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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
  • [MeSH-minor] Adult. Aged. Female. Gastric Mucosa / pathology. Humans. Immunohistochemistry. Male. Middle Aged. Retrospective Studies

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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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2. Tu CH, Lee CT, Perng DS, Chang CC, Hsu CH, Lee YC: Esophageal adenocarcinoma arising from Barrett's epithelium in Taiwan. J Formos Med Assoc; 2007 Aug;106(8):664-8
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  • [Title] Esophageal adenocarcinoma arising from Barrett's epithelium in Taiwan.
  • The prevalence of Barrett's esophagus (BE) in Eastern countries is rising to match the prevalence in the West.
  • However, a corresponding trend of BE-associated adenocarcinoma has yet to be observed in Asia.
  • Historically, adenocarcinoma complicating BE has been considered a rare event in Taiwan.
  • In the present report, we collected three Taiwanese cases of esophageal adenocarcinoma arising from BE.
  • The second case was a 63-year-old man who presented with odynophagia and was found to have an ulcerative tumor centered on the characteristic Barrett's mucosa.
  • Our report emphasizes the need for an updated epidemiologic study to determine the incidence of BE-associated adenocarcinoma in Taiwan.

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  • (PMID = 17711800.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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3. 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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4. Tischoff I, Hengge UR, Vieth M, Ell C, Stolte M, Weber A, Schmidt WE, Tannapfel A: Methylation of SOCS-3 and SOCS-1 in the carcinogenesis of Barrett's adenocarcinoma. Gut; 2007 Aug;56(8):1047-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methylation of SOCS-3 and SOCS-1 in the carcinogenesis of Barrett's adenocarcinoma.
  • AIMS: This study was performed to elucidate the role of SOCS-1 and SOCS-3 in Barrett's adenocarcinoma and its precursor lesions.
  • 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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5. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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6. Vats HS, Banerjee TK, Resnick J, Khan Q: Esophageal adenocarcinoma arising from Barrett's dysplasia: a case report of double occurrence and prolonged survival after chemotherapy. Clin Med Res; 2006 Sep;4(3):184-8
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  • [Title] Esophageal adenocarcinoma arising from Barrett's dysplasia: a case report of double occurrence and prolonged survival after chemotherapy.
  • A relatively young patient with chronic gastroesophageal reflux disease (GERD), obesity, smoking, and alcohol intake presented with widespread metastatic disease in lymph nodes, liver and lungs from a lower esophageal adenocarcinoma extending into the gastroesophageal junction associated with Barrett's mucosa and dysplasia.A complete response was achieved with six cycles of chemotherapy that sustained for more than 4 years without further recurrence.
  • Unfortunately, there was presence of esophageal metaplasia after complete response which eventually converted to low to high grade dysplasia and ultimately to a second primary localized lower esophageal adenocarcinoma that was treated with thoracoabdominal esophagectomy and lymphadenectomy.
  • The pathogenesis of a recent increase in the incidence of GERD, Barrett's esophagus and lower esophageal adenocarcinoma are discussed.
  • Lower esophageal adenocarcinoma is frequently associated with Barrett's high-grade dysplasia.
  • Since there has been a dramatic increase in the incidence of Barrett's dysplasia, appropriate surveillance with upper gastrointestinal endoscopy and preventive strategies, such as the use of aspirin, cyclo-oxygenase II inhibitors and other nonsteroidal antiinflammatory drugs known to be chemopreventive agents against colon, esophagus, gastric and bladder cancers, need to be studied.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology

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  • (PMID = 16988098.001).
  • [ISSN] 1539-4182
  • [Journal-full-title] Clinical medicine & research
  • [ISO-abbreviation] Clin Med Res
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC1570486
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7. 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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8. 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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9. 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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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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11. 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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12. 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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13. 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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14. 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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15. 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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16. 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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17. 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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  • [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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18. Jaquet Y, Pilloud R, Grosjean P, Radu A, Monnier P: [Endoscopic mucosal resection for the treatment of superficial adenocarcinima developed on the Barrett's mucosa]. Rev Med Suisse; 2005 Oct 19;1(37):2385-6, 2389-90
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  • [Title] [Endoscopic mucosal resection for the treatment of superficial adenocarcinima developed on the Barrett's mucosa].
  • [Transliterated title] La mucosectomie endoscopique pour le traitement des adénocarcinomes superficiels développés sur la muqueuse de Barrett.
  • We present a new technique of endoscopic mucosal resection for the treatment of extended superficial lesions of the esophagus such as early squamous cell carcinoma, high grade intraepithelial neoplasia or early adenocarcinoma arising in Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / complications. Carcinoma, Squamous Cell / surgery. Endoscopy / methods. Esophageal Neoplasms / surgery

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  • (PMID = 16300281.001).
  • [ISSN] 1660-9379
  • [Journal-full-title] Revue médicale suisse
  • [ISO-abbreviation] Rev Med Suisse
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Switzerland
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19. Ko Y, Sato Y, Tanaka S, Okuda T, Fujimi A, Doi T, Kanisawa Y, Iwai K, Ohta H: [A case of early esophageal adenocarcinoma arising from esophageal cardiac glands]. Nihon Shokakibyo Gakkai Zasshi; 2009 Sep;106(9):1327-33
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  • [Title] [A case of early esophageal adenocarcinoma arising from esophageal cardiac glands].
  • We found no Barrett's mucosa around the lesion.
  • A biopsy specimen of this tumor showed well-differentiated adenocarcinoma.
  • Eventually, the histological diagnosis after resection was esophageal adenocarcinoma arising from cardiac glands, limited to the mucosal layer (M2).
  • This origin of the esophageal adenocarcinoma is rare.
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology

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  • (PMID = 19734704.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 19
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20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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21. 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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  • [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.
  • 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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22. Maru DM: Barrett's esophagus: diagnostic challenges and recent developments. Ann Diagn Pathol; 2009 Jun;13(3):212-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Barrett's esophagus: diagnostic challenges and recent developments.
  • Inclusion of histologic classification into the risk assessment of adenocarcinoma arising from Barrett's esophagus (BE) has placed surgical pathologist in the center of clinical care and research endeavors.
  • (1) Discuss the definition of BE and features differentiating BE vs intestinal metaplasia involving cardia. (2) Describe the morphological approach of diagnosing and grading of dysplasia and differentiation of high-grade dysplasia from intramucosal carcinoma. (3) Role of special stains in diagnosis of BE and dysplasia. (4) Brief review the literature on histologic and endoscopic factors associated with progression of BE to adenocarcinoma. (5) Discuss the biomarkers in progression of BE to adenocarcinoma.
  • Because of the controversy in defining BE, the histologic type of columnar mucosa and presence or absence of intestinal metaplasia should be specified in pathology report.
  • The extent of high-grade dysplasia, high-grade dysplasia with certain endoscopic abnormalities, and low-grade dysplasia, when diagnosed with consensus by 2 or 3 gastrointestinal pathologists, has higher risk of progression to adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / diagnosis. Precancerous Conditions / diagnosis

