoma in the United States is still small, the incidence of this cancer has increased dramatically in the last 40 years, and adenocarcinoma is now the predominant form of esophageal cancer in this country.
  • Recent evidence suggests that Barrett's esophagus is more prevalent in asymptomatic individuals than previously appreciated.
  • The pathogenesis of Barrett's esophagus is poorly understood.
  • Given that some subjects will have repeated bouts of severe erosive esophagitis and never develop Barrett's esophagus, host factors must play an important role.
  • The utility of neoadjuvant radiation and chemotherapy in those with adenocarcinoma, although they are widely practiced, is not of clear benefit, and some authorities recommend against it.
  • The value of chemoprevention in subjects with dysplastic Barrett's esophagus by use of cyclooxygenase 2 inhibitors, nonsteroidal anti-inflammatory drugs, or proton pump inhibitors is unknown.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / therapy. Barrett Esophagus / pathology. Barrett Esophagus / therapy. Esophageal Neoplasms / pathology. Esophageal Neoplasms / therapy

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  • (PMID = 15887151.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K23DK59311-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 130
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83. Levine MS: Barrett esophagus: update for radiologists. Abdom Imaging; 2005 Mar-Apr;30(2):133-41
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  • [Title] Barrett esophagus: update for radiologists.
  • Barrett esophagus is a well-recognized entity in which there is progressive columnar metaplasia of the lower esophagus due to longstanding gastroesophageal reflux and reflux esophagitis [1].
  • This condition is important because it is associated with an increased risk of developing esophageal adenocarcinoma by a well-established sequence from dysplasia to carcinoma [2].
  • During the past decade, however, an explosion of new data has dramatically affected our understanding of Barrett esophagus.
  • Not only have revised histopathologic criteria been developed for this condition, but it is currently believed that patients with Barrett esophagus should be classified as having "short-segment" or "long-segment" disease based on the extent of columnar metaplasia in the distal esophagus.
  • This distinction has important implications for the risk of developing esophageal adenocarcinoma and subsequent need for endoscopic surveillance.
  • The purpose of this article is to present these new concepts about Barrett esophagus and provide radiologists with a more current framework for diagnosing this condition.
  • [MeSH-major] Barrett Esophagus / radiography

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  • (PMID = 15602646.001).
  • [ISSN] 0942-8925
  • [Journal-full-title] Abdominal imaging
  • [ISO-abbreviation] Abdom Imaging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 56
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84. Lin X, Finkelstein SD, Zhu B, Ujevich BJ, Silverman JF: Loss of heterozygosities in Barrett esophagus, dysplasia, and adenocarcinoma detected by esophageal brushing cytology and gastroesophageal biopsy. Cancer; 2009 Feb 25;117(1):57-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of heterozygosities in Barrett esophagus, dysplasia, and adenocarcinoma detected by esophageal brushing cytology and gastroesophageal biopsy.
  • The authors also found that LOHs at 1p36, 9p21, and 17p13 may play an important role in Barrett esophagus (BE), LOHs at 10q23, 17p13, and 17q12 in low-grade dysplasia (LGD), LOHs at 5q23 and 17q21 in high-grade dysplasia (HGD), and LOHs at 5q23 and 21q22 in adenocarcinoma.
  • CONCLUSIONS: Detection of LOHs targeting tumor suppressor genes can be useful in evaluating gastroesophageal lesions, studying oncogenesis of gastroesophageal adenocarcinoma, and, in combination with EBC and GEB, determining surveillance for BE and LGD and/or treatment for HGD and adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Cell Transformation, Neoplastic / genetics. Cytodiagnosis / methods. Esophageal Neoplasms / genetics. Precancerous Conditions / genetics

