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1. Chen X, Zhu LR, Hou XH: The characteristics of Barrett's esophagus: an analysis of 4120 cases in China. Dis Esophagus; 2009;22(4):348-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The characteristics of Barrett's esophagus: an analysis of 4120 cases in China.
  • Our objective was to investigate the endoscopic and clinico-pathological characteristics in patients with Barrett's esophagus (BE) in China.
  • Using the terms 'Barrett's esophagus' and 'Barrett's esophagus, China' as key words, literatures published in Chinese and English journals were searched in Chinese data banks, as well as PubMed and ISI Web of Science from 1989 to 2007.
  • The island-type BE was predominant (56.80%), and the occurrence of BE with special intestinal metaplasia (SIM) was 36.58%, but SIM was more common in tongue-type BE than island-type and circumferential-type BE (both P < 0.001), as well as in long segment BE (LSBE) than in short segment BE (SSBE) (P < 0.001).
  • The incidence of adenocarcinoma was 0.61% patient-years of total follow up.
  • In China, the endoscopic prevalence of BE is lower, but the average age of diagnosis is younger; a high proportion of H. pylori infection is found in patients with BE, and about half of the patients have no typical symptoms of GERD; the tongue-type BE and the LSBE are apt to SIM.

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  • [ErratumIn] Dis Esophagus. 2009;22(5):475. Hou, Kiao-Hua [corrected to Hou, Xiao-hua]
  • (PMID = 19191861.001).
  • [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] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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2. Kim CW, Lee BI, Kim BW, Kim JI, Park SH, Kim JK, Han SW, Jung IS, Sun HS, Lee AW, Lee KY: [Immunohistochemical expression of the p53 and Ki-67 proteins in Barrett's esophagus in Korea]. Korean J Gastroenterol; 2005 Sep;46(3):189-95
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  • [Title] [Immunohistochemical expression of the p53 and Ki-67 proteins in Barrett's esophagus in Korea].
  • BACKGROUND/AIMS: Barrett's esophagus is a premalignant lesion of the esophagus in which normal squamous epithelium is replaced by intestinalized columnar epithelium.
  • In Korea, adenocarcinoma associated with Barrett's esophagus is rare compared with that of Western country.
  • The purpose of this study was to investigate the immunohistochemical expression of p53 and Ki-67 in Barrett's esophagus which had predictive value for cancer risk in Korea.
  • METHODS: Ninety five patients (43 male and 52 female, median age 44, range 21-75) who have been suspected to have Barrett's esophagus by endoscopic assessment were enrolled in this study.
  • Alcian blue (pH 2.5) and high ion diamine stain for the evaluation of specialized intestinal metaplasia (SIM) and immunohistochemical stain for p53 and Ki-67 were done.
  • RESULTS: 57.9% (55/95) of biopsies from the columnar lined esophagus showed SIM, but no dysplasia.
  • 56.4% (31/55) of Barrett's esophagus showed sulfomucin positive colonic metaplasia.
  • The p53 expression was observed in 10.9% (6/55) of the patients of Barrett's esophagus and all of them showed colonic metaplasia.
  • CONCLUSIONS: In Korea, 10.9% of Barrett's esophagus had p53 mutation and moreover all of them had colonic metaplasia.
  • Consequently, we expect that these patients have high risk of developing dysplasia and adenocarcinoma and need careful follow-up.
  • [MeSH-major] Barrett Esophagus / metabolism. Ki-67 Antigen / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / genetics. Adult. Aged. Esophageal Neoplasms / etiology. Esophageal Neoplasms / genetics. Female. Humans. Immunohistochemistry. Male. Middle Aged. Risk Factors

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  • (PMID = 16179838.001).
  • [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)
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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3. Tantau M, Mosteanu O, Pop T, Tantau A, Mester G: Endoscopic therapy of Barrett's esophagus and esophageal adenocarcinoma. J Gastrointestin Liver Dis; 2010 Jun;19(2):213-7
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  • [Title] Endoscopic therapy of Barrett's esophagus and esophageal adenocarcinoma.
  • The normal squamous esophageal epithelium reacts as a chronic inflammation to the severe gastro-esophageal reflux.
  • Esophagitis will progress to Barrett metaplasia in 10% of patients who would be of minor clinical interest if it then did not advance to low, high grade dysplasia and invasive carcinoma.
  • The rise of esophageal adenocarcinoma (EAC) incidence surpasses any other cancer, including melanoma, lymphoma and small cell lung cancer.
  • A multimodal approach of Barrett's esophagus with high grade dysplasia is required, including endoscopic mucosal resection, photodynamic therapy and thermal ablation.
  • The correction of the malignant esophageal obstruction improves the symptomatology and life quality, but not survival.
  • [MeSH-major] Adenocarcinoma / therapy. Barrett Esophagus / therapy. Esophageal Neoplasms / therapy. Esophagoscopy

