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6. Liu G, Zhou W, Yeap BY, Su L, Wain JC, Poneros JM, Nishioka NS, Lynch TJ, Christiani DC: XRCC1 and XPD polymorphisms and esophageal adenocarcinoma risk. Carcinogenesis; 2007 Jun;28(6):1254-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] XRCC1 and XPD polymorphisms and esophageal adenocarcinoma risk.
  • DNA damage is important in the pathogenesis of esophageal adenocarcinoma (EA).
  • [MeSH-major] Adenocarcinoma / genetics. DNA-Binding Proteins / genetics. Esophageal Neoplasms / genetics. Genetic Predisposition to Disease. Polymorphism, Genetic. Xeroderma Pigmentosum Group D Protein / genetics

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  • (PMID = 17264068.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109193; United States / NCI NIH HHS / CA / CA110822; United States / NCI NIH HHS / CA / CA74386; United States / NCI NIH HHS / CA / ES/CA06409
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
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7. Yong TY, Klebe S, Li JY: Acute critical leg ischemia: an uncommon initial manifestation of esophageal adenocarcinoma. J Palliat Med; 2009 Sep;12(9):841-4
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  • [Title] Acute critical leg ischemia: an uncommon initial manifestation of esophageal adenocarcinoma.
  • This report describes a patient who presented with acute critical right leg ischemia leading to the diagnosis of esophageal adenocarcinoma with widespread metastases.
  • However, he died 3 weeks after presentation due to progressive cancer.
  • [MeSH-major] Esophageal Neoplasms / complications. Ischemia / etiology. Leg / blood supply
  • [MeSH-minor] Acute Disease. Adenocarcinoma / complications. Adenocarcinoma / pathology. Adult. Disease Progression. Fatal Outcome. Humans. Male. Risk Factors. Time Factors

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  • (PMID = 19719377.001).
  • [ISSN] 1557-7740
  • [Journal-full-title] Journal of palliative medicine
  • [ISO-abbreviation] J Palliat Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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8. DeMeester SR: Reflux, Barrett's, and adenocarcinoma of the esophagus: can we disrupt the pathway? J Gastrointest Surg; 2010 Jun;14(6):941-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reflux, Barrett's, and adenocarcinoma of the esophagus: can we disrupt the pathway?
  • [MeSH-major] Adenocarcinoma / physiopathology. Barrett Esophagus / physiopathology. Esophageal Neoplasms / physiopathology. Esophagus / pathology. Gastroesophageal Reflux / physiopathology

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  • (PMID = 20094815.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
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9. Onwuegbusi BA, Rees JR, Lao-Sirieix P, Fitzgerald RC: Selective loss of TGFbeta Smad-dependent signalling prevents cell cycle arrest and promotes invasion in oesophageal adenocarcinoma cell lines. PLoS One; 2007 Jan 31;2(1):e177
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  • [Title] Selective loss of TGFbeta Smad-dependent signalling prevents cell cycle arrest and promotes invasion in oesophageal adenocarcinoma cell lines.
  • In cancer, Transforming Growth Factor beta (TGFbeta) increases proliferation and promotes invasion via selective loss of signalling pathways.
  • Oesophageal adenocarcinoma arises from Barrett's oesophagus, progresses rapidly and is usually fatal.
  • We therefore investigated the role of TGFbeta in Barrett's associated oesophageal adenocarcinoma using a panel of cell lines (OE33, TE7, SEG, BIC, FLO).
  • 4/5 adenocarcinoma cell lines failed to cell cycle arrest, down-regulate c-Myc or induce p21 in response to TGFbeta, and modulation of a Smad3/4 specific promoter was inhibited.
  • These hyperproliferative adenocarcinoma cell lines displayed a TGFbeta induced increase in the expression of the extracellular matrix degrading proteinases, urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor 1 (PAI-1), which correlated with an invasive cell phenotype as measured by in vitro migration, invasion and cell scattering assays.
  • These data would support a dual role for TGFbeta in oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Signal Transduction / physiology. Smad3 Protein / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Barrett Esophagus / complications. Cell Cycle / physiology. Cell Line, Tumor. Cell Proliferation. Enzyme Activation. Enzyme Inhibitors / metabolism. Extracellular Matrix / metabolism. Extracellular Signal-Regulated MAP Kinases / genetics. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression Regulation. Humans. JNK Mitogen-Activated Protein Kinases / genetics. JNK Mitogen-Activated Protein Kinases / metabolism. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Transcription, Genetic

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  • (PMID = 17264880.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Smad3 Protein; 0 / Transforming Growth Factor beta; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1766472
  • [General-notes] NLM/ Original DateCompleted: 20070723
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10. Murray L, Romero Y: Role of obesity in Barrett's esophagus and cancer. Surg Oncol Clin N Am; 2009 Jul;18(3):439-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of obesity in Barrett's esophagus and cancer.
  • The incidence of esophageal adenocarcinoma (EAC) has increased dramatically in the western world, and there also appears to have been an increase in the incidence of Barrett's esophagus and gastroesophageal reflux disease in recent years.
  • This article reviews current evidence for the role that overweight/obesity and body fat distribution have in development of the esophagitis metaplasia-dysplasia-adenocarcinoma sequence.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / etiology. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / etiology. Obesity / complications


11. Weimann A, Rieger A, Zimmermann M, Gross M, Hoffmann P, Slevogt H, Morawietz L: Comparison of six immunohistochemical markers for the histologic diagnosis of neoplasia in Barrett's esophagus. Virchows Arch; 2010 Nov;457(5):537-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of six immunohistochemical markers for the histologic diagnosis of neoplasia in Barrett's esophagus.
  • In esophageal neoplasms, the histopathologic differentiation between Barrett's esophagus with or without intraepithelial neoplasia and adenocarcinoma is often challenging.
  • The expression of CDX2, LI-cadherin, mucin 2 (MUC2), blood group 8 (BG8, Lewis(y)), claudin-2, and villin was investigated in normal gastroesophageal (n = 23) and in Barrett's (n = 17) mucosa, in low-grade (n = 12) and high-grade (n = 9) intraepithelial neoplasia (IEN) as well as in esophageal adenocarcinoma (n = 16), using immunohistochemistry.
  • For CDX2 and LI-cadherin, the immunoreactivity score was highest in IEN while for MUC2, BG8, and villin, it dropped gradually from Barrett's via IEN to adenocarcinoma, and expression of Claudin-2 was only weak and focal in all lesions.
  • MUC2 and LI-cadherin are useful immunohistochemical markers for the differentiation between normal glandular mucosa, Barrett's mucosa, IEN, and invasive carcinoma of the esophagus; however, none of the examined markers was helpful for the differentiation between low-grade and high-grade IEN.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Biomarkers, Tumor / analysis. Esophageal Neoplasms / diagnosis

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  • (PMID = 20844891.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDH17 protein, human; 0 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / CLDN2 protein, human; 0 / Cadherins; 0 / Claudins; 0 / Homeodomain Proteins; 0 / MUC2 protein, human; 0 / Membrane Proteins; 0 / Microfilament Proteins; 0 / Mucin-2; 0 / villin
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12. Ku GY, Ilson DH: Role of neoadjuvant therapy for esophageal adenocarcinoma. Surg Oncol Clin N Am; 2009 Jul;18(3):533-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of neoadjuvant therapy for esophageal adenocarcinoma.
  • This article examines the role of neoadjuvant therapy in the treatment of locally advanced esophageal adenocarcinoma.
  • Primary chemoradiotherapy is the accepted standard of care for medically inoperable patients, whereas adjuvant chemoradiotherapy may be considered for patients who undergo primary resection of lower esophageal/gastroesophageal junction tumors.
  • [MeSH-major] Adenocarcinoma / therapy. Esophageal Neoplasms / therapy. Neoadjuvant Therapy / methods