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  • [Copyright] (c) 2009 American Cancer Society.
  • (PMID = 19347831.001).
  • [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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85. Wijnhoven BP, Hussey DJ, Watson DI, Tsykin A, Smith CM, Michael MZ, South Australian Oesophageal Research Group: MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma. Br J Surg; 2010 Jun;97(6):853-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND: The genetic changes that drive metaplastic progression from squamous oesophageal mucosa toward intestinal metaplasia and adenocarcinoma are unclear.
  • This study examined whether miRNAs play a role in the development of oesophageal adenocarcinoma.
  • METHODS: RNA was extracted from mucosa of normal oesophageal squamous epithelium, normal gastric epithelium, Barrett's oesophagus with intestinal metaplasia and oesophageal adenocarcinoma obtained from 16 individuals.
  • Expression of miR-143, miR-145 and miR-215 was lower in oesophageal adenocarcinoma than in Barrett's oesophagus.
  • MiR-205 levels were lower in gastric epithelium than in both Barrett's oesophagus and adenocarcinoma.
  • Dysregulation of specific miRNAs could contribute to metaplastic and neoplastic processes in the oesophageal mucosa.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. MicroRNAs / analysis. RNA, Messenger / analysis

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  • (PMID = 20301167.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger
  • [Investigator] Wijnhoven BP; Hussey DJ; Watson DI; Smith CM; Mayne GC; Michael MZ; Astill D; Van der Hoek MB; Tsykin A; Tilanus HW; Wijnhoven BP
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86. Botelho NK, Schneiders FI, Lord SJ, Freeman AK, Tyagi S, Nancarrow DJ, Hayward NK, Whiteman DC, Lord RV: Gene expression alterations in formalin-fixed, paraffin-embedded Barrett esophagus and esophageal adenocarcinoma tissues. Cancer Biol Ther; 2010 Jul 15;10(2):172-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression alterations in formalin-fixed, paraffin-embedded Barrett esophagus and esophageal adenocarcinoma tissues.
  • BACKGROUND AND AIM: Widespread applicability of tissue-based mRNA expression screening for Barrett esophagus (BE) is likely to require (1) accurate methods for assaying archival formalin-fixed, paraffin-embedded (FFPE) histopathology specimens taken at endoscopy, and (2) validation studies of promising biomarkers in different patient cohorts.
  • METHODS: mRNA was isolated from 54 FFPE small endoscopic biopsies from patients with Barrett intestinal metaplasia (BE), esophageal adenocarcinoma (EAC), or control patients with a normal squamous-lined esophagus.
  • This study's findings for many highly differentially expressed genes are very similar to those previously reported, suggesting that these genes should be tested further in longitudinal studies for their potential role as biomarkers of progression to more advanced Barrett disease.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Gene Expression Profiling / methods. Polymerase Chain Reaction / methods

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  • (PMID = 20543560.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 1HG84L3525 / Formaldehyde
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87. Siewert JR, Bartels H, Stein HJ: [Abdomino-right-thoracic esophagectomy with intrathoracic anastomosis in Barrett's cancer]. Chirurg; 2005 Jun;76(6):588-94
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  • [Title] [Abdomino-right-thoracic esophagectomy with intrathoracic anastomosis in Barrett's cancer].
  • [Transliterated title] Abdomino-rechts-thorakale Osophagusresektion mit intrathorakaler Anastomose beim Barrett-Karzinom.
  • The modified technique of abdomino-right-thoracic esophagectomy (the Lewis-Tanner approach) is increasingly being favoured as the surgical procedure of choice in patients with resectable adenocarcinoma of the distal esophagus, so-called Barrett's cancer.
  • [MeSH-major] Abdomen / surgery. Adenocarcinoma / surgery. Anastomosis, Surgical / methods. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophagectomy / methods. Precancerous Conditions / surgery. Thoracotomy / methods

