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1. Chemaly M, Scalone O, Durivage G, Napoleon B, Pujol B, Lefort C, Hervieux V, Scoazec JY, Souquet JC, Ponchon T: Miniprobe EUS in the pretherapeutic assessment of early esophageal neoplasia. Endoscopy; 2008 Jan;40(1):2-6
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  • We conducted a retrospective study, which summarized our clinical experience with various miniprobe techniques in the assessment of early squamous cell carcinoma (SCC) and superficial adenocarcinoma on Barrett's mucosa (SAB).
  • [MeSH-major] Adenocarcinoma / ultrasonography. Barrett Esophagus / ultrasonography. Carcinoma, Squamous Cell / ultrasonography. Endosonography / instrumentation. Esophageal Neoplasms / ultrasonography. Neoplasm Invasiveness / pathology

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  • [CommentIn] Endoscopy. 2008 Jan;40(1):71-2 [18210344.001]
  • (PMID = 18058614.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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2. Tomizawa Y, Wang KK: Changes in screening, prognosis and therapy for esophageal adenocarcinoma in Barrett's esophagus. Curr Opin Gastroenterol; 2009 Jul;25(4):358-65
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  • [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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3. 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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4. Naritaka Y, Ogawa K, Shimakawa T, Wagatsuma Y, Isohata N, Asaka S, Miyaki A, Shiozawa S, Katsube T, Yoshimatsu K, Aiba M, Ide H: Collision carcinoma of the residual cervical esophagus 27 years after esophageal cancer surgery. Anticancer Res; 2007 Jan-Feb;27(1B):505-11
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  • A case of collision carcinoma (squamous cell carcinoma and Barrett's adenocarcinoma) in the residual cervical esophagus of a 68-year-old woman at 27 years after subtotal esophagectomy for thoracic esophageal carcinoma is reported.
  • Pathological examination showed squamous cell carcinoma on the esophageal side of the esophagogastric anastomosis and columnar epithelium with a tongue-shaped extension across the anastomotic line that included Barrett's epithelium, as well as adenocarcinoma, on the gastric tube side.
  • The squamous cell carcinoma and adenocarcinoma were contiguous, but there was a distinct border between them and no morphological transition.
  • Immunohistochemical staining showed positivity for p53 in the squamous carcinoma cells, while it was negative in the adenocarcinoma cells.
  • In contrast, HER2 (c-erb-2) was strongly positive in the adenocarcinoma cells, but negative in the squamous carcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology


5. Lovat LB, Jamieson NF, Novelli MR, Mosse CA, Selvasekar C, Mackenzie GD, Thorpe SM, Bown SG: Photodynamic therapy with m-tetrahydroxyphenyl chlorin for high-grade dysplasia and early cancer in Barrett's columnar lined esophagus. Gastrointest Endosc; 2005 Oct;62(4):617-23
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  • [Title] Photodynamic therapy with m-tetrahydroxyphenyl chlorin for high-grade dysplasia and early cancer in Barrett's columnar lined esophagus.
  • BACKGROUND: Many patients with high-grade dysplasia and localized adenocarcinoma in Barrett's esophagus have localized disease but are either unfit for major surgery or decline esophagectomy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Barrett Esophagus / drug therapy. Esophageal Neoplasms / drug therapy. Mesoporphyrins / therapeutic use. Photochemotherapy / methods. Photosensitizing Agents / therapeutic use. Precancerous Conditions / drug therapy

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  • (PMID = 16185985.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Grant] United Kingdom / Worldwide Cancer Research / / 00-0296
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mesoporphyrins; 0 / Photosensitizing Agents; FU21S769PF / temoporfin
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6. Casson AG, Zheng Z, Evans SC, Veugelers PJ, Porter GA, Guernsey DL: Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma. Carcinogenesis; 2005 Sep;26(9):1536-41
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  • [Title] Polymorphisms in DNA repair genes in the molecular pathogenesis of esophageal (Barrett) adenocarcinoma.
  • To test the hypothesis that aberrations of DNA repair contribute to susceptibility for the progression of gastroesophageal reflux disease (GERD) into Barrett esophagus (BE) and esophageal adenocarcinoma (EADC), we studied the frequency of polymorphisms of selected DNA repair genes in patients with GERD (n = 126), BE (n = 125) and EADC (n = 56) enrolled in a 2-year prospective case-control study.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. DNA Repair / genetics. Esophageal Neoplasms / genetics. Polymorphism, Genetic

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  • (PMID = 15878910.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / X-ray repair cross complementing protein 1; 0 / X-ray repair cross complementing protein 3
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7. Brankley SM, Wang KK, Harwood AR, Miller DV, Legator MS, Lutzke LS, Kipp BR, Morrison LE, Halling KC: The development of a fluorescence in situ hybridization assay for the detection of dysplasia and adenocarcinoma in Barrett's esophagus. J Mol Diagn; 2006 May;8(2):260-7
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  • [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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8. 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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9. Matono S, Fujita H, Sueyoshi S, Tanaka T, Yamana H, Shirouzu K: Long-term survival after three-field lymph-adenectomy for an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node. Jpn J Thorac Cardiovasc Surg; 2006 Jan;54(1):11-5
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  • [Title] Long-term survival after three-field lymph-adenectomy for an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node.
  • Here, we report a case of long-term survival after resection of an adenocarcinoma in Barrett's esophagus with metastasis to Virchow's node.
  • They were pathologically found to be an adenocarcinoma in the esophagus which had metastasised to the lymph node.
  • The pathological diagnosis was adenocarcinoma in Barrett's esophagus with the UICC stage classification of pT1, pN1, pM1-LYM, Stage IVB.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / surgery. Lymph Node Excision / methods

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  • (PMID = 16482930.001).
  • [ISSN] 1344-4964
  • [Journal-full-title] The Japanese journal of thoracic and cardiovascular surgery : official publication of the Japanese Association for Thoracic Surgery = Nihon Kyobu Geka Gakkai zasshi
  • [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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10. Wolfsen HC, Hemminger LL: Salvage photodynamic therapy for persistent esophageal cancer after chemoradiation therapy. Photodiagnosis Photodyn Ther; 2006 Mar;3(1):11-4
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  • RESULTS: Two patients had squamous carcinoma while five patients had Barrett's adenocarcinoma (Barrett's median segment length=8cm; range 5-10cm).
  • The other five patients treated for Barrett's carcinoma have remained disease free although one had died 33 months from metastatic colon cancer.