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  • (PMID = 19433303.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 58
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23. 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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24. Agarwal B, Swisher SG, Ajani J, Kelly K, Komaki RR, Abu-Hamda E, Correa AM, Roth JA: Differential response to preoperative chemoradiation and surgery in esophageal adenocarcinomas based on presence of Barrett's esophagus and symptomatic gastroesophageal reflux. Ann Thorac Surg; 2005 May;79(5):1716-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential response to preoperative chemoradiation and surgery in esophageal adenocarcinomas based on presence of Barrett's esophagus and symptomatic gastroesophageal reflux.
  • BACKGROUND: Barrett's esophagus and gastroesophageal reflux disease (GERD) are recognized to predispose to esophageal adenocarcinoma.
  • Abdel-Latif and colleagues recently suggested that esophageal adenocarcinoma patients with GERD might be resistant to multimodality treatment.
  • In this study, we investigated potential differences in clinical outcomes in esophageal adenocarcinoma patients based on the presence of identifiable Barrett's mucosa and/or history of symptomatic GERD.
  • METHODS: Eighty-four patients with resectable esophageal adenocarcinoma, who completed the planned preoperative chemoradiation and underwent a potentially curative esophageal resection were retrospectively evaluated.
  • Postoperative survival was compared between patients with or without underlying Barrett's esophagus and history of symptomatic GERD.
  • Patients with pathologic complete response (path CR) and those with partial or no response (path PR) were compared to determine if presence of Barrett's esophagus and history of symptomatic GERD influence the path CR rates.
  • RESULTS: We found significantly lower postoperative survival in patients with Barrett's associated adenocarcinoma (vs adenocarcinoma arising de novo, p = 0.031) and patients with symptomatic GERD (vs patients without symptomatic GERD, p = 0.019).
  • Furthermore, the subset of patients with path PR (vs path CR) after chemoradiation have a significantly higher proportion of patients with Barrett's esophagus (HR = 4.38, confidence interval [CI] = 1.39 to 13.83, p = 0.012) and patients with GERD (HR = 2.71, CI = 1.13 to 6.50, p = 0.026).
  • CONCLUSIONS: Patients with esophageal adenocarcinoma may have differences in response to preoperative chemoradiation based on the presence of Barrett's esophagus and history of symptomatic GERD.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / surgery. Gastroesophageal Reflux / complications


25. Leers JM, DeMeester SR, Ayazi S, Tang AL, Peyre CG, Lipham JC, Hagen JA, DeMeester TR: Recurrence of intramucosal esophageal adenocarcinoma arising in a former esophagostomy site: a unique case report. Dis Esophagus; 2009;22(6):E17-20
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  • [Title] Recurrence of intramucosal esophageal adenocarcinoma arising in a former esophagostomy site: a unique case report.
  • A 75-year-old male with a long history of gastroesophageal reflux symptoms developed adenocarcinoma proximally within a long segment of Barrett's esophagus.
  • Pathology showed an intramucosal adenocarcinoma, limited to the muscularis mucosa with surrounding high-grade dysplasia and intestinal metaplasia.
  • The proximal esophageal margin showed no tumor cells, but there was low-grade dysplasia within Barrett's esophagus.
  • Biopsy revealed an implant metastasis of esophageal adenocarcinoma.

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  • (PMID = 19021685.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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26. 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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27. 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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28. 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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29. Alrawi SJ, Winston J, Tan D, Gibbs J, Loree TR, Hicks W, Rigual N, Lorè JM Jr: Primary adenocarcinoma of cervical esophagus. J Exp Clin Cancer Res; 2005 Jun;24(2):325-30
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  • [Title] Primary adenocarcinoma of cervical esophagus.
  • Most upper esophageal malignancies are squamous cell carcinomas, rarely adenocarcinomas arising from Barrett's esophagus and very rarely adenocarcinomas from heterotopic gastric mucosa without evidence of Barrett's especially in the cervical part of the esophagus.
  • We report a case of adenocarcinoma of the polypoid type in the upper esophagus (cervical esophagus) arising from ectopic gastric mucosa, in a 60 year-old man who presented with progressive dysphagia.
  • Accurate diagnosis by esophagogram revealed a large mass in the cervical esophagus; CAT scan showed intraluminal mass at the level of thoracic inlet, esophagogastroscopy showed a fleshy polyp (3.2cm x 3.0cm) at 20 cm from the incisors with a biopsy confirming moderately differentiated adenocarcinoma with no evidence of Barrett's esophagus.
  • It seems this tumor has a much better prognosis than adenocarcinomas arising from Barrett's.
  • [MeSH-major] Adenocarcinoma / diagnosis. Esophageal Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Cell Differentiation. Deglutition Disorders. Esophagus / pathology. Gastric Mucosa / pathology. Humans. Male. Middle Aged. Prognosis. Tomography, X-Ray Computed

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  • (PMID = 16110768.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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30. 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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31. 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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32. 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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33. 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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34. 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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35. 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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36. 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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37. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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38. Möbius C, Freire J, Becker I, Feith M, Brücher BL, Hennig M, Siewert JR, Stein HJ: VEGF-C expression in squamous cell carcinoma and adenocarcinoma of the esophagus. World J Surg; 2007 Sep;31(9):1768-72; discussion 1773-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] VEGF-C expression in squamous cell carcinoma and adenocarcinoma of the esophagus.
  • METHODS: The expression of VEGF-C was evaluated using immunohistochemistry (IHC) on 59 paraffin-embedded archival specimens from patients with squamous cell esophageal carcinomas and 54 paraffin-embedded archival specimens of patients with esophageal adenocarcinomas arising in Barrett's mucosa.
  • In patients with adenocarcinoma of the esophagus there was no correlation between VEGF-C expression and clinicopathological parameters.
  • High VEGF-C expression tended to be correlated with poor survival in squamous cell cancer but not in adenocarcinoma of the esophagus.
  • This seems not to be true for the adenocarcinoma of the esophagus.
  • These data could help with the understanding of the different onset and characteristics of lymph node metastasis in squamous cell carcinoma and adenocarcinoma of the esophagus.
  • [MeSH-major] Adenocarcinoma / chemistry. Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / chemistry. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / chemistry. Esophageal Neoplasms / pathology. Vascular Endothelial Growth Factor C / analysis

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  • (PMID = 17354029.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor C
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39. 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 Kyōbu Geka Gakkai zasshi
  • [ISO-abbreviation] Jpn. J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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40. 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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41. Hara T, Kijima H, Yamamoto S, Kise Y, Hanashi T, Nishi T, Chino O, Shimada H, Tanaka M, Inokuchi S, Makuuchi H: Immunohistochemical expression of p63 in esophageal Barrett's adenocarcinoma. Mol Med Rep; 2008 Jul-Aug;1(4):473-7
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  • [Title] Immunohistochemical expression of p63 in esophageal Barrett's adenocarcinoma.
  • We examined p63 expression patterns in esophageal Barrett's adenocarcinoma, including early-stage cancers, as well as its clinicopathological significance.
  • The role of the p63 gene is thought to be different in esophageal Barrett's adenocarcinoma compared with esophageal squamous cell carcinoma. p63 immunoreactivity was most useful as a predictor of lymph node metastasis.

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  • (PMID = 21479434.001).
  • [ISSN] 1791-2997
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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42. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


43. Jenkins JT, Charles A, Mitchell KG, Fullarton GM: Photodynamic therapy for Barretts' adenocarcinoma associated with an Angelchik device. Photodiagnosis Photodyn Ther; 2005 Sep;2(3):197-200

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Photodynamic therapy for Barretts' adenocarcinoma associated with an Angelchik device.
  • We present a novel case of an elderly patient with a Barrett's adenocarcinoma in the presence of an Angelchik prosthesis.
  • We aim to draw attention to issues relating to metaplastic Barretts' oesphagus and its adenocarcinoma complications and highlight relevant issues in multimodal endoscopic management and palliation using photodynamic therapy in the presence of the device.