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  • [Cites] Chirurg. 2004 Nov;75(11):1063-70 [15517114.001]
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  • (PMID = 15875146.001).
  • [ISSN] 0009-4722
  • [Journal-full-title] Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen
  • [ISO-abbreviation] Chirurg
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
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88. Lewis JT, Wang KK, Abraham SC: Muscularis mucosae duplication and the musculo-fibrous anomaly in endoscopic mucosal resections for barrett esophagus: implications for staging of adenocarcinoma. Am J Surg Pathol; 2008 Apr;32(4):566-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Muscularis mucosae duplication and the musculo-fibrous anomaly in endoscopic mucosal resections for barrett esophagus: implications for staging of adenocarcinoma.
  • Endoscopic mucosal resection (EMR) is increasingly used for management of Barrett esophagus (BE)-related neoplasia.
  • The frequency, morphologic characteristics, and effect of MM duplication in adenocarcinoma staging in EMRs have not yet been evaluated.
  • Carcinomas reaching the level of submucosa were classified as invasive adenocarcinoma (INV); those confined to lamina propria or MM were classified as intramucosal adenocarcinoma (IMAC).
  • Of 122 EMRs, 11 (9%) reached mucosa only, 109 (89%) extended to submucosa, and 2 (2%) extended into muscularis propria.
  • Final pathologic diagnoses were 9 (7%) no specialized Barrett mucosa, 4 (3%) BE without dysplasia, 13 (11%) low-grade dysplasia, 51 (42%) high-grade dysplasia, 33 (27%) IMAC, and 12 (10%) INV.
  • It is closely associated with the presence of BE but is not affected by neoplastic progression in the Barrett epithelium.
  • Level of IMAC may be a critical feature because of potential access to lymphatic spaces between duplicated MM layers, and we therefore recommend including an explicit statement about the depth of adenocarcinoma invasion rather than using only broad terms such as IMAC or INV in the diagnostic report.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Diagnostic Errors / prevention & control. Esophageal Neoplasms / pathology. Esophagectomy / methods. Esophagoscopy. Esophagus / pathology. Precancerous Conditions / pathology

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  • (PMID = 18300796.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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89. Brown IS, Whiteman DC, Lauwers GY: Foveolar type dysplasia in Barrett esophagus. Mod Pathol; 2010 Jun;23(6):834-43
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  • [Title] Foveolar type dysplasia in Barrett esophagus.
  • Adenocarcinoma of the lower esophagus and esophagogastric junction is increasing in incidence in Western countries.
  • A metaplasia (Barrett esophagus)-dysplasia-carcinoma sequence induced by gastroesophageal reflux disease is established.
  • Two patterns of Barrett dysplasias have been described-adenomatous (type 1) and non-adenomatous (type 2 or foveolar/hyperplastic type).
  • Esophagogastrectomy cases from 41 patients with glandular dysplasia with and without associated invasive adenocarcinoma of the lower esophagus were evaluated for expression of MUC2, MUC5AC, CDX2, villin, Ki67 and p53.
  • In conclusion, our study provides evidence for a non intestinal pathway to neoplastic development in Barrett esophagus, that is, gastric metaplasia-foveolar dysplasia-adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Precancerous Conditions / pathology

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  • (PMID = 20228780.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Ki-67 Antigen; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Microfilament Proteins; 0 / Mucin 5AC; 0 / Mucin-2; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / villin
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90. de Jonge PJ, Steyerberg EW, Kuipers EJ, Honkoop P, Wolters LM, Kerkhof M, van Dekken H, Siersema PD: Risk factors for the development of esophageal adenocarcinoma in Barrett's esophagus. Am J Gastroenterol; 2006 Jul;101(7):1421-9
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  • [Title] Risk factors for the development of esophageal adenocarcinoma in Barrett's esophagus.
  • OBJECTIVE: To identify risk factors for esophageal adenocarcinoma (EAC) in patients with Barrett's esophagus (BE).
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology