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  • (PMID = 25049021.001).
  • [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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11. 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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  • [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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12. Pech O, Behrens A, May A, Nachbar L, Gossner L, Rabenstein T, Manner H, Guenter E, Huijsmans J, Vieth M, Stolte M, Ell C: Long-term results and risk factor analysis for recurrence after curative endoscopic therapy in 349 patients with high-grade intraepithelial neoplasia and mucosal adenocarcinoma in Barrett's oesophagus. Gut; 2008 Sep;57(9):1200-6
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  • [Title] Long-term results and risk factor analysis for recurrence after curative endoscopic therapy in 349 patients with high-grade intraepithelial neoplasia and mucosal adenocarcinoma in Barrett's oesophagus.
  • OBJECTIVE: Endoscopic therapy is increasingly being used in the treatment of high-grade intraepithelial neoplasia (HGIN) and mucosal adenocarcinoma (BC) in patients with Barrett's oesophagus.
  • 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


13. 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
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  • [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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14. Wijnhoven BP, Hussey DJ, Watson DI, Tsykin A, Smith CM, Michael MZ, South Australian Oesophageal Research Group: MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma. Br J Surg; 2010 Jun;97(6):853-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND: The genetic changes that drive metaplastic progression from squamous oesophageal mucosa toward intestinal metaplasia and adenocarcinoma are unclear.
  • This study examined whether miRNAs play a role in the development of oesophageal adenocarcinoma.
  • METHODS: RNA was extracted from mucosa of normal oesophageal squamous epithelium, normal gastric epithelium, Barrett's oesophagus with intestinal metaplasia and oesophageal adenocarcinoma obtained from 16 individuals.
  • Expression of miR-143, miR-145 and miR-215 was lower in oesophageal adenocarcinoma than in Barrett's oesophagus.
  • MiR-205 levels were lower in gastric epithelium than in both Barrett's oesophagus and adenocarcinoma.
  • Dysregulation of specific miRNAs could contribute to metaplastic and neoplastic processes in the oesophageal mucosa.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. MicroRNAs / analysis. RNA, Messenger / analysis

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  • (PMID = 20301167.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger
  • [Investigator] Wijnhoven BP; Hussey DJ; Watson DI; Smith CM; Mayne GC; Michael MZ; Astill D; Van der Hoek MB; Tsykin A; Tilanus HW; Wijnhoven BP
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15. 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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16. 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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17. 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


18. 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
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  • 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

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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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19. 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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20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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21. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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22. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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23. Souza RF: Molecular mechanisms of acid exposure in Barrett's esophagus. Inflammopharmacology; 2007 Jun;15(3):95-100
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  • [Title] Molecular mechanisms of acid exposure in Barrett's esophagus.
  • Esophageal adenocarcinoma is one of the most deadly gastrointestinal tumors.
  • Gastroesophageal reflux has been established as a major risk factor for esophageal adenocarcinoma and Barrett's esophagus, the condition in which the normal squamous cells of the esophagus are replaced by metaplastic, specialized intestinal cells that are predisposed to malignancy.
  • Data from ex vivo and in vitro model systems suggests that acid exposure has pro-proliferative and anti-apoptotic effects which may facilitate neoplastic progression of Barrett's esophagus.
  • Such data have led some authorities to propose complete elimination of gastric acid production as a chemopreventive strategy for Barrett's patients.
  • Such distinction may help in optimizing the level of gastric acid suppression for the prevention of cancer in Barrett's esophagus.
  • This report describes the molecular mechanisms whereby acid exposure directly and indirectly, through inducing inflammation, may contribute to the neoplastic progression of Barrett's esophagus and the potential role for acid suppression as a chemopreventive strategy in patients with Barrett's esophagus.
  • [MeSH-major] Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Gastroesophageal Reflux / complications

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  • (PMID = 19847948.001).
  • [ISSN] 0925-4692
  • [Journal-full-title] Inflammopharmacology
  • [ISO-abbreviation] Inflammopharmacology
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK63621
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Acids; 0 / Cytokines; 0 / NF-kappa B; 0 / Reactive Nitrogen Species; 0 / Reactive Oxygen Species
  • [Number-of-references] 53
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24. 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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25. Tischoff I, Hengge UR, Vieth M, Ell C, Stolte M, Weber A, Schmidt WE, Tannapfel A: Methylation of SOCS-3 and SOCS-1 in the carcinogenesis of Barrett's adenocarcinoma. Gut; 2007 Aug;56(8):1047-53
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  • [Title] Methylation of SOCS-3 and SOCS-1 in the carcinogenesis of Barrett's adenocarcinoma.
  • AIMS: This study was performed to elucidate the role of SOCS-1 and SOCS-3 in Barrett's adenocarcinoma and its precursor lesions.
  • METHODS: DNA of specimens from 19 Barrett's adenocarcinomas, 56 Barrett's intraepithelial neoplasias (n = 29 low grade and n = 27 high grade), 30 Barrett's mucosa without neoplasia, 20 samples of normal squamous and gastric epithelium and four cell lines were studied using methylation specific PCR for the SOCS-1 and SOCS-3 promoter following microdissection.
  • RESULTS: In normal squamous epithelium and normal gastric mucosa, neither SOCS-3 nor SOCS-1 methylation was observed.
  • In Barrett's mucosa without intraepithelial neoplasia, SOCS-3 methylation occurred in 4/30 cases (13%) whereas SOCS-1 was unmethylated.
  • A hypermethylated SOCS-3 promoter was found in 14/19 Barrett's adenocarcinomas (74%) and in 20/29 high and 6/27 low grade intraepithelial neoplasias (69% and 22%, respectively).
  • CONCLUSIONS: These data indicate that promoter methylation and subsequent transcript downregulation of SOCS-3 transcripts and, to a much lesser extent, SOCS-1 are involved in the multistep carcinogenesis of Barrett's adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Suppressor of Cytokine Signaling Proteins / genetics


26. Singh R, Ragunath K, Jankowski J: Barrett's Esophagus: Diagnosis, Screening, Surveillance, and Controversies. Gut Liver; 2007 Dec;1(2):93-100
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  • [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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27. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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28. Sayana H, Wani S, Sharma P: Esophageal adenocarcinoma and Barrett's esophagus. Minerva Gastroenterol Dietol; 2007 Jun;53(2):157-69
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  • [Title] Esophageal adenocarcinoma and Barrett's esophagus.
  • Esophageal adenocarcinoma (EAC) is the most rapidly rising incidence cancer associated with a poor 5-year survival rate.
  • Barrett's esophagus (BE) is a well established premalignant condition for the development of EAC and hence it is imperative that patients with BE or at risk for developing BE should be identified and managed appropriately.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / etiology

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  • (PMID = 17557044.001).
  • [ISSN] 1121-421X
  • [Journal-full-title] Minerva gastroenterologica e dietologica
  • [ISO-abbreviation] Minerva Gastroenterol Dietol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 95
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29. 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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  • [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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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. Horváth OP, Kalmár K: Early-stage adenocarcinoma in Barrett's esophagus: aspects of surgical therapies. Dig Dis; 2009;27(1):45-53
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  • [Title] Early-stage adenocarcinoma in Barrett's esophagus: aspects of surgical therapies.
  • Adenocarcinomas in Barrett's esophagus are increasingly diagnosed at early stages thanks to effective surveillance programs.
  • Subtotal esophagectomy with extended lymphadenectomy is considered the best curative treatment for patients with early adenocarcinoma of the esophagus.
  • An individualized strategy should be employed based on staging (tumor penetration into the mucosa/submucosa, presence of lymph node metastasis), multicentricity of tumor, length of the underlying Barrett's mucosa and risk factors of the affected patient.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophagectomy. Esophagoscopy
  • [MeSH-minor] Ablation Techniques. Humans. Lymph Node Excision. Lymphatic Metastasis. Minimally Invasive Surgical Procedures. Neoplasm Recurrence, Local. Neoplasm Staging. Respiratory Mucosa / pathology. Respiratory Mucosa / surgery