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  • (PMID = 20593060.001).
  • [ISSN] 1841-8724
  • [Journal-full-title] Journal of gastrointestinal and liver diseases : JGLD
  • [ISO-abbreviation] J Gastrointestin Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Romania
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4. Chen X, Qin R, Liu B, Ma Y, Su Y, Yang CS, Glickman JN, Odze RD, Shaheen NJ: Multilayered epithelium in a rat model and human Barrett's esophagus: similar expression patterns of transcription factors and differentiation markers. BMC Gastroenterol; 2008 Jan 11;8:1
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  • [Title] Multilayered epithelium in a rat model and human Barrett's esophagus: similar expression patterns of transcription factors and differentiation markers.
  • BACKGROUND: In rats, esophagogastroduodenal anastomosis (EGDA) without concomitant chemical carcinogen treatment leads to gastroesophageal reflux disease, multilayered epithelium (MLE, a presumed precursor in intestinal metaplasia), columnar-lined esophagus, dysplasia, and esophageal adenocarcinoma.
  • Previously we have shown that columnar-lined esophagus in EGDA rats resembled human Barrett's esophagus (BE) in its morphology, mucin features and expression of differentiation markers (Lab. Invest. 2004;84:753-765).
  • Tissue sections were immunohistochemically stained for a variety of transcription factors and differentiation markers of esophageal squamous epithelium and intestinal columnar epithelium.
  • As expected, both rat and human squamous epithelium, but not intestinal metaplasia, expressed squamous transcription factors and differentiation markers (p63, Sox2, CK14 and CK4) in all cases.
  • Both rat and human intestinal metaplasia, but not squamous epithelium, expressed intestinal transcription factors and differentiation markers (Cdx2, GATA4, HNF1alpha, villin and Muc2) in all cases.

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  • (PMID = 18190713.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA75683; United States / NIDDK NIH HHS / DK / R21 DK063650; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / U56 CA092077; United States / NIDDK NIH HHS / DK / DK63650; United States / NCI NIH HHS / CA / CA092077; United States / NCI NIH HHS / CA / R01 CA075683
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2267197
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5. Bai JG, Lv Y, Dang CX: Adenocarcinoma of the Esophagogastric Junction in China according to Siewert's classification. Jpn J Clin Oncol; 2006 Jun;36(6):364-7
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  • [Title] Adenocarcinoma of the Esophagogastric Junction in China according to Siewert's classification.
  • On the basis of the classification, this study aims to research into the clinicopathological characteristics and surgical modes of adenocarcinoma of the esophagogastric junction in China.
  • METHODS: The study reviewed the data of the distal esophageal cancer, the cancer of cardia and the proximal gastric cancer at the First Hospital of Xi'an Jiaotong University from January 1995 to December 1999.
  • RESULTS: Among the 203 patients, there were 29 patients with adenocarcinoma of the distal esophagus (Type I); 80 patients with true carcinoma of cardia (Type II); and 94 patients with subcardial carcinoma (Type III).
  • [MeSH-major] Adenocarcinoma / classification. Esophageal Neoplasms / classification. Esophagectomy. Esophagogastric Junction. Lymph Node Excision. Stomach Neoplasms / classification
  • [MeSH-minor] Barrett Esophagus / pathology. Cardia. China / epidemiology. Female. Gastrectomy. Gastric Mucosa / pathology. Humans. Lymph Nodes / pathology. Male. Metaplasia. Middle Aged. Morbidity. Postoperative Complications / etiology. Survival Rate

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  • (PMID = 16766566.001).
  • [ISSN] 0368-2811
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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6. Takubo K, Vieth M, Aida J, Sawabe M, Kumagai Y, Hoshihara Y, Arai T: Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia. Digestion; 2009;80(4):248-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia.
  • METHODS: Here we discuss four such important differences: the definition of the esophagogastric junction (EGJ), the possible precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus (BE), and the histologic criteria for mucosal adenocarcinoma.
  • If an area of columnar-lined esophagus (CLE) is only partially involved by intestinal metaplasia, then the latter cannot always be demonstrated in biopsy specimens.
  • Therefore, we do not think that a definition of BE as CLE with histologic intestinal metaplasia is practical.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Gastroenterology / standards. Precancerous Conditions / diagnosis. Terminology as Topic
  • [MeSH-minor] Esophagogastric Junction / pathology. Esophagoscopy. Gastroscopy. Humans. Stomach Neoplasms / diagnosis