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  • (PMID = 19500742.001).
  • [ISSN] 1558-5042
  • [Journal-full-title] Surgical oncology clinics of North America
  • [ISO-abbreviation] Surg. Oncol. Clin. N. Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin
  • [Number-of-references] 60
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13. Gladman L, Chapman W, Iqbal TH, Gearty JC, Cooper BT: Barrett's oesophagus: an audit of surveillance over a 17-year period. Eur J Gastroenterol Hepatol; 2006 Mar;18(3):271-6
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  • [Title] Barrett's oesophagus: an audit of surveillance over a 17-year period.
  • OBJECTIVE: To audit whether our patients with Barrett's oesophagus (BO) enter into our endoscopic surveillance programme and whether they continue with it after entry.
  • We have determined the incidence of oesophageal adenocarcinoma among our surveyed patients.
  • RESULTS: During these years, 466 patients with BO were diagnosed (392 long segment, >or=3 cm), 29 had oesophageal adenocarcinoma at diagnosis, 232 [195 with intestinal metaplasia (IM) on biopsy] had at least one follow-up endoscopy, and 205 have not been re-endoscoped.
  • Of the remaining 178 out of 205 with IM, 30 were within 2 years of diagnosis and 148 have not been re-endoscoped for the following reasons: age (51), non-attendance (35), not referred back by general practitioner (30), non-oesophageal cancer (14), severe concurrent illness (12), death (three), refused follow-up (two), left the area (one).
  • Ninety-seven out of 195 patients remain under active endoscopic surveillance but 98 discontinued for the following reasons: age (31), non attendance (21), death (21 including one from oesophageal adenocarcinoma), refused follow up (seven), concurrent illness (six), left the area (four), no IM on repeat biopsies (three).
  • Of the 195 patients with IM, four developed low-grade dysplasia, two high-grade dysplasia and four adenocarcinoma (incidence 0.37%); 178 out of 195 have been maintained on proton pump inhibitor (PPI) therapy.
  • The incidence of adenocarcinoma was low compared with many published series, and we speculate whether this is the result of maintenance PPI therapy.
  • [MeSH-major] Barrett Esophagus / therapy. Esophagoscopy. Medical Audit / methods. Patient Selection
  • [MeSH-minor] Adenocarcinoma / complications. Adenocarcinoma / diagnosis. Adult. Aged. Aged, 80 and over. Anti-Ulcer Agents / therapeutic use. Esophageal Neoplasms / complications. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Female. Histamine H2 Antagonists / therapeutic use. Hospitals, Teaching. Humans. Male. Metaplasia. Middle Aged. Proton Pump Inhibitors. Retrospective Studies

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  • (PMID = 16462540.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors
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4. Dvorakova K, Payne CM, Ramsey L, Bernstein H, Holubec H, Chavarria M, Bernstein C, Sampliner RE, Riley C, Prasad A, Garewal H: Apoptosis resistance in Barrett's esophagus: ex vivo bioassay of live stressed tissues. Am J Gastroenterol; 2005 Feb;100(2):424-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoptosis resistance in Barrett's esophagus: ex vivo bioassay of live stressed tissues.
  • BACKGROUND AND AIMS: Barrett's esophagus (BE) is a premalignant lesion of the distal esophagus in which squamous epithelial cells are replaced by metaplastic intestinal-like columnar epithelium that contains goblet cells.
  • The factors that contribute to the progression from normal squamous mucosa to BE, Barrett's dysplasia, and adenocarcinoma are not well understood at the molecular level.
  • This will result in the survival of cells with unrepaired DNA damage, and a consequent increase in genomic instability leading to cancer progression.
  • The major goal of this study is to compare sensitivity to apoptosis induced by the bile acid, deoxycholate (DOC), a known inducer of apoptosis, in normal esophageal squamous epithelium, normal colon epithelium, and BE.
  • METHODS: Thirteen patients with a confirmed diagnosis of BE and four patients who had undergone clinically indicated colectomy were included in the present study.
  • RESULTS: Our results indicate that BE is resistant to apoptosis induced by DOC compared to esophageal squamous epithelium and normal colon epithelium.
  • Altogether, the data indicate that reduced apoptosis capability in BE tissue may contribute to progression to esophageal adenocarcinoma.
  • [MeSH-major] Apoptosis / drug effects. Barrett Esophagus / pathology. Deoxycholic Acid / pharmacology. Esophagus / pathology

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  • (PMID = 15667503.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P50 CA 95060; United States / NCI NIH HHS / CA / CA 23074; United States / NCI NIH HHS / CA / CA 72008; United States / NIEHS NIH HHS / ES / ES 06694
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 005990WHZZ / Deoxycholic Acid; 68238-35-7 / Keratins; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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15. Sarosi GA Jr: Introduction: esophagus, dysplasia, and early esophageal adenocarcinoma: managing the transition. J Gastrointest Surg; 2010 Jun;14(6):935-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Introduction: esophagus, dysplasia, and early esophageal adenocarcinoma: managing the transition.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology

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  • [Cites] J Natl Cancer Inst. 2005 Jan 19;97(2):142-6 [15657344.001]
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  • (PMID = 20162375.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Introductory Journal Article
  • [Publication-country] United States
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16. Konda Vani JA, Chennat J, Waxman I: New directions in endoscopic therapy of Barrett' s esophagus. Minerva Gastroenterol Dietol; 2010 Dec;56(4):421-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New directions in endoscopic therapy of Barrett' s esophagus.
  • The key to prevention and early treatment of esophageal adenocarcinoma is the detection and eradication of neoplasia found in patients with Barrett's esophagus (BE).
  • The goals of endoscopic therapy of Barrett's neoplasia are to preserve the esophagus while ablating or removing the entire Barrett's segment.
  • Endoscopic resection is a tool to accurately provide a histological diagnosis of lesions in addition to treat neoplasia.
  • [MeSH-major] Adenocarcinoma / therapy. Barrett Esophagus / therapy. Esophageal Neoplasms / therapy. Esophagoscopy / trends. Precancerous Conditions / therapy

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  • (PMID = 21139541.001).
  • [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
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17. Eisen GM: Capsule endoscopy. New applications. J Fam Pract; 2005 Dec;Suppl:9-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal / methods. Gastroesophageal Reflux / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Clinical Trials as Topic. Esophageal Neoplasms / diagnosis. Humans. Reproducibility of Results. Video Recording / methods

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  • (PMID = 16321338.001).
  • [ISSN] 0094-3509
  • [Journal-full-title] The Journal of family practice
  • [ISO-abbreviation] J Fam Pract
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 21
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18. Bhat MA, Naikoo ZA, Dass TA, Lone RA, Dar AM: Role of intraoperative sentinel lymph node mapping in the management of carcinoma of the esophagus. Saudi J Gastroenterol; 2010 Jul-Sep;16(3):168-73
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  • [Title] Role of intraoperative sentinel lymph node mapping in the management of carcinoma of the esophagus.
  • BACKGROUND/AIM: Precise evaluation of lymph node status is one of the most important factors in determining clinical outcome in treating gastro-intestinal (GI) cancer.
  • Sentinel lymph node (SLN) mapping clearly has become highly feasible and accurate in staging GI cancer.
  • This study aims to investigate the feasibility and accuracy of detection of SLN using methylene blue dye in patients with carcinoma of the esophagus and assess its potential role in determining the rational extent of lymphadenectomy in esophageal cancer surgery.
  • MATERIALS AND METHODS: Thirty-two patients of esophageal cancer diagnosed on endoscopic biopsy were enrolled in this prospective study.
  • The SLNs of esophageal cancer were only found in N1 area in 21 (80.77%) cases, and in N2 or N3 area in only 19.33%.
  • SLN had a sensitivity of 85.71% in mid esophageal tumors and 93.33% in lower esophageal tumors.
  • The SLN biopsy had sensitivity of 87.5% in the case of squamous cell carcinoma and 92.86% in the cases of adenocarcinoma of the esophagus.
  • The accuracy of the procedure for squamous cell carcinoma and adenocarcinoma was 60% and 76.47%, respectively.
  • CONCLUSION: SLN mapping is an accurate diagnostic procedure for detecting lymph node metastasis in patients with esophageal cancer and may indicate rational extent of lymphadenectomy in these patients.
  • SLN mapping provides "right nodes" to the pathologists for detailed analysis and appropriate staging, thereby helping in individualizing the multi-modal treatment for esophageal cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / surgery. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Sentinel Lymph Node Biopsy