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  • (PMID = 19439960.001).
  • [ISSN] 1421-9875
  • [Journal-full-title] Digestive diseases (Basel, Switzerland)
  • [ISO-abbreviation] Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 55
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32. Clemons NJ, McColl KE, Fitzgerald RC: Nitric oxide and acid induce double-strand DNA breaks in Barrett's esophagus carcinogenesis via distinct mechanisms. Gastroenterology; 2007 Oct;133(4):1198-209
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nitric oxide and acid induce double-strand DNA breaks in Barrett's esophagus carcinogenesis via distinct mechanisms.
  • BACKGROUND & AIMS: The luminal microenvironment including acid and nitric oxide (NO) has been implicated in Barrett's esophagus carcinogenesis.
  • METHODS: Transformed and primary Barrett's esophagus and adenocarcinoma cells were exposed to either acid, (pH 3.5), +/- antioxidant or NO from a donor or generated by acidification of nitrite in the presence of ascorbate +/- NO scavenger.
  • Exposure to physiologic concentrations of NO produced from the NO donor or acidification of salivary nitrite induced DSBs in a dose- (>25 micromol/L) and cell-dependent manner (adenocarcinoma >Barrett's esophagus, P < .05).
  • NO also induced DSBs in primary Barrett's esophagus cells treated ex vivo.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / complications. Cell Transformation, Neoplastic / metabolism. DNA Breaks, Single-Stranded. Esophageal Neoplasms / metabolism. Gastric Acid / metabolism. Nitric Oxide / metabolism


33. Sarbia M, zur Hausen A, Feith M, Geddert H, von Rahden BH, Langer R, von Weyhern C, Siewert JR, Höfler H, Stein HJ: Esophageal (Barrett's) adenocarcinoma is not associated with Epstein-Barr virus infection: an analysis of 162 cases. Int J Cancer; 2005 Nov 20;117(4):698-700
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  • [Title] Esophageal (Barrett's) adenocarcinoma is not associated with Epstein-Barr virus infection: an analysis of 162 cases.
  • [MeSH-major] Adenocarcinoma / complications. Barrett Esophagus / complications. Epstein-Barr Virus Infections / complications. Esophageal Neoplasms / complications

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  • (PMID = 15929074.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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34. 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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36. Marx AH, Zielinski M, Kowitz CM, Dancau AM, Thieltges S, Simon R, Choschzick M, Yekebas E, Kaifi JT, Mirlacher M, Atanackovic D, Brümmendorf TH, Fiedler W, Bokemeyer C, Izbicki JR, Sauter G: Homogeneous EGFR amplification defines a subset of aggressive Barrett's adenocarcinomas with poor prognosis. Histopathology; 2010 Sep;57(3):418-26
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  • [Title] Homogeneous EGFR amplification defines a subset of aggressive Barrett's adenocarcinomas with poor prognosis.
  • The aim of this study was performed to determine the potential impact of tumour heterogeneity on anti-EGFR therapy in Barrett's adenocarcinoma (BAC).
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Gene Amplification. Receptor, Epidermal Growth Factor / genetics

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  • [Copyright] © 2010 Blackwell Publishing Limited.
  • (PMID = 20840671.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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37. 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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38. 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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39. 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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40. Messmann H: [Barrett's esophagus carcinoma]. Praxis (Bern 1994); 2006 Jun 21;95(25-26):1029-35
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  • [Title] [Barrett's esophagus carcinoma].
  • The incidence of Barrett's esophagus, long segment as well as short segment, has increased over the last few years.
  • However there is a simultaneous increase of Barrett's adenocarcinoma in the Western world, while the number of squamous epithelium cancer decreases.
  • Due to available data it is clear that the risk of Barrett's esophagus has been overestimated, mainly because of a publication bias.
  • The risk of a Barrett's esophagus carcinoma has been published with 0.5%/year.
  • The diagnosis of Barrett's esophagus is made endoscopically and histologically, this means 4 quadrant biopsies every 1-2 cm are gold standard.
  • In patients with proven Barrett's esophagus regular surveillance endoscopies depending on the presence of intraepithelial neoplasia are recommended.
  • While patients with Barrett's esophagus and no or with low grade intraepithelial neoplasia need only surveillance, those with high grade intraepithelial neoplasia should be treated.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / pathology

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  • (PMID = 16836063.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Switzerland
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41. 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 / 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; OU13V1EYWQ / SB 203580; PQ6CK8PD0R / Ascorbic Acid
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42. 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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43. Casson AG, Zheng Z, Porter GA, Guernsey DL: Genetic polymorphisms of microsomal epoxide hydroxylase and glutathione S-transferases M1, T1 and P1, interactions with smoking, and risk for esophageal (Barrett) adenocarcinoma. Cancer Detect Prev; 2006;30(5):423-31
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  • [Title] Genetic polymorphisms of microsomal epoxide hydroxylase and glutathione S-transferases M1, T1 and P1, interactions with smoking, and risk for esophageal (Barrett) adenocarcinoma.
  • BACKGROUND: The aim of this case-control study was to test the hypothesis that polymorphisms of the microsomal epoxide hydroxylase (mEH) and glutathione S-transferase (GST) genes modulate the susceptibility to esophageal adenocarcinoma (EADC) associated with smoking.
  • METHODS: Cases included patients with gastroesophageal reflux disease (GERD) (n=126), Barrett esophagus (BE) (n=125), and EADC (n=56); controls comprised 95 strictly asymptomatic individuals.
  • [MeSH-minor] Adenocarcinoma / genetics. Alleles. Barrett Esophagus / genetics. Case-Control Studies. Female. Gastroesophageal Reflux / genetics. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Risk Factors

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  • (PMID = 17064856.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1; EC 3.3.2.- / Epoxide Hydrolases
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44. Sappati Biyyani RS, Chessler L, McCain E, Nelson K, Fahmy N, King J: Familial trends of inheritance in gastro esophageal reflux disease, Barrett's esophagus and Barrett's adenocarcinoma: 20 families. Dis Esophagus; 2007;20(1):53-7
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  • [Title] Familial trends of inheritance in gastro esophageal reflux disease, Barrett's esophagus and Barrett's adenocarcinoma: 20 families.
  • We reported four families with familial Barrett's esophagus (FBE) in 1993.
  • This follow-up study includes an additional 16 families with FBE, gastroesophageal reflux disease (GERD) and BE-related adenocarcinoma (BEAC) highlighting the familial trends of inheritance.