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  • (PMID = 16863542.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anti-Ulcer Agents
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91. Zou H, Molina JR, Harrington JJ, Osborn NK, Klatt KK, Romero Y, Burgart LJ, Ahlquist DA: Aberrant methylation of secreted frizzled-related protein genes in esophageal adenocarcinoma and Barrett's esophagus. Int J Cancer; 2005 Sep 10;116(4):584-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant methylation of secreted frizzled-related protein genes in esophageal adenocarcinoma and Barrett's esophagus.
  • Hypermethylation of secreted frizzled-related proteins (SFRP) genes frequently occurs with several cancers but has not been studied in esophageal adenocarcinoma or its precursor-Barrett's esophagus.
  • To explore the role of SFRP methylation in the neoplastic progression of Barrett's esophagus and to evaluate methylated SFRP genes as biomarkers for Barrett's esophagus and cancer, methylation of SFRP genes was determined in esophageal adenocarcinomas, Barrett's esophagus and normal epithelia using methylation-specific PCR.
  • The mRNA expression of SFRP genes was quantified by real-time reverse-transcription PCR in esophageal adenocarcinoma cell lines with and without demethylation by 5-aza-2'deoxycytidine and inhibition of deacetylation by trichostatin A treatment.
  • Hypermethylation of SFRP1, 2, 4 and 5 was detected in 93%, 83%, 73% and 85% of 40 cancers; 81%, 89%, 78% and 73% of 37 Barrett's epithelia; 25%, 64%, 32% and 21% of 28 adjacent normal epithelia from Barrett's patients; and 10%, 67%, 0% and 13% of 30 normal esophagogastric epithelia from healthy individuals, respectively (p < 0.001 for SFRP1, 4 and 5; p < 0.05 for SFRP2).
  • Thus, hypermethylation of SFRP genes is a common early event in the evolution of esophageal adenocarcinoma, and methylation of SFRP1, 4 and 5 might serve as biomarkers for Barrett's neoplasia.
  • Aberrant promoter methylation appears to functionally silence SFRP gene expression in esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Barrett Esophagus / genetics. Barrett Esophagus / pathology. DNA Methylation. Esophageal Neoplasms / genetics. Esophageal Neoplasms / pathology. Eye Proteins / genetics. Eye Proteins / metabolism. Gene Expression Profiling. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / genetics. Membrane Proteins / metabolism. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15825175.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Eye Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / SFRP1 protein, human; 0 / SFRP4 protein, human; 0 / SFRP5 protein, human
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92. Linares Torres P, Castañón López C, Llano Alonso C, Alvarez Posadilla M, Vivas Alegre S, Espinel Díez J, Ribas Arino MT: [Association of adenocarcinoma of esophagus and breast cancer in a male with Madelung' disease]. An Med Interna; 2006 Mar;23(3):133-5
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  • [Title] [Association of adenocarcinoma of esophagus and breast cancer in a male with Madelung' disease].
  • [Transliterated title] Asociación de adenocarcinoma de esófago y cáncer de mama en un varón con enfermedad de Madelung.
  • We report a case of adenocarcinoma of the esophagus in a man diagnosed of benign symmetrical lipomatosis (Madelung' disease), who had received adjuvant radiotherapy three years before for breast cancer.
  • [MeSH-major] Adenocarcinoma / complications. Breast Neoplasms, Male / complications. Carcinoma, Ductal, Breast / complications. Esophageal Neoplasms / complications. Lipomatosis, Multiple Symmetrical / complications. Neoplasms, Radiation-Induced / etiology. Neoplasms, Second Primary / etiology. Radiotherapy, Adjuvant / adverse effects
  • [MeSH-minor] Aged. Alcohol Drinking / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Barrett Esophagus / complications. Chemotherapy, Adjuvant. Combined Modality Therapy. Deglutition Disorders / etiology. Fatal Outcome. Hematemesis / etiology. Humans. Lymph Node Excision. Male. Mastectomy, Modified Radical. Risk Factors. Smoking / adverse effects


93. Veugelers PJ, Porter GA, Guernsey DL, Casson AG: Obesity and lifestyle risk factors for gastroesophageal reflux disease, Barrett esophagus and esophageal adenocarcinoma. Dis Esophagus; 2006;19(5):321-8
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  • [Title] Obesity and lifestyle risk factors for gastroesophageal reflux disease, Barrett esophagus and esophageal adenocarcinoma.
  • The aim of this study was to examine the association of obesity with esophageal adenocarcinoma, and with the precursor lesions Barrett esophagus and gastroesophageal reflux disease (GERD).
  • This case-control study included cases with GERD (n = 142), Barrett esophagus (n = 130), and esophageal adenocarcinoma (n = 57).
  • Relative to normal weight, obese individuals were at increased risk for esophageal adenocarcinoma (Odds Ratio [OR] 4.67, 95% Confidence Interval [CI] 1.27-17.9).
  • Diets high in vitamin C were associated with a lower risk for GERD (OR 0.40, 95% CI 0.19-0.87), Barrett esophagus (OR 0.44, 95% CI 0.20-0.98), and esophageal adenocarcinoma (OR 0.21, 95% CI 0.06-0.77).
  • For the more established risk factors, we confirmed that smoking was a significant risk factor for esophageal adenocarcinoma, and that increased liquor consumption was associated with GERD and Barrett esophagus.
  • In light of the current obesity epidemic, esophageal adenocarcinoma incidence rates are expected to continue to increase.