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  • (PMID = 20616411.001).
  • [ISSN] 1998-4049
  • [Journal-full-title] Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association
  • [ISO-abbreviation] Saudi J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; T42P99266K / Methylene Blue
  • [Other-IDs] NLM/ PMC3003219
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19. Gockel I, Sultanov FS, Domeyer M, Trinh TT, Gönner U, Junginger T: [Surgical therapy for esophageal carcinoma: a prospective 20-year analysis]. Zentralbl Chir; 2008 Jun;133(3):260-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgical therapy for esophageal carcinoma: a prospective 20-year analysis].
  • [Transliterated title] Chirurgische Therapie des Osophaguskarzinoms: Eine prospektive 20-Jahres-Analyse.
  • BACKGROUND: The aim of our study was the analysis of long-term developments in the surgical therapy for esophageal carcinoma at our hospital over a period of 20 years with a differentiated view on the two predominant histological tumour types.
  • PATIENTS AND METHODS: Between September 1985 and September 2005, esophageal resections were performed in 470 patients at our clinic on account of a malignant tumour of the esophagus.
  • The abdomino-thoracic resection with abdominal and extended mediastinal lymph node dissection as well as intrathoracic anastomosis was the standard treatment in the case of squamous cell carcinoma, whereas in adenocarcinoma a transhiatal resection with abdominal and dorsal mediastinal lymphadenectomy and cervical esophagogastrostomy was carried out.
  • A proportionally identical amount of transhiatal resections for squamous cell carcinoma was found in both intervals, whereas the transhiatal procedures for adenocarcinoma increased in the last decade (3.6 % in the period between 9 / 1985 and 9 / 1995, as compared with 23.6 % between 10 / 1995 and 9 / 2005) (p < 0.05).
  • While the overall prognosis for squamous cell carcinoma did not significantly differ in the two decades (p = 0.2040), patients with adenocarcinoma were found to have a significantly improved long-term survival (log-rank test: p = 0.0365) in the second decade.
  • The prognosis for adenocarcinoma, therefore, could be improved in the course of time with a 3-year survival rate of finally 40 % (as compared with 17.5 % in the first decade), and a 5-year survival rate of 25 % (as compared with 15 %).
  • CONCLUSION: Surgical therapy for esophageal carcinoma has undergone distinct changes over the past 20 years.
  • Especially with adenocarcinoma of the esophagus, these changes have led to a significantly more favourable long-term prognosis.
  • [MeSH-major] Adenocarcinoma / surgery. Carcinoma, Squamous Cell / surgery. Diffusion of Innovation. Esophageal Neoplasms / surgery. Thoracotomy / trends
  • [MeSH-minor] Adult. Aged. Anastomosis, Surgical. Diaphragm / surgery. Disease-Free Survival. Esophagus / surgery. Female. Follow-Up Studies. Humans. Lymph Node Excision. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Stomach / surgery

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  • (PMID = 18563693.001).
  • [ISSN] 0044-409X
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
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20. Haghdoost AA, Hosseini H, Chamani G, Zarei MR, Rad M, Hashemipoor M, Zahedi MJ, Darvish-Moghadam S: Rising incidence of adenocarcinoma of the esophagus in Kerman, Iran. Arch Iran Med; 2008 Jul;11(4):364-70
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  • [Title] Rising incidence of adenocarcinoma of the esophagus in Kerman, Iran.
  • BACKGROUND: The fall in the incidence of esophageal squamous cell cancer and noncardia gastric cancers in western countries parallels a concomitant rise in the incidence of gastric cardia cancer and distal adenocarcinoma of the esophagus.
  • We aimed to investigate the incidence trend of different gastric and esophageal cancers in Kerman, southeast Iran.
  • METHODS: The information of all newly diagnosed patients with gastric and esophageal cancers were collected actively from all histopathology departments around the Kerman Province during 1991 - 2002 retrospectively.
  • RESULTS: The annual age standardized incidence risks of esophageal and gastric cancers in Kerman were 1.9 and 6.9 per 100,000 populations.
  • In average, the risks of gastric and esophageal squamous cell cancers were more or less constant, while the risk of adenocarcinoma of the esophagus increased around 11% annually.
  • The rising incidence of adenocarcinoma of the esophagus in Kerman parallels its temporal pattern in western countries.
  • [MeSH-major] Adenocarcinoma / epidemiology. Esophageal Neoplasms / epidemiology. Stomach Neoplasms / epidemiology

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  • (PMID = 18588366.001).
  • [ISSN] 1029-2977
  • [Journal-full-title] Archives of Iranian medicine
  • [ISO-abbreviation] Arch Iran Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
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21. Madani K, Zhao R, Lim HJ, Casson SM, Casson AG: Obesity is not associated with adverse outcome following surgical resection of oesophageal adenocarcinoma. Eur J Cardiothorac Surg; 2010 Nov;38(5):604-8
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  • [Title] Obesity is not associated with adverse outcome following surgical resection of oesophageal adenocarcinoma.
  • OBJECTIVE: To study the impact of obesity on postoperative morbidity and outcome following surgical resection of primary oesophageal adenocarcinoma (EADC).
  • DFS and OS at 5 years were increased for patients who were obese at the time of oesophageal resection (P=0.008).
  • CONCLUSIONS: Obesity is not associated with increased postoperative complication rates or adverse outcome following oesophageal resection, and should therefore not be considered a relative contraindication to the surgical management of EADC.
  • The improved survival of obese patients who underwent oesophageal resection for EADC suggests that further investigation of the association between obesity and oesophageal malignancy is now warranted.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagectomy / adverse effects. Obesity / complications

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  • [Copyright] Copyright © 2010 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.
  • [ErratumIn] Eur J Cardiothorac Surg. 2010 Dec;38(6):820-1
  • (PMID = 20444616.001).
  • [ISSN] 1873-734X
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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22. Hennig EE, Mikula M, Orlowska J, Jarosz D, Bielasik A, Regula J, Ostrowski J: Large intra- and inter-individual variability of genes expression levels limits potential predictive value of molecular diagnosis of dysplasia in Barrett's esophagus. J Mol Med (Berl); 2008 Feb;86(2):233-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large intra- and inter-individual variability of genes expression levels limits potential predictive value of molecular diagnosis of dysplasia in Barrett's esophagus.
  • Barrett's esophagus represents a well-defined precursor lesion of esophageal adenocarcinoma, although only a subset of patients with these lesions advances to invasive cancer.
  • Currently, reliable markers predicting neoplastic progression in Barrett's esophagus are lacking.
  • Thus, identification of biomarkers of potential prognostic value in dysplasia development in Barrett's esophagus is highly important.
  • The aim of the study was to determine if expression levels of selected genes support histologic diagnosis of dysplastic changes in Barrett's esophagus.
  • Upon rigorous sampling and independent histopathologic examination of endoscopic specimens by two experienced gastrointestinal pathologists, 56 patients with Barrett's esophagus (16 negative for dysplasia, 15 with indefinite, 21 with low-grade, and 4 with high-grade dysplasia) were selected for molecular analysis.
  • Although expression of nine genes showed trends toward down- or upregulation during progression from Barrett's esophagus without dysplasia to Barrett's esophagus with high-grade dysplasia, only a decrease in S100A2 mRNA levels was statistically significant (P<0.05).
  • In conclusion, expression of this set of ten genes cannot be used as a molecular marker aiding histological examination of dysplasia in Barrett's esophagus.
  • [MeSH-major] Barrett Esophagus / diagnosis. Esophageal Neoplasms / etiology. Esophagoscopy. Esophagus / pathology. Genetic Markers. Genetic Testing. Genetic Variation. Molecular Diagnostic Techniques

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  • (PMID = 17952395.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chemotactic Factors; 0 / Genetic Markers; 0 / RNA, Messenger; 0 / S100 Proteins; 0 / S100A2 protein, human
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23. Islami F, Kamangar F: Helicobacter pylori and esophageal cancer risk: a meta-analysis. Cancer Prev Res (Phila); 2008 Oct;1(5):329-38
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  • [Title] Helicobacter pylori and esophageal cancer risk: a meta-analysis.
  • We conducted this meta-analysis to examine the association between Helicobacter pylori and esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma.
  • Case-control or nested case-control studies were selected if they used serology or endoscopic methods to detect H. pylori in the stomach and if control subjects were not restricted to upper gastrointestinal tract cancer or peptic ulcer disease patients.
  • For esophageal squamous cell carcinoma, the summary OR (95% CI) was 1.10 (0.78-1.55).
  • [MeSH-major] Adenocarcinoma / etiology. Carcinoma, Squamous Cell / etiology. Esophageal Neoplasms / etiology. Helicobacter Infections / epidemiology. Helicobacter pylori / physiology