7. Hao J, Liu B, Yang CS, Chen X: Gastroesophageal reflux leads to esophageal cancer in a surgical model with mice. BMC Gastroenterol; 2009 Jul 23;9:59
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastroesophageal reflux leads to esophageal cancer in a surgical model with mice.
  • BACKGROUND: Esophago-gastroduodenal anastomosis with rats mimics the development of human Barrett's esophagus and esophageal adenocarcinoma by introducing mixed reflux of gastric and duodenal contents into the esophagus.
  • Therefore, a mouse model of esophageal adenocarcinoma is needed.
  • RESULTS: At week 20, we observed metaplasia in wild-type mice (5%, 1/20) and p53A135V mice (5.3%, 1/19).
  • At week 40, metaplasia was found in wild-type mice (16.2%, 6/37), p53A135V mice (4.8%, 2/42), and wild-type mice also receiving gastrectomy and iron (6.7%, 1/15).
  • Esophageal squamous cell carcinoma developed in INK4a/Arf+/- mice (7.1%, 1/14), and wild-type mice receiving gastrectomy and iron (21.4%, 3/14).
  • None of these mice developed esophageal adenocarcinoma.
  • CONCLUSION: Surgically induced gastroesophageal reflux produced esophageal squamous cell carcinoma, but not esophageal adenocarcinoma, in mice.
  • Dominant negative p53 mutation, heterozygous loss of INK4a/Arf, antacid treatment, iron supplementation, or gastrectomy failed to promote esophageal adenocarcinoma in these mice.
  • Further studies are needed in order to develop a mouse model of esophageal adenocarcinoma.

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  • (PMID = 19627616.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / R01 CA75683; United States / NCI NIH HHS / CA / R03 CA125804; United States / NCI NIH HHS / CA / U56 CA092077
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Tumor Suppressor Protein p53; E1UOL152H7 / Iron; KG60484QX9 / Omeprazole
  • [Other-IDs] NLM/ PMC2723127
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8. Punia RS, Arya S, Mohan H, Duseja A, Bal A: Spectrum of clinico-pathological changes in Barrett oesophagus. J Assoc Physicians India; 2006 Mar;54:187-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: Barrett oesophagus is replacement of squamous epithelium to specialised intestinal metaplasia.
  • It is associated with an increased risk for adenocarcinoma which develops through dysplasia.
  • Associated dysplasia was not seen in any of the case, while one case showed associated adenocarcinoma.
  • There is a paucity of patients with pure dysplasia in Barrett metaplasia.
  • Despite the fact that there are a number of patients presenting with Barrett esophagus and carcinoma, very few patients present with dysplasia, indicating that Barrett oesophagus is a silent disease presenting later as a carcinoma.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / pathology. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology
  • [MeSH-minor] Adult. Age Factors. Aged. Biopsy. Esophagoscopy. Female. Humans. India. Male. Metaplasia. Middle Aged. Retrospective Studies. Sex Factors. Staining and Labeling

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  • (PMID = 16800342.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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9. Finley JC, Reid BJ, Odze RD, Sanchez CA, Galipeau P, Li X, Self SG, Gollahon KA, Blount PL, Rabinovitch PS: Chromosomal instability in Barrett's esophagus is related to telomere shortening. Cancer Epidemiol Biomarkers Prev; 2006 Aug;15(8):1451-7
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  • [Title] Chromosomal instability in Barrett's esophagus is related to telomere shortening.
  • Barrett's esophagus is a useful model for the study of carcinogenesis, as the metaplastic columnar epithelium that replaces squamous esophageal epithelium is at elevated risk for development of adenocarcinoma.
  • We examined telomere length and chromosomal instability (CIN) in Barrett's esophagus biopsies using fluorescence in situ hybridization.
  • To study CIN, we selected centromere and locus-specific arm probes to chromosomes 17/17p (p53), 11/11q (cyclin D1), and 9/9p (p16 INK4A), loci reported to be involved in early stages of Barrett's esophagus neoplasia.
  • Telomere shortening was observed in Barrett's esophagus epithelium at all histologic grades, whereas CIN was highest in biopsies with dysplastic changes; there was, however, considerable heterogeneity between patients in each variable.
  • We conclude that CIN is related to telomere shortening in Barrett's esophagus but varies by chromosome.
  • Because telomere shortening and CIN are early events in Barrett's esophagus neoplastic progression and are highly variable among patients, it will be important to determine whether they identify a subset of patients that is at risk for more rapid neoplastic evolution.
  • [MeSH-major] Barrett Esophagus / genetics. Chromosomal Instability. Esophageal Neoplasms / genetics. Telomere / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Aged. Anaphase / genetics. Chromosomes, Human / genetics. Esophagus / metabolism. Flow Cytometry. Gastroesophageal Reflux / genetics. Gastroesophageal Reflux / pathology. Humans. In Situ Hybridization, Fluorescence / methods. Metaplasia / genetics. Middle Aged