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  • (PMID = 16984526.001).
  • [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] 0 / Vitamins
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94. Dunn LJ, Robertson AG, Immanuel A, Griffin SM: Barrett's adenocarcinoma 52 years after subtotal esophagectomy for pediatric peptic stricture. Ann Thorac Surg; 2010 Feb;89(2):604-6
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  • [Title] Barrett's adenocarcinoma 52 years after subtotal esophagectomy for pediatric peptic stricture.
  • Barrett's esophagus results from the long-term effects of both acid and bile reflux.
  • Development of Barrett's epithelium in the esophageal remnant has been reported.
  • Here we report the case of a man who was diagnosed with adenocarcinoma in his esophageal remnant on a background of Barrett's change 52 years after undergoing one of the first esophageal resections for benign disease as a child.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophageal Stenosis / surgery. Esophagitis, Peptic / surgery. Postoperative Complications / surgery

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  • [Copyright] 2010 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20103354.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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95. Alvarez H, Koorstra JB, Hong SM, Boonstra JJ, Dinjens WN, Foratiere AA, Wu TT, Montgomery E, Eshleman JR, Maitra A: Establishment and characterization of a bona fide Barrett esophagus-associated adenocarcinoma cell line. Cancer Biol Ther; 2008 Nov;7(11):1753-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment and characterization of a bona fide Barrett esophagus-associated adenocarcinoma cell line.
  • Esophageal adenocarcinoma currently has one of the most rapidly increasing tumor incidences in the United States, with the vast majority of cases occurring on the backdrop of metaplastic epithelium (Barrett esophagus).
  • The identity of several of the widely utilized esophageal adenocarcinoma cell lines (BIC-1, SEG-1 and TE-7) have recently been called into question.
  • Here we describe the establishment and characterization of a bona fide esophageal cancer cell line, JH-EsoAd1, from a patient with Barrett-associated adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / complications. Barrett Esophagus / complications

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  • [Cites] Cancer Cell. 2005 May;7(5):469-83 [15894267.001]
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  • (PMID = 18787394.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vimentin
  • [Other-IDs] NLM/ NIHMS440953; NLM/ PMC3596869
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96. Hur C, Broughton DE, Ozanne E, Yachimski P, Nishioka NS, Gazelle GS: Patient preferences for the chemoprevention of esophageal adenocarcinoma in Barrett's esophagus. Am J Gastroenterol; 2008 Oct;103(10):2432-42
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  • [Title] Patient preferences for the chemoprevention of esophageal adenocarcinoma in Barrett's esophagus.
  • OBJECTIVES: Although evidence suggests that aspirin and celecoxib may reduce the risk of esophageal adenocarcinoma (EAC) in patients with Barrett's esophagus (BE), these drugs can also cause harmful side effects.

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  • (PMID = 18775019.001).
  • [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 / K07 CA107060; United States / NCI NIH HHS / CA / K07CA107060
  • [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 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib; R16CO5Y76E / Aspirin
  • [Other-IDs] NLM/ NIHMS495397; NLM/ PMC3736801
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97. Sagatys E, Garrett CR, Boulware D, Kelley S, Malafa M, Cheng JQ, Sebti S, Coppola D: Activation of the serine/threonine protein kinase Akt during the progression of Barrett neoplasia. Hum Pathol; 2007 Oct;38(10):1526-31
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  • [Title] Activation of the serine/threonine protein kinase Akt during the progression of Barrett neoplasia.
  • Esophageal adenocarcinoma has demonstrated a rapid increase in incidence over the last 10 years.
  • This increase mirrors a dramatic rise in that of Barrett esophagus, which is associated with esophageal adenocarcinoma in at least 95% of cases.
  • In an attempt to understand the pathogenesis of esophageal adenocarcinoma, attention has turned to the antiapoptotic and oncogenic pathways.
  • Here we demonstrated that Akt was frequently activated in Barrett esophagus-related adenocarcinoma.
  • After institutional review board ethics approval, 60 archival tissue specimens of esophageal adenocarcinoma arising on a background of Barrett esophagus were selected for immunohistochemical staining with phosphorylated Akt (p-Akt) antibody.
  • Approximately 80% of high-grade dysplasia and esophageal adenocarcinoma cases demonstrated strong to moderate Akt activity.
  • Sixty-two percent of Barrett mucosa revealed low Akt activity, the remaining cases being p-Akt negative.
  • None of the low-grade dysplasia cases exhibited strong p-Akt staining, whereas only weak p-Akt activity is seen in a portion of metaplastic Barrett mucosa, Akt is highly activated in high-grade dysplasia and esophageal adenocarcinoma arising from Barrett esophagus.
  • These findings suggest a role of p-Akt in the progression of Barrett esophagus to esophageal adenocarcinoma and provide the rationale for using p-Akt inhibitor API-2/triciribine, which is currently in clinical trial, in the treatment of esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Barrett Esophagus / pathology. Esophageal Neoplasms / enzymology. Proto-Oncogene Proteins c-akt / biosynthesis