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  • (PMID = 19138977.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / cagA protein, Helicobacter pylori
  • [Other-IDs] NLM/ NIHMS419215; NLM/ PMC3501739
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24. Wang RH, Ou-Yang Q, Chen X, Li GD, Xiang JY: [Chemoprevention of Barrett's esophagus by celecoxib in rats]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2009 Sep;38(5):498-504
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  • [Title] [Chemoprevention of Barrett's esophagus by celecoxib in rats].
  • OBJECTIVE: To examine the chemopreventive effect of selective cyclooxygenase-2 (COX-2) inhibitor celecoxib for Barrett's esophagus in rats.
  • METHODS: Fifty 8-week-old male Sprague Dawley rats underwent esophagojejunostomy to induce Barrett's esophagus model.
  • The degree of inflammation, Barrett's esophagus, adenocarcinoma, COX-2 expression and PGE(2) of animals were assessed.
  • The incidence of mild, moderate and severe degree esophageal inflammation in celecoxib group and control group was 14/19(73.68%), 4/19(21.05%), 1/19(5.26%); 4/17(23.53%), 5/17(29.41%), 8/17(47.06%)(P<0.05), respectively.
  • The incidence of Barrett's esophagus was 7/19(36.84%), 13/17(76.47%) in two group respectively(P<0.05); The incidence of Barrett's esophagus with dysplasia was 2/19(10.53%), 8/17(47.06%)(P<0.05), respectively.
  • No esophageal pathological changes were found in sham operation group.
  • CONCLUSION: Selective COX-2 inhibitors celecoxib can inhibit inflammations, development of Barrett's esophagus and esophagus adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / prevention & control. Cyclooxygenase 2 Inhibitors / therapeutic use. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use

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  • (PMID = 19830863.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
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25. Souza RF: Molecular mechanisms of acid exposure in Barrett's esophagus. Inflammopharmacology; 2007 Jun;15(3):95-100
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  • [Title] Molecular mechanisms of acid exposure in Barrett's esophagus.
  • Esophageal adenocarcinoma is one of the most deadly gastrointestinal tumors.
  • Gastroesophageal reflux has been established as a major risk factor for esophageal adenocarcinoma and Barrett's esophagus, the condition in which the normal squamous cells of the esophagus are replaced by metaplastic, specialized intestinal cells that are predisposed to malignancy.
  • Data from ex vivo and in vitro model systems suggests that acid exposure has pro-proliferative and anti-apoptotic effects which may facilitate neoplastic progression of Barrett's esophagus.
  • However, it is not clear whether the effects of acid exposure on proliferation and apoptosis are a direct result of the acid exposure itself, or whether they result indirectly from the effects of acid on inducing esophageal inflammation.
  • Such distinction may help in optimizing the level of gastric acid suppression for the prevention of cancer in Barrett's esophagus.
  • This report describes the molecular mechanisms whereby acid exposure directly and indirectly, through inducing inflammation, may contribute to the neoplastic progression of Barrett's esophagus and the potential role for acid suppression as a chemopreventive strategy in patients with Barrett's esophagus.
  • [MeSH-major] Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications

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  • (PMID = 19847948.001).
  • [ISSN] 0925-4692
  • [Journal-full-title] Inflammopharmacology
  • [ISO-abbreviation] Inflammopharmacology
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK63621
  • [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] Switzerland
  • [Chemical-registry-number] 0 / Acids; 0 / Cytokines; 0 / NF-kappa B; 0 / Reactive Nitrogen Species; 0 / Reactive Oxygen Species
  • [Number-of-references] 53
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26. Vakil N, Malfertheiner P, Salis G, Flook N, Hongo M: An international primary care survey of GERD terminology and guidelines. Dig Dis; 2008;26(3):231-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM: To determine the knowledge of primary care physicians with regard to: terminology related to GERD, their understanding of related complications and extra-esophageal symptoms/conditions, and their use of guidelines relating to GERD.
  • Gastroesophageal reflux disease/GERD (84%) or reflux/reflux disease (47%) were the terms mostly often used to record a diagnosis for patients with reflux-related symptoms or clinical manifestations; dyspepsia (15%), epigastric pain (10%), and gastritis (9%) were infrequently used.
  • Erosive esophagitis, Barrett's esophagus, stricture, and esophageal adenocarcinoma were recognized as being associated with GERD by 88, 71, 61 and 51% of physicians, respectively.
  • Extra-esophageal problems of cough, sleep-related disorders, laryngitis and asthma were recognized to be associated with GERD by 74, 50, 48 and 47% of respondents.
  • (1) GERD is well recognized, but its related terminology is variable throughout the world. (2) There was variable and incomplete recognition of extra-esophageal manifestations GERD. (3) Recognition of extra-esophageal diseases caused by GERD is variable. (4) Current GERD guidelines are infrequently used by primary care physicians.

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18463441.001).
  • [ISSN] 1421-9875
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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27. Chang EY, Li X, Jerosch-Herold M, Priest RA, Enestvedt CK, Xu J, Springer CS Jr, Jobe BA: The evaluation of esophageal adenocarcinoma using dynamic contrast-enhanced magnetic resonance imaging. J Gastrointest Surg; 2008 Jan;12(1):166-75
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  • [Title] The evaluation of esophageal adenocarcinoma using dynamic contrast-enhanced magnetic resonance imaging.
  • Although neoadjuvant chemoradiation eradicates esophageal adenocarcinoma in a substantial proportion of patients, conventional imaging techniques cannot accurately detect this response.
  • This pilot study evaluates the ability of this method to discriminate adenocarcinoma from normal esophageal tissue.
  • Patients with esophageal adenocarcinoma and control subjects underwent scanning.
  • Five esophageal adenocarcinoma patients and two tumor-free control subjects underwent scanning.
  • The mean Ktrans value was 5.7 times greater in esophageal adenocarcinoma, and taui is 2.0 times smaller, than in the control subjects.
  • DCE MRI of the esophagus is feasible.
  • Ktrans, a parameter that has demonstrated discriminative ability in other malignancies, also shows promise in differentiating esophageal adenocarcinoma from benign tissue.
  • [MeSH-major] Adenocarcinoma / diagnosis. Contrast Media / administration & dosage. Esophageal Neoplasms / diagnosis. Heterocyclic Compounds. Magnetic Resonance Imaging / methods. Organometallic Compounds
  • [MeSH-minor] Diagnosis, Differential. Gadolinium. Humans. Injections, Intravenous. Male. Pilot Projects. Reproducibility of Results

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  • (PMID = 17768665.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB00422; United States / NINDS NIH HHS / NS / R01 NS40801
  • [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 / Contrast Media; 0 / Heterocyclic Compounds; 0 / Organometallic Compounds; 0199MV609F / gadoteridol; AU0V1LM3JT / Gadolinium
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28. 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.
  • [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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29. Cooper SC, Croft S, Day R, Thomson CS, Trudgill NJ: The risk of oesophageal cancer is not affected by a diagnosis of breast cancer. Eur J Cancer Prev; 2010 May;19(3):182-5
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  • [Title] The risk of oesophageal cancer is not affected by a diagnosis of breast cancer.
  • Oesophageal adenocarcinoma (OAC) is less common and develops at a later age in women compared with men.
  • A cohort of women with breast cancer, a tumour commonly treated with oestrogen antagonists, was examined to identify the subsequent risk of developing OAC.
  • Earlier studies have implicated radiotherapy in increasing oesophageal cancer (OC) risk among women with breast cancer.
  • West Midlands Cancer Intelligence Unit data recording cancer diagnosis and treatment information was examined to identify patients with a first malignant primary breast cancer during 1977-2004.
  • Patients were followed until diagnosis of a second primary cancer, death or end of the time period examined.
  • No difference was identified when examined by OC morphology.There was no association between breast cancer and a second primary OC.
  • Radiotherapy that avoids deep irradiation in the treatment of breast cancer, local nodes or recurrence was not associated with an increased risk of developing a second primary OC.
  • [MeSH-major] Breast Neoplasms / complications. Esophageal Neoplasms / etiology. Neoplasms, Second Primary / etiology