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  • (PMID = 17227311.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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45. Selaru FM, Wang S, Yin J, Schulmann K, Xu Y, Mori Y, Olaru AV, Sato F, Hamilton JP, Abraham JM, Schneider P, Greenwald BD, Brabender J, Meltzer SJ: Beyond Field Effect: Analysis of Shrunken Centroids in Normal Esophageal Epithelia Detects Concomitant Esophageal Adenocarcinoma. Bioinform Biol Insights; 2007;1:127-136
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  • [Title] Beyond Field Effect: Analysis of Shrunken Centroids in Normal Esophageal Epithelia Detects Concomitant Esophageal Adenocarcinoma.
  • BACKGROUND AND AIMS: Because of the extremely low neoplastic progression rate in Barrett's esophagus, it is difficult to diagnose patients with concomitant adenocarcinoma early in their disease course.
  • If biomarkers existed in normal squamous esophageal epithelium to identify patients with concomitant esophageal adenocarcinoma, potential applications would be far-reaching.
  • The aim of the current study was to identify global gene expression patterns in normal esophageal epithelium capable of revealing simultaneous esophageal adenocarcinoma, even located remotely in the esophagus.
  • METHODS: Tissues comprised normal esophageal epithelia from 9 patients with esophageal adenocarcinoma, 8 patients lacking esophageal adenocarcinoma or Barrett's, and 6 patients with Barrett's esophagus alone. cDNA microarrays were performed, and pattern recognition in each of these subgroups was achieved using shrunken nearest centroid predictors.
  • RESULTS: Our method accurately discriminated normal esophageal epithelia of 8/8 patients without esophageal adenocarcinoma or Barrett's esophagus and of 6/6 patients with Barrett's esophagus alone from normal esophageal epithelia of 9/9 patients with Barrett's esophagus and concomitant esophageal adenocarcinoma.
  • Thus, based on their corresponding normal esophageal epithelia alone, our method accurately diagnosed patients who had concomitant esophageal adenocarcinoma.
  • CONCLUSIONS: These global gene expression patterns, along with individual genes culled from them, represent potential biomarkers for the early diagnosis of esophageal adenocarcinoma from normal esophageal epithelia.
  • Genes discovered in normal esophagus that are differentially expressed in patients with vs. without esophageal adenocarcinoma merit further pursuit in molecular genetic, functional, and therapeutic interventional studies.

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  • (PMID = 18425214.001).
  • [Journal-full-title] Bioinformatics and biology insights
  • [ISO-abbreviation] Bioinform Biol Insights
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA001808; United States / NCI NIH HHS / CA / CA001808-05; United States / NCI NIH HHS / CA / R01 CA095323; United States / NCI NIH HHS / CA / CA095323-13; United States / NCI NIH HHS / CA / R21 CA106763; United States / NCI NIH HHS / CA / CA106763-02; United States / NIDDK NIH HHS / DK / T32 DK067872; United States / NCI NIH HHS / CA / U01 CA085069; United States / NCI NIH HHS / CA / CA085069-07
  • [Publication-type] JOURNAL ARTICLE
  • [Publication-country] United States
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46. Sabo E, Beck AH, Montgomery EA, Bhattacharya B, Meitner P, Wang JY, Resnick MB: Computerized morphometry as an aid in determining the grade of dysplasia and progression to adenocarcinoma in Barrett's esophagus. Lab Invest; 2006 Dec;86(12):1261-71
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  • [Title] Computerized morphometry as an aid in determining the grade of dysplasia and progression to adenocarcinoma in Barrett's esophagus.
  • The aims of this study were to use computerized morphometry in order to differentiate between the degree of dysplasia and to predict progression to invasive adenocarcinoma in Barrett's esophagus (BE).
  • Moreover, histomorphometric quantification of nuclear texture is a powerful tool for predicting progression to invasive adenocarcinoma in patients with HGD.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / pathology. Esophageal Neoplasms / etiology. Image Interpretation, Computer-Assisted / methods. Precancerous Conditions / pathology

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  • (PMID = 17075582.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR17695
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
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47. Villette S, Pigaglio-Deshayes S, Vever-Bizet C, Validire P, Bourg-Heckly G: Ultraviolet-induced autofluorescence characterization of normal and tumoral esophageal epithelium cells with quantitation of NAD(P)H. Photochem Photobiol Sci; 2006 May;5(5):483-92
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  • The autofluorescence emission of squamous cell carcinoma, adenocarcinoma on Barrett's mucosa and normal cells was characterized by microspectrofluorimetry on monolayers and by spectrofluorimetry on cell suspensions.
  • [MeSH-minor] Barrett Esophagus / pathology. Cell Line, Tumor. Flavin Mononucleotide / analysis. Flavin-Adenine Dinucleotide / analysis. Flow Cytometry. Fluorescence. Humans. Spectrometry, Fluorescence. Ultraviolet Rays

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  • (PMID = 16685326.001).
  • [ISSN] 1474-905X
  • [Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • [ISO-abbreviation] Photochem. Photobiol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 146-14-5 / Flavin-Adenine Dinucleotide; 53-59-8 / NADP; 7N464URE7E / Flavin Mononucleotide
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48. 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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49. Vissers KJ, Dinjens WN, Riegman PH, Tilanus HW, van Dekken H: Allelic imbalance on distal 7q (7q36.1-q36.3) in gastric cardia and oesophageal (Barrett's) adenocarcinoma. Anticancer Res; 2005 Mar-Apr;25(2A):913-6
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  • [Title] Allelic imbalance on distal 7q (7q36.1-q36.3) in gastric cardia and oesophageal (Barrett's) adenocarcinoma.
  • BACKGROUND: Oesophageal (Barrett's) and gastric cardia adenocarcinomas are cancers arising at and around the gastro-oesophageal junction.
  • MATERIALS AND METHODS: We investigated the 7q region with a set of 5 polymorphic markers spanning 7q36.1-q36.3 in 33 Barrett-related carcinomas.
  • RESULTS: Overall, the number of allelic loss was higher in Barrett's cancers than in gastric cardia carcinomas (p=0.04).
  • In Barrett's adenocarcinomas, imbalance varied from 28% to 45% (of informative cases) with the highest prevalence at marker D7S483.
  • CONCLUSION: Marker D7S483 can aid in discriminating oesophageal (Barrett's) and gastric cardia carcinomas.
  • Further, this region possibly harbours cancer gene(s) involved in Barrett-related adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / genetics. Allelic Imbalance. Barrett Esophagus / genetics. Cardia / pathology. Chromosomes, Human, Pair 7 / genetics. Esophageal Neoplasms / genetics. Stomach Neoplasms / genetics

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  • (PMID = 15868927.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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50. 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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51. 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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52. Han JQ, Liu Q, Liang RX, Qu FS, Yan TX, Sun YH, Li XQ: [Clinical analysis of 108 cases with adenocarcinoma Barretts's esophagus]. Zhonghua Zhong Liu Za Zhi; 2007 Jun;29(6):470-3
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  • [Title] [Clinical analysis of 108 cases with adenocarcinoma Barretts's esophagus].
  • OBJECTIVE: To investigate the prognostic factors and to analyze the efficacy of chemotherapy and/or radiotherapy for Barrett's esophageal adenocarcinoma after radical surgical resection.
  • METHODS: The clinical data of 108 patients with adenocarcinoma Barrett's esophagus picking out from 783 esophageal adenocarcinoma patients surgically treated between June 1978 to June 2001 in the Shandong Provincial Hospital and Shandong Qianfoshan Hospital were analyzed retrospectively.
  • CONCLUSION: Chemotherapy plus radiotherapy after radical surgical resection may improve the survival of patients with adenocarcinoma in Barrett's esophagus adenocarcinoma patient.
  • [MeSH-major] Adenocarcinoma / therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Barrett Esophagus / therapy. Esophageal Neoplasms / therapy. Radiotherapy, High-Energy / methods