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  • (PMID = 17640711.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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98. Ikeda K, Isomoto H, Oda H, Shikuwa S, Mizuta Y, Iwasaki K, Kohno S: Endoscopic submucosal dissection of a minute intramucosal adenocarcinoma in Barrett's esophagus. Dig Endosc; 2009 Jan;21(1):34-6
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  • [Title] Endoscopic submucosal dissection of a minute intramucosal adenocarcinoma in Barrett's esophagus.
  • A 73-year-old man with short segmental Barrett's esophagus underwent esophagoscopy, and a slightly depressed, discolored lesion was found on the anterior wall of the lower esophagus.
  • Under a provisional diagnosis of differentiated adenocarcinoma without local lymph node metastasis, endoscopic submucosal dissection (ESD) was carried out.
  • Histopathological examination confirmed intramucosal well-differentiated tubular adenocarcinoma without angiolymphatic invasion adjacent to the muscularis mucosae.
  • Considering that Barrett's esophagus is a precancerous condition, one may recommend eradication of both the neoplastic and non-neoplastic lesion with using ESD.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / surgery

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  • (PMID = 19691799.001).
  • [ISSN] 1443-1661
  • [Journal-full-title] Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
  • [ISO-abbreviation] Dig Endosc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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99. Prasad GA, Wu TT, Wigle DA, Buttar NS, Wongkeesong LM, Dunagan KT, Lutzke LS, Borkenhagen LS, Wang KK: Endoscopic and surgical treatment of mucosal (T1a) esophageal adenocarcinoma in Barrett's esophagus. Gastroenterology; 2009 Sep;137(3):815-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic and surgical treatment of mucosal (T1a) esophageal adenocarcinoma in Barrett's esophagus.
  • BACKGROUND & AIMS: Endoscopic therapy is emerging as an alternative to surgical therapy in patients with mucosal (T1a) esophageal adenocarcinoma (EAC) given the low likelihood of lymph node metastases.

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  • (PMID = 19524578.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21CA122426-01; United States / NCI NIH HHS / CA / R01CA097048; United States / NCI NIH HHS / CA / R01 CA111603; United States / NCI NIH HHS / CA / R03 CA135991; United States / NCI NIH HHS / CA / R03CA135991-01; United States / NCI NIH HHS / CA / R01CA111603-01A1; United States / NCI NIH HHS / CA / R01 CA097048; United States / NCI NIH HHS / CA / R21 CA122426
  • [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 / Proton Pump Inhibitors
  • [Other-IDs] NLM/ NIHMS123990; NLM/ PMC3815672
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100. Wani S, Puli SR, Shaheen NJ, Westhoff B, Slehria S, Bansal A, Rastogi A, Sayana H, Sharma P: Esophageal adenocarcinoma in Barrett's esophagus after endoscopic ablative therapy: a meta-analysis and systematic review. Am J Gastroenterol; 2009 Feb;104(2):502-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Esophageal adenocarcinoma in Barrett's esophagus after endoscopic ablative therapy: a meta-analysis and systematic review.
  • OBJECTIVES: The extent of reduction of esophageal adenocarcinoma (EAC) incidence in Barrett's esophagus (BE) patients after endoscopic ablation is not known.
  • [MeSH-major] Ablation Techniques. Adenocarcinoma / epidemiology. Barrett Esophagus / therapy. Endoscopy. Esophageal Neoplasms / epidemiology






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