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  • (PMID = 20145541.001).
  • [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] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogens
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30. Bosetti C, Gallus S, Garavello W, La Vecchia C: Smoking cessation and the risk of oesophageal cancer: An overview of published studies. Oral Oncol; 2006 Nov;42(10):957-64
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  • [Title] Smoking cessation and the risk of oesophageal cancer: An overview of published studies.
  • The epidemiologic studies on oesophageal cancer and smoking cessation published before December 2005 were reviewed here.
  • The results from at least 10 cohort and 10 case-control studies indicated that former smokers had a lower risk of squamous-cell or unspecified oesophageal cancer than current smokers.
  • Most investigations showed that the risk of oesophageal cancer remains elevated many years (at least 10) after cessation of smoking, to decline by about 40% only thereafter.
  • A few studies investigated the effect of smoking cessation on adenocarcinoma, and did not report a clear reduction of risk.
  • Data on oesophageal adenocarcinoma are however too limited to provide adequate inference on the relation with time since smoking cessation.
  • In conclusion, cessation of smoking could have an appreciable impact in reducing (squamous-cell) oesophageal cancer, and represents an obvious priority for prevention and public-health purposes.
  • [MeSH-major] Esophageal Neoplasms / epidemiology. Smoking / adverse effects. Smoking Cessation
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / etiology. Carcinoma, Squamous Cell / epidemiology. Carcinoma, Squamous Cell / etiology. Case-Control Studies. Cohort Studies. Humans. Risk Factors

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  • (PMID = 16919996.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137686859
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 29
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31. Soma T, Kaganoi J, Kawabe A, Kondo K, Tsunoda S, Imamura M, Shimada Y: Chenodeoxycholic acid stimulates the progression of human esophageal cancer cells: A possible mechanism of angiogenesis in patients with esophageal cancer. Int J Cancer; 2006 Aug 15;119(4):771-82
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  • [Title] Chenodeoxycholic acid stimulates the progression of human esophageal cancer cells: A possible mechanism of angiogenesis in patients with esophageal cancer.
  • Bile acids are known to promote the growth of gastrointestinal cancer.
  • In vitro, esophageal squamous cell carcinoma (ESCC) cells and esophageal adenocarcinoma cells were studied.
  • Our results suggest that bile acids, important constituents of duodenal fluid, stimulate the development of human esophageal cancer by promoting angiogenesis via the COX-2 pathway.
  • [MeSH-major] Chenodeoxycholic Acid / pharmacology. Esophageal Neoplasms / blood supply. Esophageal Neoplasms / pathology

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16557574.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Vascular Endothelial Growth Factor A; 0GEI24LG0J / Chenodeoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; K7Q1JQR04M / Dinoprostone
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32. van Heijl M, Sprangers MA, de Boer AG, Lagarde SM, Reitsma HB, Busch OR, Tilanus HW, van Lanschot JJ, van Berge Henegouwen MI: Preoperative and early postoperative quality of life predict survival in potentially curable patients with esophageal cancer. Ann Surg Oncol; 2010 Jan;17(1):23-30
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  • [Title] Preoperative and early postoperative quality of life predict survival in potentially curable patients with esophageal cancer.
  • BACKGROUND: In patients with esophageal cancer, evidence for prognostic significance of preoperative quality of life (QoL) is limited, while the prognostic significance of postoperative QoL has not been investigated at all.
  • AIM: To determine whether preoperative and postoperative QoL measurements can predict survival independently from clinical and pathological factors, in patients with potentially curable esophageal adenocarcinoma.
  • CONCLUSION: In the present paper the first large consecutive series of potentially curable esophageal cancer patients is presented in whom prospectively collected QoL data before and after potentially curative surgical resection were used to predict survival.
  • Both preoperative (physical symptoms) and postoperative (social functioning, pain, and activity level) QoL subscales are independent predictors of survival in potentially curable patients with esophageal adenocarcinoma.
  • [MeSH-major] Carcinoma, Squamous Cell / mortality. Esophageal Neoplasms / mortality. Quality of Life

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  • (PMID = 19830496.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
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33. Chung SM, Kao J, Hyjek E, Chen YT: p53 in esophageal adenocarcinoma: a critical reassessment of mutation frequency and identification of 72Arg as the dominant allele. Int J Oncol; 2007 Dec;31(6):1351-5
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  • [Title] p53 in esophageal adenocarcinoma: a critical reassessment of mutation frequency and identification of 72Arg as the dominant allele.
  • p53 alterations have been implicated in the progression of Barrett's esophagus to esophageal adenocarcinoma.
  • However, the wide range of reported p53 alteration frequencies in esophageal adenocarcinoma makes using p53 as a marker of malignant transformation of Barrett's esophagus problematic.
  • To determine the utility of p53 in Barrett's esophagus monitoring, the frequency of p53 alteration was critically reassessed using esophagectomy specimens of 40 cases of esophageal adenocarcinoma, including 10 with Barrett's esophagus and high-grade dysplasia, 8 with low-grade dysplasia and 7 with no dysplasia.
  • Mutations in p53 were identified in 75% (30/40) of the esophageal adenocarcinoma. p53 protein overexpression, detected by immunohistochemistry, was found in 58% (23/40) of the esophageal adenocarcinoma, 60% (6/10) of Barrett's esophagus with high-grade dysplasia, 12% (1/8) of Barrett's esophagus with low-grade dysplasia, and 0% of Barrett's esophagus without dysplasia.
  • However, p53 appeared to be a late marker in the neoplastic transformation, and no p53 change was found in approximately 25% of the adenocarcinoma.
  • We concluded that p53 is insufficient as a single marker for Barrett's esophagus monitoring but may be useful as part of a panel due to its high specificity.
  • [MeSH-major] Adenocarcinoma / genetics. Alleles. Esophageal Neoplasms / genetics. Genes, p53. Mutation

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  • (PMID = 17982662.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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34. Michor F, Polyak K: The origins and implications of intratumor heterogeneity. Cancer Prev Res (Phila); 2010 Nov;3(11):1361-4
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  • This phenotypic and genetic heterogeneity plays an important role in neoplasia, cancer progression, and therapeutic resistance.
  • In this issue of the journal (beginning on page 1388), Merlo et al. report their use of molecular data from 239 patients with Barrett's esophagus to evaluate the propensity of major diversity indices for predicting progression to esophageal adenocarcinoma.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20959519.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U54 CA143798; United States / NCI NIH HHS / CA / U54CA143798
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS240068; NLM/ PMC3633425
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35. Jenkins GJ, D'Souza FR, Suzen SH, Eltahir ZS, James SA, Parry JM, Griffiths PA, Baxter JN: Deoxycholic acid at neutral and acid pH, is genotoxic to oesophageal cells through the induction of ROS: The potential role of anti-oxidants in Barrett's oesophagus. Carcinogenesis; 2007 Jan;28(1):136-42
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  • [Title] Deoxycholic acid at neutral and acid pH, is genotoxic to oesophageal cells through the induction of ROS: The potential role of anti-oxidants in Barrett's oesophagus.
  • Bile acids are often refluxed into the lower oesophagus and are candidate carcinogens in the development of oesophageal adenocarcinoma.
  • The higher levels of cell death and low cell survival rates at acidic pH may imply that acid bile exposure is toxic rather than carcinogenic, as dead cells do not seed cancer development.
  • [MeSH-major] Antioxidants / therapeutic use. Barrett Esophagus / metabolism. DNA Damage / drug effects. Deoxycholic Acid / toxicity. Detergents / toxicity. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Ascorbic Acid / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / metabolism. Cell Survival / drug effects. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / metabolism. Humans. Hydrogen-Ion Concentration. Micronucleus Tests. Tumor Cells, Cultured. Tumor Suppressor Protein p53