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  • (PMID = 17974287.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate; CMF regimen; FAM protocol
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53. Rokkas T, Pistiolas D, Sechopoulos P, Robotis I, Margantinis G: Relationship between Helicobacter pylori infection and esophageal neoplasia: a meta-analysis. Clin Gastroenterol Hepatol; 2007 Dec;5(12):1413-7, 1417.e1-2
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  • RESULTS: In adenocarcinoma patients there were inverse significant relationships with both the H. pylori prevalence (pooled odds ratio [OR], 0.52; 95% confidence interval [CI], 0.37-0.73; P < .001) and the prevalence of H. pylori cagA-positive strain (pooled OR, 0.51; 95% CI, 0.31-0.82; P = .006).
  • Similarly in patients with Barrett's esophagus there were inverse significant relationships (pooled OR, 0.64; 95% CI, 0.43-0.94; P = .025 and pooled OR, 0.39; 95% CI, 0.21-0.76; P = .005, respectively).
  • CONCLUSIONS: The results showed an inverse statistically significant relationship of H. pylori infection with both esophageal adenocarcinoma and Barrett's esophagus, which might suggest a protective role of the infection in these entities.
  • [MeSH-major] Adenocarcinoma / etiology. Esophageal Neoplasms / etiology. Helicobacter Infections / complications. Helicobacter pylori / isolation & purification

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  • (PMID = 17997357.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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54. 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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  • [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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55. Ferguson HR, Wild CP, Anderson LA, Murphy SJ, Johnston BT, Murray LJ, Watson RG, McGuigan J, Reynolds JV, Hardie LJ: Cyclooxygenase-2 and inducible nitric oxide synthase gene polymorphisms and risk of reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. Cancer Epidemiol Biomarkers Prev; 2008 Mar;17(3):727-31
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  • [Title] Cyclooxygenase-2 and inducible nitric oxide synthase gene polymorphisms and risk of reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma.
  • The incidence of esophageal adenocarcinoma has increased in recent years, and Barrett's esophagus is a recognized risk factor.
  • Increased expression of these enzymes has been found in esophageal adenocarcinoma, Barrett's esophagus, and reflux esophagitis.
  • In a population-based case-control study, we examined associations of the COX-2 8473 T>C and iNOS Ser(608) Leu (C>T) 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), and reflux esophagitis (n = 230) and normal population controls frequency matched for age and sex (n = 248).
  • The presence of at least one COX-2 8473 C allele was associated with a significantly increased risk of esophageal adenocarcinoma (adjusted odds ratio, 1.58; 95% confidence interval, 1.04-2.40).
  • There was no significant association between this polymorphism and risk of Barrett's esophagus or reflux esophagitis or between the iNOS Ser 608 Leu polymorphism and risk of these esophageal conditions.
  • Our study suggests that the COX-2 8473 C allele is a potential genetic marker for susceptibility to esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Barrett Esophagus / enzymology. Barrett Esophagus / genetics. Cyclooxygenase 2 / genetics. Esophageal Neoplasms / enzymology. Esophageal Neoplasms / genetics. Esophagitis, Peptic / enzymology. Esophagitis, Peptic / genetics. Nitric Oxide Synthase Type II / genetics. Polymorphism, Genetic

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  • (PMID = 18349295.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.99.1 / Cyclooxygenase 2
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56. 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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57. 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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58. 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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  • [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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59. Ruffato A, Mattioli S, Lugaresi ML, D'Ovidio F, Antonacci F, Di Simone MP: Long-term results after Heller-Dor operation for oesophageal achalasia. Eur J Cardiothorac Surg; 2006 Jun;29(6):914-9
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  • Seven out of 173 patients (4%), 6 of whom were pre-operatively classified as sigmoid achalasia, subsequently underwent oesophagectomy, 3 for epidermoid cancer, 1 for Barrett's adenocarcinoma, 2 for stasis oesophagitis and recurrent sepsis, 1 for severe dysphagia.

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  • (PMID = 16675239.001).
  • [ISSN] 1010-7940
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Germany
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60. 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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61. 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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62. Murphy SJ, Anderson LA, Ferguson HR, Johnston BT, Watson PR, McGuigan J, Comber H, Reynolds JV, Murray LJ, Cantwell MM: Dietary antioxidant and mineral intake in humans is associated with reduced risk of esophageal adenocarcinoma but not reflux esophagitis or Barrett's esophagus. J Nutr; 2010 Oct;140(10):1757-63
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  • [Title] Dietary antioxidant and mineral intake in humans is associated with reduced risk of esophageal adenocarcinoma but not reflux esophagitis or Barrett's esophagus.
  • The role of antioxidants in the pathogenesis of reflux esophagitis (RE), Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC) remains unknown.
  • We performed an assessment of dietary antioxidant intake in a case control study of RE (n = 219), BE (n = 220), EAC (n = 224), and matched population controls (n = 256) (the Factors Influencing the Barrett's Adenocarcinoma Relationship study) using a modification of a validated FFQ.
  • [MeSH-major] Adenocarcinoma / prevention & control. Antioxidants / administration & dosage. Barrett Esophagus / prevention & control. Diet. Gastroesophageal Reflux / prevention & control. Minerals / administration & dosage


63. O'Riordan JM, Abdel-latif MM, Ravi N, McNamara D, Byrne PJ, McDonald GS, Keeling PW, Kelleher D, Reynolds JV: Proinflammatory cytokine and nuclear factor kappa-B expression along the inflammation-metaplasia-dysplasia-adenocarcinoma sequence in the esophagus. Am J Gastroenterol; 2005 Jun;100(6):1257-64
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  • [Title] Proinflammatory cytokine and nuclear factor kappa-B expression along the inflammation-metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.
  • BACKGROUND: The incidence of esophageal adenocarcinoma has increased significantly in the western world over the last 20 yr.
  • Most cases arise in a background of chronic gastroesophageal reflux, and specialized intestinal metaplasia in Barrett's esophagus is frequently an antecedent phenotype or evident in association with adenocarcinoma.
  • The molecular events that characterize the pathway from inflammation to metaplasia to dysplasia and adenocarcinoma are poorly understood.
  • AIMS: To examine the expression of the proinflammatory cytokines IL-8 and IL-1beta along the esophagitis, metaplasia, dysplasia, and adenocarcinoma pathway, and to correlate this with histological changes and expression of the transcription factor NF-kappaB.
  • PATIENTS AND METHODS: Fresh biopsy specimens were collected from patients with reflux esophagitis (n=15), Barrett's esophagus (n=35), Barrett's adjacent to adenocarcinoma (n=8), and esophageal adenocarcinoma (n=35).
  • RESULTS: Elevated expression of NF-kappaB was found in 2 (13%) out of 15 patients with reflux esophagitis, 21 (60%) out of 35 patients with Barrett's esophagus, and 28 (80%) out of 35 patients with esophageal adenocarcinoma.
  • All 5 patients with Barrett's esophagus and high-grade dysplasia showed elevated expression of NF-kappaB.
  • IL-8 and IL-1beta were significantly increased in esophagitis, Barrett's, and adenocarcinoma compared with squamous epithelium, and in adenocarcinoma compared with all other groups.
  • There was a stepwise increase in the expression of IL-8, IL-1beta, and NF-kappaB from normal through Barrett's epithelium to adenocarcinoma in eight cases of esophageal adenocarcinoma.
  • The levels of both IL-8 and IL-1beta in adenocarcinoma patients correlated with stage of disease.
  • Patients with adenocarcinoma who were NF-kappaB positive had significantly higher levels of both IL-8 (p=0.04) and IL-1beta (p=0.03) compared to adenocarcinoma patients who were NF-kappaB negative.
  • CONCLUSIONS: The proinflammatory cytokines IL-8 and IL-1beta are elevated in esophagitis and Barrett's epithelium, and markedly elevated in adenocarcinoma.
  • NF-kappaB activation is infrequent in esophagitis, but is increased in Barrett's epithelium and adenocarcinoma.
  • The association of NF-kappaB activation with cytokine upregulation was only evident in patients with adenocarcinoma.
  • These patterns may play an important role in Barrett's inflammation and tumourigenesis, and inhibition of the NF-kappaB/proinflammatory cytokine pathway may be an important target for future chemoprevention strategies.
  • [MeSH-major] Adenocarcinoma / metabolism. Esophageal Neoplasms / metabolism. Esophagitis / metabolism. Interleukin-1 / biosynthesis. Interleukin-8 / biosynthesis. NF-kappa B / biosynthesis
  • [MeSH-minor] Barrett Esophagus / metabolism. Barrett Esophagus / pathology. Biomarkers / metabolism. Biopsy. Electrophoresis. Endoscopy, Digestive System. Enzyme-Linked Immunosorbent Assay. Female. Gastroesophageal Reflux / metabolism. Gastroesophageal Reflux / pathology. Humans. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Metaplasia / metabolism. Metaplasia / pathology. Middle Aged. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Prospective Studies