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  • (PMID = 25048770.001).
  • [ISSN] 1572-1000
  • [Journal-full-title] Photodiagnosis and photodynamic therapy
  • [ISO-abbreviation] Photodiagnosis Photodyn Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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44. Nishi T, Makuuchi H, Shimada H, Chino O, Yamamoto S, Hara T: [Present state and measures of Barrett's cancer in Japan]. Nihon Rinsho; 2005 Aug;63(8):1470-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Present state and measures of Barrett's cancer in Japan].
  • Barrett's adenocarcinoma is common esophageal cancer in western countries but very rare in Japan.
  • We reviewed 206 cases of Barrett's cancer in Japanese literature that issued from 2000 to 2004.
  • There was no mucosal Barrett's cancer with lymph nodes metastasis, therefore EMR (endoscopic mucosal resection) method is an appropriate way for mucosal cancer.
  • Barrett's cancer with submucosal invasion occur lymph nodes metastasis, so surgical operation should be applied for deeper invasion to submucosal cancer.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / therapy. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Esophageal Neoplasms / therapy

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  • (PMID = 16101242.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 7
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45. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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46. Hoshihara Y, Kogure T, Yamamoto T, Hashimoto M, Hoteya O: [Endoscopic diagnosis of Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1394-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Endoscopic diagnosis of Barrett's esophagus].
  • In Japan Barrett's mucosa is defined as columnar lined esophagus (CLE).
  • The prevalence of Barrett's esophagus and Barrett's adenocarcinoma is very low.
  • But in Western countries Barrett's mucosa is defined as CLE with intestinal metaplasia, and many cases of Barrett's esophagus and Barrett's adenocarcinoma are reported.
  • The definite endoscopic diagnosis of Barrett's mucosa cannot be so easy.
  • In no cases were the longitudinal vessels observed under the gastric mucosa beyond the esophageal hiatus.
  • When longitudinal vessels are found only under the columnar epithelium at the oral side over the esophageal hiatus from the stomach, this indicates Barrett's epithelium.
  • Thus the definite diagnosis of Barrett's epithelium can be made by endoscopy.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / pathology. Endoscopy, Gastrointestinal

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  • (PMID = 16101228.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 17
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47. Rugge M, Fassan M, Zaninotto G, Pizzi M, Giacomelli L, Battaglia G, Rizzetto C, Parente P, Ancona E: Aurora kinase A in Barrett's carcinogenesis. Hum Pathol; 2010 Oct;41(10):1380-6
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  • [Title] Aurora kinase A in Barrett's carcinogenesis.
  • In Barrett's mucosa, both aneuploidy and TP53 mutations are consistently recognized as markers of an increased risk of Barrett's adenocarcinoma.
  • Eighty-seven esophageal biopsy samples representative of all the phenotypic lesions occurring in the multistep process of Barrett's carcinogenesis (gastric metaplasia in 25, intestinal metaplasia in 25, low-grade intraepithelial neoplasia in 16, high-grade intraepithelial neoplasia in 11, and Barrett's adenocarcinoma in 10) were obtained from long segments of Barrett's mucosa.
  • Twenty-five additional biopsy samples of native esophageal mucosa were used for control purposes.
  • Nine of 10 Barrett's adenocarcinomas showed AURKA immunostaining.
  • AURKA overexpression is significantly associated with Barrett's mucosa progressing to Barrett's adenocarcinoma and contributes to esophageal carcinogenesis via chromosome instability.
  • The identification of AURKA as a novel molecular target of cancer progression in Barrett's mucosa provides a lead for the development of new therapeutic approaches in Barrett's mucosa patients.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Cell Transformation, Neoplastic / metabolism. Esophageal Neoplasms / enzymology. Esophagus / enzymology. Protein-Serine-Threonine Kinases / biosynthesis
  • [MeSH-minor] Aurora Kinase A. Aurora Kinases. Carcinoma in Situ / enzymology. Carcinoma in Situ / pathology. Cell Nucleus Size. Gastric Mucosa / enzymology. Gastric Mucosa / pathology. Humans. Immunohistochemistry. Intestinal Mucosa / enzymology. Intestinal Mucosa / pathology. Metaplasia. Mucous Membrane / enzymology. Mucous Membrane / pathology. Oligonucleotide Array Sequence Analysis. Retrospective Studies. Tumor Suppressor Protein p53 / biosynthesis

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20656315.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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48. Werther M, Saure C, Pahl R, Schorr F, Rüschoff J, Alles JU, Heinmöller E: Molecular genetic analysis of surveillance biopsy samples from Barrett's mucosa--significance of sampling. Pathol Res Pract; 2008;204(5):285-94
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  • [Title] Molecular genetic analysis of surveillance biopsy samples from Barrett's mucosa--significance of sampling.
  • Our aim was to determine the spectrum and accumulation of mutations in surveillance biopsies from Barrett's mucosa of individual patients during follow-up.
  • We performed loss of heterozygosity (LOH) analysis of six recently described tumor suppressor genes relevant for the carcinogenesis of Barrett's adenocarcinoma from laser-microdissected, paraffin-embedded biopsy samples of Barrett's mucosa without or with low-grade dysplastic change.
  • In two patients, Barrett's adenocarcinoma was diagnosed 6 months after the first diagnosis of Barrett's mucosa.
  • From our microsatellite marker panel, we were not able to define a single surrogate marker that could serve as a potential biomarker, indicating an increased risk of progression to Barrett's adenocarcinoma.
  • Our results raise important questions regarding the biological dynamics of mutations in Barrett's mucosa in addition to the influence of sampling, especially with regard to the number of biopsies taken from Barrett's mucosa.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Esophagus / pathology. Genes, Tumor Suppressor. Mutation. Precancerous Conditions / genetics

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  • (PMID = 18337019.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Germany
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49. 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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50. Kinoshita Y, Yuki T: [Medical treatment of Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1449-53
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  • [Title] [Medical treatment of Barrett's esophagus].
  • In patients with Barrett's esophagus, medical treatment is necessary for the control of reflux symptom, healing of accompanying erosive esophagitis, and prevention of carcinogenesis.
  • The values of PPI and aspirin/NSAIDs for the prevention of Barrett's carcinoma are still under investigation all over the world.
  • Since many groups are actively working to find the appropriate methods for preventing carcinogenesis on the Barrett's esophagus, we will have an evidence-based strategy for the prevention of Barrett's adenocarcinoma in near future.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Barrett Esophagus / drug therapy. Cyclooxygenase Inhibitors / therapeutic use. Enzyme Inhibitors / therapeutic use
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Animals. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Drug Therapy, Combination. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / drug therapy. Humans. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / physiology. Proton Pump Inhibitors

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  • (PMID = 16101238.001).
  • [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 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Proton Pump Inhibitors; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; R16CO5Y76E / Aspirin
  • [Number-of-references] 24
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51. Al-Taie OH, Graf T, Illert B, Katzenberger T, Mörk H, Kraus MR, Barthelmes HU, Scheurlen M, Seufert J: Differential effects of PPARgamma activation by the oral antidiabetic agent pioglitazone in Barrett's carcinoma in vitro and in vivo. J Gastroenterol; 2009;44(9):919-29
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  • [Title] Differential effects of PPARgamma activation by the oral antidiabetic agent pioglitazone in Barrett's carcinoma in vitro and in vivo.
  • We investigated the biological effects of PPARgamma activation by the oral antidiabetic agent pioglitazone in Barrett's adenocarcinoma cells in vitro and in vivo.
  • RESULTS: PPARgamma mRNA and protein were overexpressed in endoscopic biopsies of Barrett's epithelium and the human Barrett's adenocarcinoma cancer cell line OE33 as compared to normal esophagus and stomach and the esophageal squamous epithelium cancer cell line Kyse-180.
  • Effects of systemic PPARgamma activation by the thiazolidinedione pioglitazone on tumor cell proliferation and apoptosis were then assessed in vivo in nude mice bearing transplantable Barrett's adenocarcinomas derived from OE33 cells.
  • CONCLUSION: These results indicate that PPARgamma is involved in the molecular pathogenesis of Barrett's adenocarcinoma formation and growth.
  • However, activation of PPARgamma exerts differential effects on growth of Barrett's adenocarcinoma cells in vitro and in vivo emphasizing the importance of additional cell context specific factors and systemic metabolic status for the modulation of PPARgamma action in vivo.
  • [MeSH-major] Barrett Esophagus / drug therapy. Esophageal Neoplasms / drug therapy. PPAR gamma / drug effects. Thiazolidinediones / pharmacology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Hypoglycemic Agents / pharmacology. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. RNA, Messenger