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  • (PMID = 16905748.001).
  • [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 / Antioxidants; 0 / Detergents; 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; 005990WHZZ / Deoxycholic Acid; PQ6CK8PD0R / Ascorbic Acid
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36. Lugli A, Spichtin H, Maurer R, Mirlacher M, Kiefer J, Huusko P, Azorsa D, Terracciano L, Sauter G, Kallioniemi OP, Mousses S, Tornillo L: EphB2 expression across 138 human tumor types in a tissue microarray: high levels of expression in gastrointestinal cancers. Clin Cancer Res; 2005 Sep 15;11(18):6450-8
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  • EXPERIMENTAL DESIGN: EphB2 protein expression was analyzed by immunohistochemistry on tissue microarrays that included 76 different normal tissues, >4,000 samples from 138 different cancer types, and 1,476 samples of colon cancer with clinical follow-up data.
  • RESULTS: We found most prominent EphB2 expression in the intestinal epithelium (colonic crypts) with cancer of the colorectum displaying the highest EphB2 positivity of all tumors.
  • EphB2 expression was also observed in 75 tumor categories, including serous carcinoma of the endometrium (34.8%), adenocarcinoma of the esophagus (33.3%), intestinal adenocarcinoma of the stomach (30.2%), and adenocarcinoma of the small intestine (70%).
  • The occasional finding of strong EphB2 positivity in tumors without EphB2 positivity in the corresponding normal cells [adenocarcinoma of the lung (4%) and pancreas (2.2%)] suggests that deregulation of EphB2 signaling may involve up-regulation of the protein expression.
  • Deregulated EphB2 expression may play a role in several cancer types with loss of EphB2 expression serving as an indicator of the possible pathogenetic role of EphB2 signaling in the maintenance of tissue architecture of colon epithelium.

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  • (PMID = 16166419.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, EphB2
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37. Quaroni L, Casson AG: Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy. Analyst; 2009 Jun;134(6):1240-6
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  • [Title] Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy.
  • The objective of this exploratory study was to evaluate the feasibility of using Fourier-Transform Infrared (FTIR) spectromicroscopy to characterize formalin-fixed, paraffin-embedded human esophageal tissues.
  • Matched histologically normal esophageal squamous epithelium (NS), premalignant Barrett esophagus (BE), and primary esophageal adenocarcinoma (EADC) tissues, each defined according to strict clinicopathologic criteria, were obtained from patients who underwent esophageal resection.
  • Normal esophageal epithelia were characterized by a few well defined regions, mostly of large size (tens of contiguous pixels), which correlated with tissue histology, specifically the basal cell layer.
  • The technical feasibility of using FTIR to characterize formalin-fixed, paraffin-embedded human esophageal tissues demonstrates the potential of this technique to study archival human BE tissue specimens via automated screening techniques.
  • [MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Spectroscopy, Fourier Transform Infrared / methods
  • [MeSH-minor] Adenocarcinoma / pathology. Cluster Analysis. Goblet Cells / cytology. Goblet Cells / pathology. Humans. Intestines / pathology. Light. Metaplasia / pathology. Microscopy. Synchrotrons

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  • (PMID = 19475154.001).
  • [ISSN] 1364-5528
  • [Journal-full-title] The Analyst
  • [ISO-abbreviation] Analyst
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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38. Javle M, Ailawadhi S, Yang GY, Nwogu CE, Schiff MD, Nava HR: Palliation of malignant dysphagia in esophageal cancer: a literature-based review. J Support Oncol; 2006 Sep;4(8):365-73, 379
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  • [Title] Palliation of malignant dysphagia in esophageal cancer: a literature-based review.
  • Esophageal cancer is a lethal malignancy and adenocarcinoma of the esophagus is increasing in incidence.
  • The 5-year survival rate of patients with esophageal cancer is < 20%.
  • Palliation is an important goal of esophageal cancer therapy.
  • Investigation of dysphagia includes radiographic studies such as barium or Gastrografin swallow, esophagogastroduodenoscopy, endoscopic ultrasonography, and other staging studies for esophageal cancer.
  • Current management options for the palliation of dysphagia include esophageal dilatation, intraluminal stents, Nd:YAG laser therapy, photodynamic therapy, argon laser, systemic chemotherapy, external beam radiation therapy, brachytherapy, and combined chemoradiation therapy.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / therapy. Deglutition Disorders / etiology. Deglutition Disorders / therapy. Esophageal Neoplasms / complications. Esophageal Neoplasms / therapy. Palliative Care / methods


39. Michalak J, Bansal A, Sharma P: Screening and surveillance of Barrett's esophagus. Curr Gastroenterol Rep; 2009 Jun;11(3):195-201
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  • [Title] Screening and surveillance of Barrett's esophagus.
  • Esophageal adenocarcinoma (EAC) is the most rapidly increasing cancer in the Western world and Barrett's esophagus (BE) is the only known precursor lesion for this lethal cancer.
  • [MeSH-major] Barrett Esophagus. Endoscopy, Gastrointestinal / methods. Mass Screening / methods. Population Surveillance / methods
  • [MeSH-minor] Disease Progression. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / etiology. Humans. Incidence. Precancerous Conditions. Prevalence. United States / epidemiology

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  • (PMID = 19463219.001).
  • [ISSN] 1534-312X
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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40. Mukherjee K, Chakravarthy AB, Goff LW, El-Rifai W: Esophageal adenocarcinoma: treatment modalities in the era of targeted therapy. Dig Dis Sci; 2010 Dec;55(12):3304-14
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  • [Title] Esophageal adenocarcinoma: treatment modalities in the era of targeted therapy.
  • Esophageal adenocarcinoma is an aggressive malignancy with a poor outcome, and its incidence continues to rise at an alarming rate.
  • Multiple molecular pathways including the epidermal growth factor receptor, vascular endothelial growth factor, v-erb-b2 erythroblastic leukemia viral oncogene homolog (ERBB2), and Aurora kinase pathways are activated in many esophageal adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / drug therapy. Esophageal Neoplasms / drug therapy. Molecular Targeted Therapy
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Antineoplastic Agents / pharmacology. Aurora Kinases. Barrett Esophagus / pathology. Clinical Trials as Topic. Combined Modality Therapy. Disease Progression. Esophagectomy. Humans. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / drug effects. Receptor, Epidermal Growth Factor / physiology. Treatment Outcome

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  • (PMID = 20300841.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 1 UL1 RR024975; United States / NCI NIH HHS / CA / T32 CA106183-04; United States / NCI NIH HHS / CA / T32 CA106183; United States / NCRR NIH HHS / RR / TL1 RR024978; United States / NCRR NIH HHS / RR / KL2 RR024977; United States / NCI NIH HHS / CA / R01 CA133738-01A2; United States / NCI NIH HHS / CA / R01 CA106176-07A1; United States / NCI NIH HHS / CA / CA133738; United States / NCI NIH HHS / CA / CA131225; United States / NCI NIH HHS / CA / R01 CA131225-01A2; United States / NCI NIH HHS / CA / R01 CA133738; United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / R01 CA131225; United States / NCI NIH HHS / CA / T32 CA106183-05; United States / NCRR NIH HHS / RR / UL1 RR024975; United States / NCRR NIH HHS / RR / UL1 RR024975-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS183809; NLM/ PMC2890301
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41. Raggi M, Langer R, Feith M, Friess H, Schauer M, Theisen J: Successful evaluation of a new animal model using mice for esophageal adenocarcinoma. Langenbecks Arch Surg; 2010 Apr;395(4):347-50
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  • [Title] Successful evaluation of a new animal model using mice for esophageal adenocarcinoma.
  • INTRODUCTION: For the better understanding of the pathophysiological events occurring in the sequence inflammation-metaplasia-carcinoma in esophageal adenocarcinoma, an animal model would be desirable.
  • Some demonstrated a sequence similar to the human situation whereas others failed to initiate true esophageal adenocarcinoma or even Barrett's metaplasia.
  • Intestinal metaplasia could be found in 60% of the animals after 4 months and esophageal adenocarcinoma in 55% after 5 months.
  • CONCLUSION: After a certain learning curve esophagojejunostomy is feasible in mice with an acceptable mortality rate and leads to esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagus / surgery. Jejunum / surgery

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  • (PMID = 20300770.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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42. Aklilu M, Ilson DH: Targeted agents and esophageal cancer--the next step? Semin Radiat Oncol; 2007 Jan;17(1):62-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted agents and esophageal cancer--the next step?
  • Esophageal cancer (EC) is an aggressive cancer and is a leading cause of cancer-related death worldwide.
  • In the United States and Western Europe, there has been a decline in the incidence of squamous cell carcinomas coupled with a rapid rise in incidence of adenocarcinoma of the esophagus and gastroesophageal junction.
  • [MeSH-major] Esophageal Neoplasms / drug therapy