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  • (PMID = 15929754.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Interleukin-1; 0 / Interleukin-8; 0 / NF-kappa B
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64. Turcotte S, Duranceau A: Gastroesophageal reflux and cancer. Thorac Surg Clin; 2005 Aug;15(3):341-52
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  • The causal relationship between GERD and esophageal adenocarcinoma, although unclear just a few decades ago, now is established fairly well.
  • The physiologic changes and the biocellular alterations of the damaged esophageal mucosa are documented better.
  • The absolute risk of esophageal adenocarcinoma arising from GERD is low, and, at present, does not justify population-screening programs.
  • Still, with the notion that adenocarcinoma of the esophagus is an aggressive cancer once documented, important questions still are in need of answers for patients suffering from reflux symptoms.
  • Once documented, Barrett's esophagus needs to be seen as a premalignant condition not necessarily leading to adenocarcinoma formation; despite their increased risk of tumor formation, most patients who have Barrett's esophagus die of other causes.
  • It still is unclear if medicine or surgery provides the best quality of life and the best protection against the development of dysplasia and the possible progression toward adenocarcinoma formation when intestinal metaplasia is present in the esophagus.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Gastroesophageal Reflux / pathology. Precancerous Conditions / pathology

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  • (PMID = 16104125.001).
  • [ISSN] 1547-4127
  • [Journal-full-title] Thoracic surgery clinics
  • [ISO-abbreviation] Thorac Surg Clin
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 126
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65. 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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66. Donnelly M, Anderson LA, Johnston BT, Watson RG, Murphy SJ, Comber H, McGuigan J, Reynolds JV, Murray LJ: Oesophageal cancer: caregiver mental health and strain. Psychooncology; 2008 Dec;17(12):1196-201
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Patients with oesophageal adenocarcinoma in Ireland were recruited into the FINBAR study (the main aim of which was to investigate factors influencing the Barrett's adenocarcinoma relationship).

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  • [Copyright] (c) 2008 John Wiley & Sons, Ltd.
  • (PMID = 18470954.001).
  • [ISSN] 1099-1611
  • [Journal-full-title] Psycho-oncology
  • [ISO-abbreviation] Psychooncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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67. 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
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  • [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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68. 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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69. Abela JE, Going JJ, Mackenzie JF, McKernan M, O'Mahoney S, Stuart RC: Systematic four-quadrant biopsy detects Barrett's dysplasia in more patients than nonsystematic biopsy. Am J Gastroenterol; 2008 Apr;103(4):850-5
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  • [Title] Systematic four-quadrant biopsy detects Barrett's dysplasia in more patients than nonsystematic biopsy.
  • AIMS: To compare detection of Barrett's dysplasia and adenocarcinoma by systematic versus nonsystematic surveillance biopsy protocols.
  • The surgical team adopted annual systematic four-quadrant biopsy Barrett's surveillance in 1995.
  • The medical team continued annual Barrett's surveillance with nonsystematic biopsy until 2004.
  • We compare detection of Barrett's dysplasia and esophageal adenocarcinoma in unselected patients by these two biopsy strategies over 10 yr.
  • All patients had > or = 3 cm Barrett's esophagus and histological proof of intestinal metaplasia.
  • Patients referred for dysplasia management or with prevalent adenocarcinoma were excluded.
  • Two had intramucosal adenocarcinoma.
  • No cohort A patient developed advanced cancer but three cohort B patients developed and died of invasive Barrett's adenocarcinoma (0.6% per patient-year).
  • CONCLUSIONS: Patient age, gender, Barrett's segment length, and follow-up were similar (though not identical) in both cohorts, but confounding seems unlikely to account for a 13-fold difference in detection of prevalent dysplasia between the two groups.
  • Our data support the hypothesis that systematic four-quadrant biopsy is considerably more effective than nonsystematic biopsy sampling in detecting Barrett's dysplasia and early adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Biopsy / methods


70. 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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71. Kuester D, Dar AA, Moskaluk CC, Krueger S, Meyer F, Hartig R, Stolte M, Malfertheiner P, Lippert H, Roessner A, El-Rifai W, Schneider-Stock R: Early involvement of death-associated protein kinase promoter hypermethylation in the carcinogenesis of Barrett's esophageal adenocarcinoma and its association with clinical progression. Neoplasia; 2007 Mar;9(3):236-45
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  • [Title] Early involvement of death-associated protein kinase promoter hypermethylation in the carcinogenesis of Barrett's esophageal adenocarcinoma and its association with clinical progression.
  • Esophageal Barrett's adenocarcinoma (BA) develops through a multistage process, which is associated with the transcriptional silencing of tumor-suppressor genes by promoter CpG island hypermethylation.
  • In this study, we explored the promoter hypermethylation and protein expression of proapoptotic death-associated protein kinase (DAPK) during the multistep Barrett's carcinogenesis cascade.
  • Hypermethylation of DAPK promoter was detected in 20% of normal mucosa, 50% of Barrett's metaplasia, 53% of dysplasia, and 60% of adenocarcinomas, and resulted in a marked decrease in DAPK protein expression (P < .01).
  • Thus, we consider DAPK inactivation by promoter hypermethylation as an early event in Barrett's carcinogenesis and suggest that a decreased protein expression of DAPK likely plays a role in the development and progression of BA.