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  • (PMID = 19506796.001).
  • [ISSN] 1435-5922
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Thiazolidinediones; X4OV71U42S / pioglitazone
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52. Beales IL, Ogunwobi O, Cameron E, El-Amin K, Mutungi G, Wilkinson M: Activation of Akt is increased in the dysplasia-carcinoma sequence in Barrett's oesophagus and contributes to increased proliferation and inhibition of apoptosis: a histopathological and functional study. BMC Cancer; 2007;7:97
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  • [Title] Activation of Akt is increased in the dysplasia-carcinoma sequence in Barrett's oesophagus and contributes to increased proliferation and inhibition of apoptosis: a histopathological and functional study.
  • BACKGROUND: The incidence of oesophageal adenocarcinoma is increasing rapidly in the developed world.
  • Therefore we have examined the activation of Akt in Barrett's oesophagus and oesophageal adenocarcinoma and the functional effects of Akt activation in vitro.
  • The functional effects of Akt were examined using Barrett's adenocarcinoma cells in culture.
  • RESULTS: In normal squamous oesophagus, erosive oesophagitis and non-dysplastic Barrett's oesophagus, phospho-Akt was limited to the basal 1/3 of the mucosa.
  • Image analysis confirmed that Akt activation was significantly increased in non-dysplastic Barrett's oesophagus compared to squamous epithelium and further significantly increased in high-grade dysplasia and adenocarcinoma.
  • In all cases of high grade dysplasia and adenocarcinoma Akt was activated in the luminal 1/3 of the epithelium.
  • CONCLUSION: Akt is abnormally activated in Barrett's oesophagus, high grade dysplasia and adenocarcinoma.
  • Akt activation promotes proliferation and inhibits apoptosis in Barrett's adenocarcinoma cells and both transient acid exposure and leptin stimulate Akt phosphorylation.
  • Activation of Akt in obesity and by reflux of gastric acid may be important in the pathogenesis of Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Cell Transformation, Neoplastic / metabolism. Enzyme Activation / physiology. Esophageal Neoplasms / enzymology. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 17559672.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC1899509
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53. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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54. Scheil-Bertram S, Lorenz D, Ell C, Sheremet E, Fisseler-Eckhoff A: Expression of alpha-methylacyl coenzyme A racemase in the dysplasia carcinoma sequence associated with Barrett's esophagus. Mod Pathol; 2008 Aug;21(8):961-7
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  • [Title] Expression of alpha-methylacyl coenzyme A racemase in the dysplasia carcinoma sequence associated with Barrett's esophagus.
  • Two different studies demonstrated alpha-methylacyl coenzyme A racemase (AMACR) to be a highly specific marker in Barrett's neoplastic lesions.
  • We present a retrospective study of early Barrett's adenocarcinoma treated with surgery (2000-2005, n=29; M:F=5:1, median age 67 years).
  • Barrett's epithelium that was negative for dysplasia and columnar epithelial cell changes indefinite for dysplasia (n=30) did not demonstrate AMACR immunoreactivity.
  • AMACR immunoreactivity was demonstrated in 27% (8/30) of cases of Barrett's epithelium with columnar epithelial cell changes indefinite for dysplasia.
  • Altogether 91% of cases with low-grade dysplasia were AMACR-positive and 96% of cases with high-grade dysplasia and early Barrett's adenocarcinoma were positive for AMACR.
  • In summary, the sensitivity of AMACR expression in low-grade dysplasia and subsequent early Barrett's adenocarcinoma was significantly higher in our study compared with previous data.
  • This might be a new diagnostic marker for dysplasia carcinoma sequence in Barrett's low-grade neoplastic lesions.
  • [MeSH-major] Adenocarcinoma / enzymology. Barrett Esophagus / enzymology. Esophageal Neoplasms / enzymology. Precancerous Conditions / enzymology. Racemases and Epimerases / metabolism

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  • (PMID = 18500268.001).
  • [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] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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55. Nguyen NT, Chang K, Nahidi T, Wilson SE, Luketich JD: Esophagectomy for Barrett's esophagus: indications, techniques, and outcome. Curr Treat Options Gastroenterol; 2006 Feb;9(1):85-92
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  • [Title] Esophagectomy for Barrett's esophagus: indications, techniques, and outcome.
  • Barrett's esophagus describes metaplastic changes from squamous mucosa to specialized columnar epithelium that can progress from low-grade dysplasia to high-grade dysplasia and even invasive carcinoma.
  • The treatment of Barrett's esophagus with low-grade dysplasia or Barrett's adenocarcinoma is relatively standardized; however, controversy remains regarding appropriate therapy for Barrett's esophagus with high-grade dysplasia.
  • In these patients, surgery is indicated, as esophagectomy can be curative for early stage adenocarcinoma in Barrett's esophagus.
  • In experienced centers, minimally invasive esophagectomy is now an attractive alternative for the treatment of Barrett's esophagus with high-grade dysplasia.

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  • (PMID = 16423317.001).
  • [ISSN] 1092-8472
  • [Journal-full-title] Current treatment options in gastroenterology
  • [ISO-abbreviation] Curr Treat Options Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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56. 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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57. Zaninotto G, Minnei F, Guirroli E, Ceolin M, Battaglia G, Bellumat A, Betetto G, Bozzola L, Cassaro M, Cataudella G, Dal Bò N, Farinati F, Florea G, Furlanetto A, Galliani E, Germanà B, Guerini A, Macrì E, Marcon V, Mastropaolo G, Meggio A, Miori G, Morelli L, Murer B, Norberto L, Togni R, Valiante F, Rugge M: The Veneto Region's Barrett's Oesophagus Registry: aims, methods, preliminary results. Dig Liver Dis; 2007 Jan;39(1):18-25

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  • [Title] The Veneto Region's Barrett's Oesophagus Registry: aims, methods, preliminary results.
  • BACKGROUND: The natural history of Barrett's Oeosphagus is not completely clarified and Barrett's Oeosphagus Registries are considered useful tools to expand our knowledge on this disease.
  • A Barrett's Oeosphagus Registry has been therefore established in the Veneto Region and neighbouring provinces.
  • AIMS: The aims of the Registry are to assess the demographical, endoscopical and histological characteristics of Barrett's Oeosphagus patients; the prevalence of non-invasive neoplasia and Barrett's Adenocarcinoma and the timing and incidence of Barrett's Oeosphagus progression to malignancy.
  • METHODS: An interdisciplinary committee of endoscopists, pathologists and information technology experts was established in 2004 to design a website-based Barrett's Oesophagus Registry for the Veneto Region and neighbouring north-eastern Italian provinces.
  • RESULTS: In the first 18 months, 397 patients with endoscopically visible and histologically proven Barrett's Oeosphagus were enrolled in the Registry; the median age of these patients was 66 years (male:female=3:1).
  • Most patients (75%) had a Short Segment of Barrett's Oesophagus (<or=3 cm) and only 1 in 4 had a Long Segment of Barrett's Oesophagus (>3 cm).
  • Long Segment of Barrett's Oesophagus patients were 5 years older than the Short Segment of Barrett's Oesophagus patients (p<0.05), suggesting a progression from Short Segment of Barrett's Oesophagus to Long Segment of Barrett's Oesophagus.
  • Though no data are available on the incidence of non-invasive neoplasia or Barrett's Adenocarcinoma (i.e., progression to cancer at least 12 months after enrolment), the prevalence of neoplastic lesions (found within 12 months of enrolment) was 5% for Short Segment of Barrett's Oesophagus and 19% for Long Segment of Barrett's Oesophagus, indicating that a careful multiple-biopsy endoscopic protocol is needed, especially when Long Segment of Barrett's Oesophagus are suspected at endoscopy.
  • The prevalence of Barrett's Adenocarcinoma among patients with non-invasive neoplasia was 1/17 cases of low-grade non-invasive neoplasia and 2/3 cases of high-grade non-invasive neoplasia, indicating that these patients require strict endoscopic and bioptic follow-up.
  • CONCLUSION: A regional Barrett's Oeosphagus Registry is feasible at a relatively low cost and enables significant data to be collected in a relatively short time.
  • [MeSH-major] Barrett Esophagus. Esophagoscopy. Precancerous Conditions / diagnosis. Prevalence. Registries