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  • (PMID = 17185199.001).
  • [ISSN] 1053-4296
  • [Journal-full-title] Seminars in radiation oncology
  • [ISO-abbreviation] Semin Radiat Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 85
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43. Wen D, Zhang N, Shan B, Wang S: Helicobacter pylori infection may be implicated in the topography and geographic variation of upper gastrointestinal cancers in the Taihang Mountain high-risk region in northern China. Helicobacter; 2010 Oct;15(5):416-21
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  • Chronic infection of the bacterial not only causes distal stomach cancer, but also confers risk to gastric cardia adenocarcinoma.
  • Because H. pylori infection is inversely associated with esophageal adenocarcinoma, globally the infection rate is significantly correlated with the ratio of squamous carcinoma to adenocarcinoma of the esophagus.
  • These agree with the topography of upper gastrointestinal cancer observed in the Taihang Mountain high-risk region where both gastric cardia and non-cardia adenocarcinoma coincide with esophageal squamous cancer, but with almost no distal esophageal adenocarcinoma.
  • Because H. pylori infection is a definite carcinogen to gastric adenocarcinoma and is more prevalent in the mountain than in plain areas due to undeveloped living conditions, the observation gives the impression as though H. pylori infection is implicated.
  • AIMS: This article aims to note the role of H. pylori infection in upper gastrointestinal cancer in the Taihang Mountain high-risk region in northern China.
  • MATERIALS AND METHODS: First the unique topography and geographic variation of upper gastrointestinal cancer in the region is described to indicate a possible role of H. pylori infection, then we review studies on prevalence of H. pylori infection in the high-risk region and describe difference in socioeconomic development and water hygiene between the plains and the mountains as related to the prevalence of H. pylori infection.
  • RESULTS:   Coincidence of gastric cancer in the region and a progressively increasing rate of the cancer from the plain towards the mountains indicate H. pylori infection may be implicated in upper gastrointestinal cancer.
  • CONCLUSION: International collaboration is needed to study H. pylori and upper gastrointestinal cancer in the region when rapid industrialization is just beginning.
  • [MeSH-major] Adenocarcinoma / epidemiology. Adenocarcinoma / microbiology. Gastrointestinal Neoplasms / epidemiology. Gastrointestinal Neoplasms / microbiology. Helicobacter Infections / complications. Helicobacter Infections / epidemiology. Helicobacter pylori / isolation & purification

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 21083747.001).
  • [ISSN] 1523-5378
  • [Journal-full-title] Helicobacter
  • [ISO-abbreviation] Helicobacter
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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44. Labutina IuO: [Barrett's esophagus: contemporary diagnostic and therapeutic approaches]. Klin Med (Mosk); 2006;84(11):25-9
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  • [Title] [Barrett's esophagus: contemporary diagnostic and therapeutic approaches].
  • The author considers the modern concepts of the epidemiology, pathophysiology, clinical manifestations, and diagnostics of Barrett's esophagus (BE).
  • Special attention is paid to the evaluation of BE as precancer elevating the risk of esophageal adenocarcinoma, as well as the issues of the treatment and regular medical check-up of such patients.
  • [MeSH-major] Barrett Esophagus. Endoscopy, Gastrointestinal / methods. Enzyme Inhibitors / therapeutic use. Esophagectomy / methods. Histamine H2 Antagonists / therapeutic use. Proton Pump Inhibitors

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  • (PMID = 17243606.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors
  • [Number-of-references] 39
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45. Kubo A, Levin TR, Block G, Rumore G, Quesenberry CP Jr, Buffler P, Corley DA: Cigarette smoking and the risk of Barrett's esophagus. Cancer Causes Control; 2009 Apr;20(3):303-11
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  • [Title] Cigarette smoking and the risk of Barrett's esophagus.
  • INTRODUCTION: We examined the association between smoking and the risk of Barrett's esophagus (BE), a metaplastic precursor to esophageal adenocarcinoma.
  • Patients with a new diagnosis of BE (n = 320) were matched to persons with gastroesophageal reflux disease (GERD) (n = 316) and to population controls (n = 317).
  • Stratified analyses suggested that ever smoking may be associated with an increased risk of BE among some groups (compared to population controls): persons with long-segment Barrett's esophagus (odds ratio [OR] = 1.72, 95% confidence interval [CI] 1.12-2.63); subjects without GERD symptoms (OR = 3.98, 95% CI 1.58-10.0); obese subjects (OR = 3.38, 95% CI 1.46-7.82); and persons with a large abdominal circumference (OR = 3.02, 95% CI (1.18-2.75)).

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  • (PMID = 18853262.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK063616-05; United States / NIDDK NIH HHS / DK / K08 DK002697; United States / NIDDK NIH HHS / DK / K08 DK 002697; United States / NIDDK NIH HHS / DK / R01 DK063616; United States / NIDDK NIH HHS / DK / R01 DK 63616; United States / NIDDK NIH HHS / DK / R01 DK063616-05; United States / NIDDK NIH HHS / DK / DK002697-05; United States / NIDDK NIH HHS / DK / F32 DK081271; United States / NIDDK NIH HHS / DK / K08 DK002697-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ NIHMS72089; NLM/ PMC2649684
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46. Wu G, Bybel B, Brunken R, Lin H, Neumann D: PET detection of solitary distant skeletal muscle metastasis of esophageal adenocarcinoma. Clin Nucl Med; 2005 May;30(5):335-7
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  • [Title] PET detection of solitary distant skeletal muscle metastasis of esophageal adenocarcinoma.
  • A 67-year-old man with progressive dysphagia was recently diagnosed with a gastroesophageal junction adenocarcinoma.
  • Needle biopsy was performed and confirmed metastatic esophageal adenocarcinoma.
  • A case of skeletal muscle metastases from late-stage (IV) gastroesophageal adenocarcinoma was previously reported.
  • The case supports the previous report that PET is superior in detecting distant metastases for initial staging of esophageal carcinoma over CT.
  • [MeSH-major] Adenocarcinoma / radionuclide imaging. Adenocarcinoma / secondary. Esophageal Neoplasms / radionuclide imaging. Fluorodeoxyglucose F18. Muscle Neoplasms / radionuclide imaging. Muscle Neoplasms / secondary. Positron-Emission Tomography / methods

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  • (PMID = 15827406.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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47. Sampliner RE: Managing Barrett's esophagus: what is new in 2005? Dis Esophagus; 2005;18(1):17-20
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  • [Title] Managing Barrett's esophagus: what is new in 2005?
  • The new developments in the management of Barrett's esophagus in 2005 result in refinements of decision making.
  • Endoscopic mucosal resection is being more widely applied resulting in more accurate staging of patients with early adenocarcinoma of the esophagus and helping to define patients amenable to endoscopic therapy.
  • The impact of medical therapy of GERD and anti-reflux surgery on the development of esophageal adenocarcinoma is disappointing.