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  • (PMID = 17401463.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106176; United States / NCI NIH HHS / CA / CA106176
  • [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 / Apoptosis Regulatory Proteins; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC1838580
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72. Burnat G, Rau T, Elshimi E, Hahn EG, Konturek PC: Bile acids induce overexpression of homeobox gene CDX-2 and vascular endothelial growth factor (VEGF) in human Barrett's esophageal mucosa and adenocarcinoma cell line. Scand J Gastroenterol; 2007 Dec;42(12):1460-5
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  • [Title] Bile acids induce overexpression of homeobox gene CDX-2 and vascular endothelial growth factor (VEGF) in human Barrett's esophageal mucosa and adenocarcinoma cell line.
  • OBJECTIVE: Barrett's esophagus (BE) is an acquired precancerous condition that develops from mucosal injury incurred after chronic gastroesophageal acid and bile reflux.
  • The aims of the present study were 1) to compare the mRNA and protein expression of CDX-2 in biopsies obtained from patients with BE and normal squamous epithelium and 2) to study the effect of two different bile salts, ursodeoxycholic acid (UDCA) and deoxycholic acid (DCA), on the mRNA expression of CDX-2 and vascular endothelial growth factor (VEGF) in Barrett's the adenocarcinoma cell line (OE-33).
  • MATERIAL AND METHODS: CDX-2 expression was measured in Barrett's mucosa and normal esophageal mucosa obtained from 15 patients with BE histologically diagnosed by immunohistochemistry, Western blot, and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR).
  • RESULTS: Both mRNA and protein expression of CDX-2 were significantly up-regulated in Barrett's mucosa as compared to normal esophageal mucosa.
  • DCA appears to be a stronger stimulant of the expression of VEGF than UDCA in the Barrett's carcinoma cell line, indicating a stronger carcinogenic potential of this bile salt.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Bile Acids and Salts / pharmacology. Esophageal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 17852856.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
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73. Colleypriest BJ, Ward SG, Tosh D: How does inflammation cause Barrett's metaplasia? Curr Opin Pharmacol; 2009 Dec;9(6):721-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How does inflammation cause Barrett's metaplasia?
  • Oesophageal adenocarcinoma conveys a poor prognosis and has a rapidly increasing incidence.
  • Similarly, Barrett's metaplasia (a precursor lesion for oesophageal adenocarcinoma) has an increasing incidence.
  • Both oesophageal adenocarcinoma and Barrett's metaplasia are more common in the context of inflammation as a result of acid and bile reflux.
  • The cytokine profile of Barrett's metaplasia is predominantly a T-helper 2 response that contrasts with the T-helper 1 response in normal and inflamed oesophagus and normal intestine.
  • A key transcription factor in the development of Barrett's metaplasia, CDX2, has recently been shown to be induced in response to inflammatory mediators.
  • Understanding the role of oesophageal inflammation will provide important insight into the development of Barrett's metaplasia and oesophageal cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / etiology. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Esophagitis / complications

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  • (PMID = 19828375.001).
  • [ISSN] 1471-4973
  • [Journal-full-title] Current opinion in pharmacology
  • [ISO-abbreviation] Curr Opin Pharmacol
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300415
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / NF-kappa B; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 53
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74. Maru DM: Barrett's esophagus: diagnostic challenges and recent developments. Ann Diagn Pathol; 2009 Jun;13(3):212-21
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  • [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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75. 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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  • [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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76. Heidemann J, Maaser C, Lügering A, Spahn TW, Zimmer KP, Herbst H, Rafiee P, Domschke W, Krieglstein CF, Binion DG, Kucharzik TF: Expression of vascular cell adhesion molecule-1 (CD 106) in normal and neoplastic human esophageal squamous epithelium. Int J Oncol; 2006 Jan;28(1):77-85
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  • To further delineate the differential expression patterns of VCAM-1 in the esophageal epithelium, we examined specimens from squamous cell carcinoma (SCC), adenocarcinoma, and Barrett's columnar cell metaplasia.
  • VCAM-1 was strongly expressed in squamous cell carcinoma, but not adenocarcinoma nor columnar epithelia in Barrett's esophagus.
  • [MeSH-minor] Gene Expression Profiling. Homeostasis. Humans. Inflammation. Intestinal Mucosa / cytology. Intestinal Mucosa / physiology. Neoplasm Metastasis / genetics. Neoplasm Metastasis / physiopathology

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  • (PMID = 16327982.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Vascular Cell Adhesion Molecule-1
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77. Shammas MA, Qazi A, Batchu RB, Bertheau RC, Wong JY, Rao MY, Prasad M, Chanda D, Ponnazhagan S, Anderson KC, Steffes CP, Munshi NC, De Vivo I, Beer DG, Gryaznov S, Weaver DW, Goyal RK: Telomere maintenance in laser capture microdissection-purified Barrett's adenocarcinoma cells and effect of telomerase inhibition in vivo. Clin Cancer Res; 2008 Aug 1;14(15):4971-80
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  • [Title] Telomere maintenance in laser capture microdissection-purified Barrett's adenocarcinoma cells and effect of telomerase inhibition in vivo.
  • PURPOSE: The aims of this study were to investigate telomere function in normal and Barrett's esophageal adenocarcinoma (BEAC) cells purified by laser capture microdissection and to evaluate the effect of telomerase inhibition in cancer cells in vitro and in vivo.
  • To evaluate the effect of telomerase inhibition, adenocarcinoma cell lines were continuously treated with a specific telomerase inhibitor (GRN163L) and live cell number was determined weekly.
  • For in vivo studies, severe combined immunodeficient mice were s.c. inoculated with adenocarcinoma cells and following appearance of palpable tumors, injected i.p. with saline or GRN163L.
  • The treatment of adenocarcinoma cells with telomerase inhibitor, GRN163L, led to loss of telomerase activity, reduction in telomere length, and growth arrest through induction of both the senescence and apoptosis.
  • CONCLUSIONS: We show that telomerase activity is significantly elevated whereas telomeres are shorter in BEAC and suppression of telomerase inhibits proliferation of adenocarcinoma cells both in vitro and in vivo.

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  • (PMID = 18676772.001).
  • [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 / PHS HHS / / P01-78378; United States / NCI NIH HHS / CA / R01 CA125711; United States / PHS HHS / / NIH-P50-100007; United States / NCI NIH HHS / CA / P01 CA078378; United States / NCI NIH HHS / CA / CA078378-06A10006; United States / NCI NIH HHS / CA / P01 CA078378-06A10006; United States / PHS HHS / / P50-100007
  • [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] EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ NIHMS104415; NLM/ PMC2705940
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78. Yoon HY, Kim HI, Kim CB: [Clinicopathologic characteristics of adenocarcinoma in cardia according to Siewert classification]. Korean J Gastroenterol; 2008 Nov;52(5):293-7
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  • [Title] [Clinicopathologic characteristics of adenocarcinoma in cardia according to Siewert classification].
  • RESULTS: Barrett's adenocarcinoma was recognized in two patients so called type I.
  • [MeSH-major] Adenocarcinoma / pathology. Cardia. Stomach Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Esophageal Neoplasms / classification. Esophageal Neoplasms / mortality. Esophageal Neoplasms / pathology. Female. Humans. Kaplan-Meier Estimate. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Analysis

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  • (PMID = 19077475.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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79. 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