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  • (PMID = 17141593.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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58. Gough MD, Ackroyd R, Majeed AW, Bird NC: Prediction of malignant potential in reflux disease: are cytokine polymorphisms important? Am J Gastroenterol; 2005 May;100(5):1012-8
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  • OBJECTIVES: Esophageal reflux is common in the Western world and can lead to a number of diseases, such as esophagitis, Barrett's esophagus, and adenocarcinoma.
  • Barrett's predisposes to adenocarcinoma and endoscopic surveillance may lead to earlier detection of adenocarcinoma.
  • However, clinical methods only identify one patient in 15 with Barrett's esophagus.
  • The aim of this study was to find factors that may help identify patients with Barrett's earlier.
  • METHODS: Blood samples and detailed histories were taken from 456 patients with gastroesophageal reflux who were recruited into three study groups: esophagitis, Barrett's esophagus without dysplasia, and Barrett's with dysplasia or adenocarcinoma.
  • RESULTS: IL-1 Ra +2018 genotype 2/2 was associated with Barrett's more commonly than esophagitis (OR-3.7, p= 0.0345).
  • The IL-10 +1082 genotype 2/2 was more strongly associated with Barrett's and adenocarcinoma than esophagitis (OR-1.76, p= 0.056 and OR 1.96, p= 0.025, respectively).
  • CONCLUSIONS: Cytokine polymorphisms are more commonly found in patients with Barrett's or adenocarcinoma than those with esophagitis.
  • Together with demographic data, this may help identify those patients with Barrett's who would benefit from surveillance.
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / immunology. Adult. Aged. Aged, 80 and over. Barrett Esophagus / etiology. Barrett Esophagus / immunology. Esophagitis, Peptic / etiology. Esophagitis, Peptic / immunology. Female. Forecasting. Genotype. Humans. Interleukin-1 / genetics. Interleukin-10 / genetics. Male. Middle Aged. Polymerase Chain Reaction. Receptors, Interleukin-1 / antagonists & inhibitors. Receptors, Interleukin-4 / genetics

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  • [CommentIn] Am J Gastroenterol. 2005 May;100(5):1019-20 [15842573.001]
  • (PMID = 15842572.001).
  • [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 / Interleukin-1; 0 / Interleukins; 0 / Receptors, Interleukin-1; 0 / Receptors, Interleukin-4; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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59. Singh R, Ragunath K, Jankowski J: Barrett's Esophagus: Diagnosis, Screening, Surveillance, and Controversies. Gut Liver; 2007 Dec;1(2):93-100

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Barrett's Esophagus: Diagnosis, Screening, Surveillance, and Controversies.
  • Barrett's esophagus (BE) is a frequent complication of gastroesophageal reflux disease, an acquired condition resulting from persistent mucosal injury to the esophagus.
  • The incidence of Barrett's metaplasia and Barrett's adenocarcinoma has been increasing, but the prognosis of Barrett's adenocarcinoma is worse because individuals present at a late stage.
  • Whether adequate control of gastroesophageal reflux early in the disease alters the natural history of Barrett's change once it has developed remains unanswered.

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  • (PMID = 20485625.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2871632
  • [Keywords] NOTNLM ; Barrett's esophagus / Gastroesophageal reflux
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60. Pühringer-Oppermann FA, Stein HJ, Sarbia M: Lack of EGFR gene mutations in exons 19 and 21 in esophageal (Barrett's) adenocarcinomas. Dis Esophagus; 2007;20(1):9-11
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  • [Title] Lack of EGFR gene mutations in exons 19 and 21 in esophageal (Barrett's) adenocarcinomas.
  • We analyzed exons 19 and 21 coding for the receptor tyrosine kinase of the epidermal growth factor gene in 105 samples of esophageal (Barrett's) adenocarcinoma by denaturing high-pressure liquid chromatography.
  • In conclusion, mutations within the tyrosine kinase domain of EGFR associated with sensitivity of non-small cell lung cancer patients to gefitinib are not present in esophageal (Barrett's) adenocarcinoma.

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  • (PMID = 17227303.001).
  • [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 / Antineoplastic Agents; 0 / Codon; 0 / Quinazolines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
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61. 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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62. 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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63. 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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64. 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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  • [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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65. 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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66. 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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  • [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


67. 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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68. 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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  • [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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69. 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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70. Srivastava A, Hornick JL, Li X, Blount PL, Sanchez CA, Cowan DS, Ayub K, Maley CC, Reid BJ, Odze RD: Extent of low-grade dysplasia is a risk factor for the development of esophageal adenocarcinoma in Barrett's esophagus. Am J Gastroenterol; 2007 Mar;102(3):483-93; quiz 694
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  • [Title] Extent of low-grade dysplasia is a risk factor for the development of esophageal adenocarcinoma in Barrett's esophagus.
  • OBJECTIVES: Previous studies that evaluated extent of high-grade dysplasia (HGD) as a risk factor for esophageal adenocarcinoma (EA) in Barrett's esophagus (BE) were conflicting, and no prior study has evaluated extent of low-grade dysplasia (LGD) as a risk factor.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / complications. Esophageal Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Disease Progression. Endoscopy, Gastrointestinal. Female. Follow-Up Studies. Humans. Intestinal Mucosa / pathology. Male. Middle Aged. Prognosis. Retrospective Studies. Risk Factors. Time Factors

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  • [CommentIn] Am J Gastroenterol. 2007 Sep;102(9):2111-2 [17727447.001]
  • [CommentIn] Am J Gastroenterol. 2007 Mar;102(3):494-6 [17335444.001]
  • [CommentIn] Am J Gastroenterol. 2007 Sep;102(9):2112-3 [17727448.001]
  • (PMID = 17338734.001).
  • [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 / P01 CA91955; United States / NCI NIH HHS / CA / R01 CA61202
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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71. 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
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] 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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72. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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73. Kuester D, El-Rifai W, Peng D, Ruemmele P, Kroeckel I, Peters B, Moskaluk CA, Stolte M, Mönkemüller K, Meyer F, Schulz HU, Hartmann A, Roessner A, Schneider-Stock R: Silencing of MGMT expression by promoter hypermethylation in the metaplasia-dysplasia-carcinoma sequence of Barrett's esophagus. Cancer Lett; 2009 Mar 08;275(1):117-26
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  • [Title] Silencing of MGMT expression by promoter hypermethylation in the metaplasia-dysplasia-carcinoma sequence of Barrett's esophagus.
  • To determine the relevance of MGMT in Barrett's carcinogenesis, we analyzed promotor hypermethylation and expression of MGMT in Barrett's adenocarcinomas and its paired precursor lesions from 133 patients using a methylation-specific PCR, real-time RT-PCR and immunohistochemistry.
  • Hypermethylation was detected in 78.9% of esophageal adenocarcinomas, in 100% of Barrett's intraepithelial neoplasia, in 88.9% of Barrett's metaplasia, but only in 21.4% of normal esophageal mucosa samples (P<0.001) and correlated significantly with downregulation of MGMT transcripts (P=0.048) and protein expression (P=0.02).
  • We conclude, that aberrant promoter methylation of MGMT is a frequent and early event during tumorigenesis of Barrett's esophagus.
  • High prevalence of MGMT hypermethylation may represent a candidate marker for improved diagnosis and targeted therapy in Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Carcinoma / metabolism. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Gene Silencing. Metaplasia / metabolism. Tumor Suppressor Proteins / genetics

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  • (PMID = 19027227.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK067629; United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / R01CA106176
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ NIHMS576423; NLM/ PMC4028828
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74. Dunn JM, Mackenzie GD, Oukrif D, Mosse CA, Banks MR, Thorpe S, Sasieni P, Bown SG, Novelli MR, Rabinovitch PS, Lovat LB: Image cytometry accurately detects DNA ploidy abnormalities and predicts late relapse to high-grade dysplasia and adenocarcinoma in Barrett's oesophagus following photodynamic therapy. Br J Cancer; 2010 May 25;102(11):1608-17
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  • [Title] Image cytometry accurately detects DNA ploidy abnormalities and predicts late relapse to high-grade dysplasia and adenocarcinoma in Barrett's oesophagus following photodynamic therapy.
  • BACKGROUND AND AIMS: DNA ploidy abnormalities (aneuploidy/tetraploidy) measured by flow cytometry (FC) are strong predictors of future cancer development in untreated Barrett's oesophagus, independent of histology grade.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Barrett Esophagus / drug therapy. Chromosome Aberrations. Esophagus / pathology. Image Cytometry. Photochemotherapy