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  • (PMID = 15773836.001).
  • [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; Review
  • [Publication-country] United States
  • [Number-of-references] 33
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48. Lin L, Wang Z, Prescott MS, van Dekken H, Thomas DG, Giordano TJ, Chang AC, Orringer MB, Gruber SB, Moran JV, Glover TW, Beer DG: Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3-q27 are associated with development of esophageal adenocarcinoma. Genes Chromosomes Cancer; 2006 Apr;45(4):319-31
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  • [Title] Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3-q27 are associated with development of esophageal adenocarcinoma.
  • Gene amplification is one of the mechanisms to activate oncogenes in many cancers, including esophageal adenocarcinoma (EA).
  • [MeSH-major] Adenocarcinoma / genetics. Chromosomes, Human, Pair 3. Esophageal Neoplasms / genetics


49. Takubo K, Aida J, Sawabe M, Arai T, Kato H, Pech O, Arima M: The normal anatomy around the oesophagogastric junction: a histopathologic view and its correlation with endoscopy. Best Pract Res Clin Gastroenterol; 2008;22(4):569-83
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  • The incidence of primary oesophageal adenocarcinoma in Caucasian men has recently been increasing rapidly.
  • Therefore, primary oesophageal adenocarcinoma, columnar-lined oesophagus (CLO) or Barrett's oesophagus and the normal condition of the lower segment of the oesophagus are currently receiving worldwide attention in the medical field.
  • We review definitions of the OGJ, the pattern of the squamocolumnar junction (SCJ), oesophageal cardiac-type glands beneath the squamous epithelium, the normal squamous epithelium, columnar islands in squamous-lined mucosa, squamous islands in CLO and newly reported metaplastic changes in the OGJ zone.
  • [MeSH-minor] Biopsy. Esophageal Sphincter, Upper / cytology. Humans. Stomach / cytology

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  • (PMID = 18656817.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 33
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50. Szachnowicz S, Cecconello I, Ribeiro U, Iriya K, El Ibrahim R, Takeda FR, Corbett CE, Vaz Safatle-Ribeiro A: Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study. World J Surg Oncol; 2009;7:27
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  • [Title] Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study.
  • BACKGROUND: Mucin immunoexpression in adenocarcinoma arising in Barrett's esophagus (BE) may indicate the carcinogenesis pathway.
  • The aim of this study was to evaluate resected specimens of adenocarcinoma in BE for the pattern of mucins and to correlate to the histologic classification.
  • METHODS: Specimens were retrospectively collected from thirteen patients who underwent esophageal resection due to adenocarcinoma in BE.
  • CONCLUSION: Barrett's esophagus adenocarcinoma shows either gastric or intestinal type pattern of mucin expression.
  • The two types of tumors developed in Barrett's esophagus may reflect the original cell type involved in the malignant transformation.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Mucin 5AC / analysis. Mucin-2 / analysis

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  • (PMID = 19272137.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucin-2
  • [Other-IDs] NLM/ PMC2662840
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96. Quera R, O'Sullivan K, Quigley EM: Surveillance in Barrett's oesophagus: will a strategy focused on a high-risk group reduce mortality from oesophageal adenocarcinoma? Endoscopy; 2006 Feb;38(2):162-9
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  • [Title] Surveillance in Barrett's oesophagus: will a strategy focused on a high-risk group reduce mortality from oesophageal adenocarcinoma?
  • BACKGROUND AND STUDY AIMS: The incidence of oesophageal adenocarcinoma has increased significantly in recent years.
  • While surveillance of people with Barrett's oesophagus, its usual precursor, has been advocated in order to detect dysplasia and early cancer in those considered to be at greatest risk, the impact of such a strategy on survival from oesophageal adenocarcinoma is unclear.
  • This study aimed to determine the effect of surveillance on mortality from oesophageal adenocarcinoma in a group of patients considered to be at high risk of developing Barrett's oesophagus and adenocarcinoma.
  • PATIENTS AND METHODS: After performing a Medline search of the literature published between 1985 and 2004 for studies on gastro-oesophageal reflux disease, Barrett's oesophagus and adenocarcinoma, we examined the impact of surveillance on mortality from oesophageal adenocarcinoma in a hypothetical sample of 100 high-risk patients (men aged over 50 with Barrett's oesophagus but without high-grade dysplasia at entry).
  • RESULTS: Four patients in this high-risk group developed adenocarcinoma during surveillance, with survival rates of 78.9% (95%CI 64.9%-88.5%) at 2 years and 78.6% (95%CI 62.8%-89.2%) at 5 years.
  • Meanwhile, between 515 and 2060 patients with Barrett's oesophagus were not detected or surveyed by this strategy and between 16 and 61 of these developed adenocarcinoma, with much lower survival rates of 37.1% (95%CI 25.4%-50.3%) at 2 years and 16.7% (95%CI 9%-28.3%) at 5 years.
  • Although surveillance in the high-risk group resulted in the long-term survival of three patients who would not otherwise have survived, this gain was dramatically offset by the 13 to 51 patients, excluded from surveillance by this strategy, who died from oesophageal adenocarcinoma.
  • CONCLUSIONS: A surveillance programme based on current concepts of risk cannot have an impact on mortality from oesophageal adenocarcinoma.
  • To be effective, it will be necessary for surveillance programmes to utilise more precise methods for the identification of those who are most at risk of progression to adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / mortality. Barrett Esophagus / epidemiology. Esophageal Neoplasms / mortality. Population Surveillance. Precancerous Conditions / epidemiology

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  • (PMID = 16479424.001).
  • [ISSN] 0013-726X
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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97. Bradbury PA, Zhai R, Hopkins J, Kulke MH, Heist RS, Singh S, Zhou W, Ma C, Xu W, Asomaning K, Ter-Minassian M, Wang Z, Su L, Christiani DC, Liu G: Matrix metalloproteinase 1, 3 and 12 polymorphisms and esophageal adenocarcinoma risk and prognosis. Carcinogenesis; 2009 May;30(5):793-8
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  • [Title] Matrix metalloproteinase 1, 3 and 12 polymorphisms and esophageal adenocarcinoma risk and prognosis.
  • We studied the association between four MMP polymorphisms within three MMP genes and esophageal adenocarcinoma (EA) risk and prognosis.

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  • (PMID = 19321798.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA074386
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.65 / Matrix Metalloproteinase 12; EC 3.4.24.7 / Matrix Metalloproteinase 1
  • [Other-IDs] NLM/ PMC2675656
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98. Dilemmas in managing Barrett's oesophagus. Drug Ther Bull; 2006 Sep;44(9):69-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dilemmas in managing Barrett's oesophagus.
  • In the UK, oesophageal adenocarcinoma accounts for over 7,000 deaths per year and its incidence is rising.
  • One risk factor for this cancer is Barrett's oesophagus.
  • Of people with Barrett's oesophagus, about 1% per year develop adenocarcinoma, around 30-125 times the rate in the general population.
  • So it has been suggested that people with reflux should be screened for Barrett's oesophagus, and those with the condition should be kept under surveillance to detect dysplasia or adenocarcinoma in the early stages.
  • Here we discuss the problems in managing patients with Barrett's oesophagus.
  • [MeSH-major] Barrett Esophagus / therapy

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  • (PMID = 17009567.001).
  • [ISSN] 0012-6543
  • [Journal-full-title] Drug and therapeutics bulletin
  • [ISO-abbreviation] Drug Ther Bull
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin
  • [Number-of-references] 72
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99. Shirin H, Leja M, Niv Y: Helicobacter pylori and non-malignant diseases. Helicobacter; 2008 Oct;13 Suppl 1:23-7
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  • The main problems remain unsolved: peptic ulcer disease negative for H. pylori, synergism of H. pylori infection and aspirin and other nonsteroidal anti-inflammatory drugs or cyclooxygenase 2 specific inhibitors, the role of H. pylori eradication in uninvestigated and nonulcer dyspepsia, and the possible protective effect of H. pylori infection against gastroesophageal reflux disease and its complications such as Barrett's esophagus and adenocarcinoma.

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  • (PMID = 18783518.001).
  • [ISSN] 1523-5378
  • [Journal-full-title] Helicobacter
  • [ISO-abbreviation] Helicobacter
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
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100. Nair KS, Naidoo R, Chetty R: Expression of cell adhesion molecules in oesophageal carcinoma and its prognostic value. J Clin Pathol; 2005 Apr;58(4):343-51
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  • [Title] Expression of cell adhesion molecules in oesophageal carcinoma and its prognostic value.
  • Oesophageal carcinoma remains a disease of poor prognosis.
  • This review provides a brief description of five families of CAMs (cadherins, integrins, CD44, immunoglobulin superfamily, and selectins) and highlights their altered expression in relation both to prognosis and tumour behaviour in squamous cell carcinoma and adenocarcinoma of the oesophagus.
  • [MeSH-major] Cell Adhesion Molecules / analysis. Esophageal Neoplasms / chemistry
  • [MeSH-minor] Adenocarcinoma / chemistry. Antigens, CD44 / analysis. Cadherins / analysis. Carcinoma, Squamous Cell / chemistry. Humans. Integrins / analysis. Neoplasm Metastasis. Prognosis. Selectins / analysis

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  • (PMID = 15790695.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Cadherins; 0 / Cell Adhesion Molecules; 0 / Integrins; 0 / Selectins
  • [Number-of-references] 132
  • [Other-IDs] NLM/ PMC1770622
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