80. Miller RC, Atherton PJ, Kabat BF, Fredericksen MB, Geno DM, Deschamps C, Jatoi A, Sloan JA, Romero Y: Marital status and quality of life in patients with esophageal cancer or Barrett's esophagus: the mayo clinic esophageal adenocarcinoma and Barrett's esophagus registry study. Dig Dis Sci; 2010 Oct;55(10):2860-8
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  • [Title] Marital status and quality of life in patients with esophageal cancer or Barrett's esophagus: the mayo clinic esophageal adenocarcinoma and Barrett's esophagus registry study.
  • AIMS: To quantify the association of marital status and changes in QOL over time in patients with EC and patients with Barrett's esophagus (BE).
  • METHODS: Eligible patients in the Mayo Clinic Esophageal Adenocarcinoma and Barrett's Esophagus Registry completed QOL assessments at baseline and approximately 1 year later.
  • [MeSH-major] Adenocarcinoma / epidemiology. Barrett Esophagus / epidemiology. Esophageal Neoplasms / epidemiology. Marital Status / statistics & numerical data. Quality of Life


81. 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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82. 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
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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


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


84. Szachnowicz S, Cecconello I, Ribeiro U, Iriya K, El Ibrahim R, Takeda FR, Corbett CE, Vaz Safatle-Ribeiro A: Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study. World J Surg Oncol; 2009;7:27
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  • [Title] Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study.
  • BACKGROUND: Mucin immunoexpression in adenocarcinoma arising in Barrett's esophagus (BE) may indicate the carcinogenesis pathway.
  • The aim of this study was to evaluate resected specimens of adenocarcinoma in BE for the pattern of mucins and to correlate to the histologic classification.
  • METHODS: Specimens were retrospectively collected from thirteen patients who underwent esophageal resection due to adenocarcinoma in BE.
  • CONCLUSION: Barrett's esophagus adenocarcinoma shows either gastric or intestinal type pattern of mucin expression.
  • The two types of tumors developed in Barrett's esophagus may reflect the original cell type involved in the malignant transformation.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / complications. Esophageal Neoplasms / etiology. Mucin 5AC / analysis. Mucin-2 / analysis
  • [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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85. Shami VM, Villaverde A, Stearns L, Chi KD, Kinney TP, Rogers GB, Dye CE, Waxman I: Clinical impact of conventional endosonography and endoscopic ultrasound-guided fine-needle aspiration in the assessment of patients with Barrett's esophagus and high-grade dysplasia or intramucosal carcinoma who have been referred for endoscopic ablation therapy. Endoscopy; 2006 Feb;38(2):157-61
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  • [Title] Clinical impact of conventional endosonography and endoscopic ultrasound-guided fine-needle aspiration in the assessment of patients with Barrett's esophagus and high-grade dysplasia or intramucosal carcinoma who have been referred for endoscopic ablation therapy.
  • BACKGROUND AND STUDY AIMS: Endoscopic mucosal resection and photodynamic therapy are exciting, minimally invasive curative techniques that represent an alternative to surgery in patients with Barrett's esophagus and high-grade dysplasia or intramucosal adenocarcinoma.
  • PATIENTS AND METHODS: A total of 25 consecutive patients with a diagnosis of high-grade dysplasia or intramucosal adenocarcinoma in Barrett's esophagus who had been referred to the University of Chicago for staging in preparation for endoscopic therapy between March 2002 and November 2004 were included in the study.
  • CONCLUSIONS: By detecting unsuspected malignant lymphadenopathy, conventional endosonography and endoscopic ultrasound with fine-needle aspiration dramatically changed the course of management in 20% of patients referred for endoscopic therapy of Barrett's esophagus with high-grade dysplasia or intramucosal carcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Catheter Ablation / methods. Endoscopy, Gastrointestinal. Endosonography. Esophageal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biopsy, Fine-Needle / methods. Female. Humans. Intestinal Mucosa / pathology. Intestinal Mucosa / ultrasonography. Male. Middle Aged. Retrospective Studies

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  • [CommentIn] Endoscopy. 2006 Feb;38(2):175-9 [16479426.001]
  • (PMID = 16479423.001).
  • [ISSN] 0013-726X
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK42086
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
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86. 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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87. 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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  • [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


88. 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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89. 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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90. Schauer M, Stein H, Lordick F, Feith M, Theisen J, Siewert JR: Results of a multimodal therapy in patients with stage IV Barrett's adenocarcinoma. World J Surg; 2008 Dec;32(12):2655-60
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  • [Title] Results of a multimodal therapy in patients with stage IV Barrett's adenocarcinoma.
  • BACKGROUND: Locally advanced and metastatic Barrett's carcinomas account for the majority of this tumor entity at the time of diagnosis.
  • METHODS: A total of 178 patients with Barrett's carcinoma who underwent multimodal therapy with resection of the tumor were reviewed.
  • CONCLUSIONS: This is the first study to compare the outcome of a modern multimodal therapy concept in patients with metastatic Barrett's carcinoma in comparison to patients with the locally advanced form of the disease.
  • [MeSH-major] Adenocarcinoma / secondary. Adenocarcinoma / therapy. Antineoplastic Agents / therapeutic use. Barrett Esophagus / therapy. Esophageal Neoplasms / pathology. Esophageal Neoplasms / therapy. Esophagectomy

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  • [ISSN] 0364-2313
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  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
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91. 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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  • [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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92. 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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93. 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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94. Heurgué A, Bouché O, Higuero T, Lagarde S, Diebold MD, Thiéfin G, Cadiot G: [Poorly differentiated endocrine carcinoma and adenocarcinoma on Barrett's esophagus]. Gastroenterol Clin Biol; 2005 May;29(5):613-4
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  • [Title] [Poorly differentiated endocrine carcinoma and adenocarcinoma on Barrett's esophagus].
  • [Transliterated title] Carcinome endocrine peu différencié de l'oesophage associé à un adénocarcinome sur muqueuse de Barrett.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Barrett Esophagus / complications. Barrett Esophagus / pathology. Endocrine Gland Neoplasms / etiology. Endocrine Gland Neoplasms / pathology. Esophageal Neoplasms / etiology. Esophageal Neoplasms / pathology

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  • (PMID = 15980763.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; Letter
  • [Publication-country] France
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95. 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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96. Ling FC, Baldus SE, Khochfar J, Xi H, Neiss S, Brabender J, Metzger R, Drebber U, Dienes HP, Bollschweiler E, Hoelscher AH, Schneider PM: Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer. Histopathology; 2007 Jan;50(2):203-9
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  • [Title] Association of COX-2 expression with corresponding active and chronic inflammatory reactions in Barrett's metaplasia and progression to cancer.
  • 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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97. 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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98. 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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99. 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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100. Gossner L: The role of endoscopic resection and ablation therapy for early lesions. Best Pract Res Clin Gastroenterol; 2006;20(5):867-76
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  • Endoscopic resection (ER) has gained more and more importance in the treatment of early neoplastic lesions in Barrett's oesophagus over the last few years.
  • A recently described method of EMR comprises the circumferential mucosal incision with a special type of needle-knife and subsequent en-bloc resection following prior injection under the lesions, but only a few patients with early Barrett's cancer were treated so far.
  • EMR should be considered as the treatment of choice for high-grade intraepithelial neoplasia (HGIN) and mucosal adenocarcinoma in Barrett's oesophagus.
  • Curative endoscopic treatment of early neoplastic lesions in Barrett's oesophagus should only be carried out in centers with a high-volume.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Catheter Ablation. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagoscopy
  • [MeSH-minor] Barrett Esophagus / complications. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Carcinoma in Situ / etiology. Carcinoma in Situ / pathology. Carcinoma in Situ / surgery. Humans. Neoplasm Staging

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  • (PMID = 16997166.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 33
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