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  • (PMID = 20461081.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / CRUK/ A9022
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  • [Other-IDs] NLM/ PMC2883155
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75. Brankley SM, Wang KK, Harwood AR, Miller DV, Legator MS, Lutzke LS, Kipp BR, Morrison LE, Halling KC: The development of a fluorescence in situ hybridization assay for the detection of dysplasia and adenocarcinoma in Barrett's esophagus. J Mol Diagn; 2006 May;8(2):260-7
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] The development of a fluorescence in situ hybridization assay for the detection of dysplasia and adenocarcinoma in Barrett's esophagus.
  • The goal of this study was to identify a set of fluorescence in situ hybridization probes for the detection of dysplasia and adenocarcinoma in patients with Barrett's esophagus.
  • We examined 170 brushing specimens from 138 patients with Barrett's esophagus or a history of Barrett's esophagus using fluorescence in situ hybridization with probes to 5p15, 5q21-22, centromere 7, 7p12, 8q24.12-13, centromere 9, 9p21, centromere 17, 17p13.1, 17q11.2-12, 20q13.2, and centromere Y.
  • Receiver-operator curves were used to determine the sensitivity and specificity of various four-probe combinations for detecting low-grade dysplasia, high-grade dysplasia, and esophageal adenocarcinoma.
  • Of these, a set consisting of probes to 8q24, 9p21, 17q11.2, and 20q13.2 was found to have a sensitivity and specificity, respectively, of 70% and 89% for low-grade dysplasia, 84% and 93% for high-grade dysplasia, and 94% and 93% for esophageal adenocarcinoma.
  • This probe set was chosen for future prospective clinical evaluations based on its high sensitivity and specificity, its ability to distinguish adenocarcinoma and high-grade or low-grade dysplasia from lesser diagnostic categories, and the favorable signal quality for each of the probes.

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  • (PMID = 16645214.001).
  • [ISSN] 1525-1578
  • [Journal-full-title] The Journal of molecular diagnostics : JMD
  • [ISO-abbreviation] J Mol Diagn
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097048; United States / NCI NIH HHS / CA / R0 1 CA97048-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1867582
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76. Koike T, Ohara S, Inomata Y, Abe Y, Iijima K, Shimosegawa T: The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with gastroesophageal junction adenocarcinoma in Japan. Inflammopharmacology; 2007 Apr;15(2):61-4
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for gastroesophageal junction adenocarcinoma .

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  • [Title] The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with gastroesophageal junction adenocarcinoma in Japan.
  • We have previously reported that H. 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.
  • However, the relationship between H. pylori infection, gastric acid secretion and GE junction adenocarcinoma had not yet been investigated in Japan.
  • We demonstrated that the status of gastric acid secretion was higher in patients with GE junction adenocarcinoma than in patients with early gastric cancer (EGC), and that the level was the same in patients with RE and those with BE.
  • We also found that the prevalence of H. pylori infection in patients with GE junction adenocarcinoma was significantly lower than that in patients with EGC, although not as low as that in patients with RE and BE, suggesting that preservation of gastric acid secretion may be important for the development of GE junction adenocarcinoma in Japanese people, regardless of the presence of H. pylori infection.
  • [MeSH-major] Adenocarcinoma / complications. Helicobacter Infections / complications. Helicobacter pylori. Stomach Neoplasms / complications

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  • (PMID = 17450443.001).
  • [ISSN] 0925-4692
  • [Journal-full-title] Inflammopharmacology
  • [ISO-abbreviation] Inflammopharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 42
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77. Babar M, Ennis D, Abdel-Latif M, Byrne PJ, Ravi N, Reynolds JV: Differential molecular changes in patients with asymptomatic long-segment Barrett's esophagus treated by antireflux surgery or medical therapy. Am J Surg; 2010 Feb;199(2):137-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential molecular changes in patients with asymptomatic long-segment Barrett's esophagus treated by antireflux surgery or medical therapy.
  • BACKGROUND: The Barrett's to adenocarcinoma sequence is characterized by molecular changes including activation of nuclear factor-kappaB (NF-kappaB) and related cytokines.
  • METHODS: Asymptomatic patients with long-segment Barrett's esophagus had endoscopic biopsy specimens taken from 2 cm below the squamocolumnar junction for measurement of activated NF-kappaB and a panel of cytokines and growth factors.
  • There were no differences in the length of Barrett's segment and endoscopic and histopathologic features in both groups.
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / drug therapy. Barrett Esophagus / surgery. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / prevention & control. Fundoplication. Gastroesophageal Reflux / drug therapy. Gastroesophageal Reflux / surgery. NF-kappa B / metabolism. Proton Pump Inhibitors / therapeutic use

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19306979.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [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 / Cytokines; 0 / NF-kappa B; 0 / Proton Pump Inhibitors
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78. Yu C, Zhang X, Huang Q, Klein M, Goyal RK: High-fidelity DNA histograms in neoplastic progression in Barrett's esophagus. Lab Invest; 2007 May;87(5):466-72
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] High-fidelity DNA histograms in neoplastic progression in Barrett's esophagus.
  • This study describes the high-fidelity DNA histograms in different stages of neoplastic progression to Barrett's adenocarcinoma (BAC).
  • One hundred and eighty-seven cases, including 34 normal gastrointestinal mucosa (control), 66 Barrett's-specialized intestinal metaplasia (SIM), 22 low-grade dysplasia (LGD), 22 high-grade dysplasia (HGD) and 43 BAC were investigated.
  • The high-fidelity DNA histograms suggest that (1) Barrett's SIM may already be dysplastic in nature, and all BAC may be markedly aneuploid; and (2) elevated cellular DNA heterogeneity and 5N fractions may be markers of progressive chromosomal changes and 'unstable aneuploidy' that identifies progressive lesions.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. DNA, Neoplasm / analysis. Esophageal Neoplasms / genetics. Ploidies. Precancerous Conditions / genetics
  • [MeSH-minor] Chromosomal Instability. Disease Progression. Gastric Mucosa. Humans. Image Cytometry

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  • (PMID = 17310216.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK62867
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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79. Nomura T, Yamashita K, Miyashita M, Tajiri T: [Argon plasma coagulation in Barrett's esophagus]. Nihon Rinsho; 2005 Aug;63(8):1458-62
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  • [Title] [Argon plasma coagulation in Barrett's esophagus].
  • Recently, it has been reported that Barrett's esophagus and Barrett's adenocarcinoma in situ could be successfully managed by APC.
  • The aims of this treatment are to prevent the developing of adenocarcinoma and to promote the restitution of normal squamous epithelium.
  • Shorter length of Barrett's epithelium and normalization in pH with PPI treatment were the independent predictors of sustained long-term restitution of squamous epithelium.
  • In patient with Barrett's esophagus, APC offers an effective, minimally invasive alternative to other treatments previously performed.
  • [MeSH-major] Argon / therapeutic use. Barrett Esophagus / surgery. Electrocoagulation / methods
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Combined Modality Therapy. Enzyme Inhibitors / therapeutic use. Esophageal Neoplasms / etiology. Esophageal Neoplasms / prevention & control. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / surgery. Humans. Proton Pump Inhibitors

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  • (PMID = 16101240.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Proton Pump Inhibitors; 67XQY1V3KH / Argon
  • [Number-of-references] 15
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80. 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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81. Ling FC, Khochfar J, Baldus SE, Brabender J, Drebber U, Bollschweiler E, Hoelscher AH, Schneider PM: HIF-1alpha protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasia. Dis Esophagus; 2009;22(8):694-9

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  • [Title] HIF-1alpha protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasia.
  • We examined the protein expression of HIF-1alpha within the progression of Barrett's sequence as well as the type and degree of the environmental inflammatory reaction.
  • Squamous epithelium (SE), metaplastic, low- and high-grade dysplastic lesions, and tumor tissue of 57 resection specimens from patients with Barrett's adenocarcinoma were immunohistochemically analyzed.
  • HIF-1alpha protein expression increased significantly from SE to Barrett's metaplasia (BM) (P < 0.0001).

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  • (PMID = 19302222.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
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82. Delgado JS, Mustafi R, Yee J, Cerda S, Chumsangsri A, Dougherty U, Lichtenstein L, Fichera A, Bissonnette M: Sorafenib triggers antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells. Dig Dis Sci; 2008 Dec;53(12):3055-64
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  • [Title] Sorafenib triggers antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells.
  • BACKGROUND AND PURPOSE: Current therapies offer scant benefit to patients with advanced esophageal adenocarcinoma.
  • We investigated the effects of Sorafenib, a multifunctional kinase inhibitor, on several growth regulatory pathways that control cell growth and survival in SEG-1 cells derived from Barrett's adenocarcinoma.
  • CONCLUSIONS: These results support a rational basis for future clinical studies to assess the therapeutic benefit of Sorafenib in esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Benzenesulfonates / pharmacology. Cell Proliferation / drug effects. Esophageal Neoplasms / pathology. Pyridines / pharmacology

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  • (PMID = 18512153.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA036745; United States / NIDDK NIH HHS / DK / P30DK42086
  • [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 / Benzenesulfonates; 0 / Cyclin E; 0 / MYC protein, human; 0 / Phenylurea Compounds; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Pyridines; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 136601-57-5 / Cyclin D1; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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83. Williams LJ, Guernsey DL, Casson AG: Biomarkers in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma. Curr Oncol; 2006 Feb;13(1):33-43
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  • [Title] Biomarkers in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma.
  • 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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84. Sud D, Zhong W, Beer DG, Mycek MA: Time-resolved optical imaging provides a molecular snapshot of altered metabolic function in living human cancer cell models. Opt Express; 2006 May 15;14(10):4412-26
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  • A fluorescence lifetime imaging microscopy (FLIM) method was developed and applied to investigate metabolic function in living human normal esophageal (HET-1) and Barrett's adenocarcinoma (SEG-1) cells.

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  • (PMID = 19516593.001).
  • [ISSN] 1094-4087
  • [Journal-full-title] Optics express
  • [ISO-abbreviation] Opt Express
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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85. Möbius C, Stein HJ, Spiess C, Becker I, Feith M, Theisen J, Gais P, Jütting U, Siewert JR: COX2 expression, angiogenesis, proliferation and survival in Barrett's cancer. Eur J Surg Oncol; 2005 Sep;31(7):755-9
MedlinePlus Health Information. consumer health - Esophageal Cancer.

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  • [Title] COX2 expression, angiogenesis, proliferation and survival in Barrett's cancer.
  • OBJECTIVES: To examine COX2 expression and its relation to angiogenesis, Ki67 and Bcl2 expression in Barrett's cancer.
  • METHODS: Specimens from 48 R0-resected Barrett's adenocarcinoma were immunostained for cyclooxygenase 2 (COX2), CD 31 and alpha-sm actin to discriminate between mature and immature vessels, Mib-1 and Bcl2.
  • CONCLUSIONS: Elevated COX2 expression is associated with lymph-node metastases and reduced survival in Barrett's cancer.
  • [MeSH-major] Barrett Esophagus / genetics. Barrett Esophagus / physiopathology. Esophageal Neoplasms / genetics. Esophageal Neoplasms / physiopathology. Gene Expression Profiling. Neovascularization, Pathologic. Prostaglandin-Endoperoxide Synthases / biosynthesis

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  • (PMID = 15979837.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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86. 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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87. Wang VS, Hornick JL, Sepulveda JA, Mauer R, Poneros JM: Low prevalence of submucosal invasive carcinoma at esophagectomy for high-grade dysplasia or intramucosal adenocarcinoma in Barrett's esophagus: a 20-year experience. Gastrointest Endosc; 2009 Apr;69(4):777-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low prevalence of submucosal invasive carcinoma at esophagectomy for high-grade dysplasia or intramucosal adenocarcinoma in Barrett's esophagus: a 20-year experience.
  • BACKGROUND: The rate of occult adenocarcinoma at esophagectomy in patients with Barrett's esophagus (BE) and high-grade dysplasia (HGD) has been reported to be approximately 40%.
  • OBJECTIVE: Our purpose was to determine the rate of submucosal invasive adenocarcinoma in patients undergoing esophagectomy for BE after biopsy diagnosis of HGD or intramucosal carcinoma (IMC).
  • A secondary aim was to identify clinical risk factors for submucosal invasive adenocarcinoma in these patients.
  • MAIN OUTCOME MEASUREMENTS: Submucosal invasive adenocarcinoma at esophagectomy.
  • All 4 patients with submucosal invasion at esophagectomy had either nodular or ulcerated mucosa on preoperative endoscopy.
  • CONCLUSIONS: The rate of submucosal invasive adenocarcinoma at esophagectomy in BE patients with HGD or IMC on biopsy is much lower than 40%.
  • [MeSH-major] Adenocarcinoma / epidemiology. Adenocarcinoma / pathology. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / pathology. Esophagectomy

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  • [CommentIn] Gastrointest Endosc. 2010 Feb;71(2):429 [20152322.001]
  • (PMID = 19136106.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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88. Pech O, Günter E, Dusemund F, Origer J, Lorenz D, Ell C: Accuracy of endoscopic ultrasound in preoperative staging of esophageal cancer: results from a referral center for early esophageal cancer. Endoscopy; 2010 Jun;42(6):456-61
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  • RESULTS: 179 consecutive patients (mean age 64.4 +/- 9.5 years; 142 men) underwent esophageal resection for Barrett's adenocarcinoma (n = 134) and squamous cell cancer (n = 45).
  • [MeSH-major] Adenocarcinoma / ultrasonography. Barrett Esophagus / ultrasonography. Carcinoma, Squamous Cell / ultrasonography. Endosonography. Esophageal Neoplasms / ultrasonography

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  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • (PMID = 20306385.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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89. Pech O, Behrens A, May A, Nachbar L, Gossner L, Rabenstein T, Manner H, Guenter E, Huijsmans J, Vieth M, Stolte M, Ell C: Long-term results and risk factor analysis for recurrence after curative endoscopic therapy in 349 patients with high-grade intraepithelial neoplasia and mucosal adenocarcinoma in Barrett's oesophagus. Gut; 2008 Sep;57(9):1200-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results and risk factor analysis for recurrence after curative endoscopic therapy in 349 patients with high-grade intraepithelial neoplasia and mucosal adenocarcinoma in Barrett's oesophagus.
  • OBJECTIVE: Endoscopic therapy is increasingly being used in the treatment of high-grade intraepithelial neoplasia (HGIN) and mucosal adenocarcinoma (BC) in patients with Barrett's oesophagus.
  • PATIENTS: Between October 1996 and September 2002, 61 patients with HGIN and 288 with BC were included (173 with short-segment and 176 with long-segment Barrett's oesophagus) from a total of 486 patients presenting with Barrett's neoplasia.
  • The risk factors most frequently associated with recurrence were piecemeal resection, long-segment Barrett's oesophagus, no ablative therapy of Barrett's oesophagus after CR, time until CR achieved >10 months and multifocal neoplasia.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Carcinoma in Situ / surgery. Esophageal Neoplasms / surgery. Precancerous Conditions / surgery

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  • [CommentIn] Endoscopy. 2010 Jan;42(1):42-5 [19967633.001]
  • (PMID = 18460553.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
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90. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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91. 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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92. Barritt AS 4th, Shaheen NJ: Should patients with Barrett's oesophagus be kept under surveillance? The case against. Best Pract Res Clin Gastroenterol; 2008;22(4):741-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Should patients with Barrett's oesophagus be kept under surveillance? The case against.
  • Barrett's oesophagus, or columnar metaplasia of the oesophagus, is a known risk factor for adenocarcinoma of the oesophagus.
  • Barrett's oesophagus is thought to be the result of longstanding gastro-oesophageal reflux disease, a very common diagnosis in the United States and other western countries.
  • Because Barrett's oesophagus is a transition state between a common complaint and a devastating illness, endoscopic screening and surveillance strategies are commonly employed.
  • However, neither screening nor surveillance strategies have been proven to reduce mortality from oesophageal adenocarcinoma.
  • We address the multifaceted case against surveillance for oesophageal adenocarcinoma.
  • The overall incidence of oesophageal adenocarcinoma is very low, especially compared to other cancers where surveillance is used.
  • The pace of progression from Barrett's to adenocarcinoma is not known.
  • There are drawbacks to endoscopic surveillance for dysplasia and adenocarcinoma in patients with established Barrett's oesophagus that include sampling error, inconsistent pathologic interpretation of biopsies, and cost.
  • Taken individually or together, these limitations make a strong case against surveillance endoscopy in Barrett's oesophagus.
  • [MeSH-major] Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal / contraindications. Mass Screening / methods. Population Surveillance / methods

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  • [CommentOn] Best Pract Res Clin Gastroenterol. 2008;22(4):721-39 [18656826.001]
  • (PMID = 18656827.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 29
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93. Ling FC, Baldus SE, Khochfar J, Xi H, Neiss S, Brabender J, Metzger R, Drebber U, Dienes HP, Bollschweiler E, Hoelscher AH, Schneider PM: Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer. Histopathology; 2007 Jan;50(2):203-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer.
  • AIMS: Risk reduction for Barrett's cancer in individuals taking non-steroidal anti-inflammatory drugs has been reported.
  • Cyclooxygenase (COX)-2, one of the inhibited enzymes, is putatively involved in Barrett's cancer pathogenesis.
  • The aim of this study was to examine a possible association between COX-2 protein expression and the development and progression of the Barrett's metaplasia-dysplasia-carcinoma sequence and the type and degree of associated inflammatory reaction.
  • METHODS AND RESULTS: Squamous epithelium, metaplastic, low-grade, high-grade dysplastic lesions and tumour tissue of 49 resection specimens from patients with Barrett's adenocarcinoma were immunohistochemically analysed.
  • Within the Barrett's sequence, a significant progressive increase in COX-2 expression was identified (P < 0.0001).
  • The most significant differences were detected between squamous epithelium and Barrett's metaplasia (P < 0.001) and from low- to high-grade dysplasia (P < 0.0001).
  • Active and chronic inflammation were significantly different between squamous epithelium and Barrett's metaplasia (P < 0.0001), but not during further progression in the sequence.
  • CONCLUSIONS: Increasing COX-2 expression in Barrett's metaplasia is significantly associated with a change in the local inflammatory reaction, but not during further progression through dysplasia to cancer.
  • This supports the potential of a chemoprevention strategy using COX-2 inhibitors independent of the extent and type of the inflammatory reaction in Barrett's oesophagus.
  • [MeSH-major] Barrett Esophagus / enzymology. Cyclooxygenase 2 / genetics. Esophageal Neoplasms / enzymology. Inflammation / enzymology. Membrane Proteins / genetics

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  • [ErratumIn] Histopathology. 2007 Mar;50(4):531
  • (PMID = 17222248.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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94. Parenti A, Leo G, Porzionato A, Zaninotto G, Rosato A, Ninfo V: Expression of survivin, p53, and caspase 3 in Barrett's esophagus carcinogenesis. Hum Pathol; 2006 Jan;37(1):16-22
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  • [Title] Expression of survivin, p53, and caspase 3 in Barrett's esophagus carcinogenesis.
  • The regulation of apoptosis, as a distinctive form of programmed cell death, in multistep Barrett's esophagus (BE) carcinogenesis is poorly understood.
  • Immunohistochemical expression was tested in 40 cases of BE, including 11 low-grade and 19 high-grade dysplasias (HGD), and samples were obtained from 40 surgical specimens of esophagectomy performed for HGD or Barrett's adenocarcinoma.
  • Cytoplasmic survivin location may indicate an initial antiapoptotic, more than proliferative, role in the early phases of Barrett carcinogenesis.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Caspases / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16360411.001).
  • [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] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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95. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


96. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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97. 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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  • [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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98. Abdel-Latif MM, Windle H, Terres A, Eidhin DN, Kelleher D, Reynolds JV: Helicobacter pylori extract induces nuclear factor-kappa B, activator protein-1, and cyclooxygenase-2 in esophageal epithelial cells. J Gastrointest Surg; 2006 Apr;10(4):551-62
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  • Helicobacter pylori infection is recognized as the major cause of gastritis and gastric cancer; however, its role in the development of gastroesophageal reflux disease and Barrett's adenocarcinoma is unclear.
  • The induction of such transcription factors may play a role in the specific immune response within Barrett's mucosa and may indirectly cause inflammation of the gastric cardia and the distal esophagus.

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  • (PMID = 16627221.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antioxidants; 0 / Cell Extracts; 0 / Cyclooxygenase 2 Inhibitors; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Imidazoles; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Pyridines; 0 / SB 203580; 0 / Transcription Factor AP-1; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; PQ6CK8PD0R / Ascorbic Acid
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99. Takashima T, Fujiwara Y, Hamaguchi M, Sasaki E, Tominaga K, Watanabe T, Oshitani N, Higuchi K, Arakawa T: Relationship between peroxisome proliferator-activated receptor-gamma expression and differentiation of human esophageal squamous cell carcinoma. Oncol Rep; 2005 Apr;13(4):601-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We showed that PPAR-gamma is expressed in Barrett's adenocarcinoma cell lines and inhibited the growth of these lines through the induction of G1 cell cycle arrest and apoptosis.
  • [MeSH-major] Barrett Esophagus / metabolism. Carcinoma, Squamous Cell / metabolism. Esophageal Neoplasms / metabolism. PPAR gamma / biosynthesis

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
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  • (PMID = 15756430.001).
  • [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 / 15-deoxyprostaglandin J2; 0 / Antibodies, Monoclonal; 0 / Chromans; 0 / Ligands; 0 / PPAR gamma; 0 / RNA, Messenger; 0 / Thiazolidinediones; 63231-63-0 / RNA; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; I66ZZ0ZN0E / troglitazone; LHQ7J5KV9B / Bisbenzimidazole; RXY07S6CZ2 / Prostaglandin D2; VC2W18DGKR / Thymidine
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100. Vieth M, Schubert B, Lang-Schwarz K, Stolte M: Frequency of Barrett's neoplasia after initial negative endoscopy with biopsy: a long-term histopathological follow-up study. Endoscopy; 2006 Dec;38(12):1201-5
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequency of Barrett's neoplasia after initial negative endoscopy with biopsy: a long-term histopathological follow-up study.
  • BACKGROUND: Barrett's adenocarcinoma is being diagnosed increasingly.
  • We examine possible differences between long segment and short-segment Barrett esophagus (LSBE and SSBE) in long-term follow-up on the basis of our histopathology registry.
  • METHODS AND PATIENTS: All Barrett's esophagus patients diagnosed histologically between 1990 and 1995 (n = 1071) were selected.
  • Of the remaining 748 patients with follow up for more than 5 years, 315 had documented LSBE, 246 had SSBE, and 187 had no length of Barrett esophagus recorded (NLBE).
  • CONCLUSION: The yearly incidence of Barrett esophagus cancer varies between 0.4 % and 1.7 %.
  • Despite the limitations of this retrospective and pathology-based study, the observed risk of developing cancer in Barrett esophagus without neoplasia is comparable to that found in other studies, mainly from the US and the UK, and varies between 0.7 % and 1.0 % of yearly incidence.
  • [MeSH-major] Barrett Esophagus / epidemiology. Barrett Esophagus / pathology. Esophageal Neoplasms / epidemiology. Esophageal Neoplasms / pathology. Esophagoscopy / methods. Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / epidemiology. Adenocarcinoma / pathology. Biopsy / standards. Female. Follow-Up Studies. Humans. Incidence. Male. Middle Aged. Risk Factors

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  • (PMID = 17163319.001).
  • [ISSN] 0013-726X
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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