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  • (PMID = 16896031.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA91955; United States / NIA NIH HHS / AG / P30AG13280; United States / NCI NIH HHS / CA / T32CA09437
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
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10. Fitzgerald RC: Barrett's oesophagus and oesophageal adenocarcinoma: how does acid interfere with cell proliferation and differentiation? Gut; 2005 Mar;54 Suppl 1:i21-6
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  • [Title] Barrett's oesophagus and oesophageal adenocarcinoma: how does acid interfere with cell proliferation and differentiation?
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Cell Differentiation / physiology. Cell Division / physiology. Cyclooxygenase 2. Esophagus / pathology. Gastroesophageal Reflux / complications. Humans. Hydrogen-Ion Concentration. Membrane Proteins. Metaplasia / etiology. Metaplasia / pathology. Prostaglandin-Endoperoxide Synthases / analysis

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  • (PMID = 15711004.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 57
  • [Other-IDs] NLM/ PMC1867792
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11. Mashimo H, Wagh MS, Goyal RK: Surveillance and screening for Barrett esophagus and adenocarcinoma. J Clin Gastroenterol; 2005 Apr;39(4 Suppl 2):S33-41
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  • [Title] Surveillance and screening for Barrett esophagus and adenocarcinoma.
  • Current recommendations for screening and surveillance of Barrett esophagus and related lesions are based on recent guidelines by the Practice Parameters Committee of the American College of Gastroenterology.
  • There is strong rationale for vigorous initial testing to document the baseline status and identify early adenocarcinoma, and for surveillance of high-grade dysplasia.
  • However, recommendations for surveillance of low-grade dysplasia and specialized intestinal metaplasia without dysplasia are largely opinion statements not well supported by objective data.
  • Recommendations for screening and surveillance are not evidence-based and unlikely to alter national mortality from esophageal adenocarcinoma.
  • Current recommendations are limited by inconsistent endoscopic findings and sampling errors, inconsistent histologic diagnoses of Barrett esophagus and dysplasia, and our poor understanding of the natural history of various histologic lesions.
  • Effective screening programs depend on development of simple, inexpensive, and reliable methods to identify the small group of patients truly at high risk for adenocarcinoma for endoscopic screening.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis
  • [MeSH-minor] Biopsy. Esophagoscopy. Esophagus / pathology. Humans. Mass Screening / methods. Population Surveillance. Practice Guidelines as Topic. Risk Factors. Time Factors

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  • (PMID = 15758657.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK031092; United States / NIDDK NIH HHS / DK / DK62867
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Number-of-references] 52
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12. Lord RV, Brabender J, Wickramasinghe K, DeMeester SR, Holscher A, Schneider PM, Danenberg PV, DeMeester TR: Increased CDX2 and decreased PITX1 homeobox gene expression in Barrett's esophagus and Barrett's-associated adenocarcinoma. Surgery; 2005 Nov;138(5):924-31
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  • [Title] Increased CDX2 and decreased PITX1 homeobox gene expression in Barrett's esophagus and Barrett's-associated adenocarcinoma.
  • Forced expression of Cdx2 alone in the murine stomach results in gastric intestinal metaplasia (IM).
  • METHODS: CDX2 and PITX1 messenger RNA (mRNA) expression levels, relative to the control gene beta-actin, were measured by reverse transcription-polymerase chain reaction in specimens of Barrett's IM (n = 21), dysplasia (n = 18), adenocarcinoma (n = 20), and matching normal squamous esophagus tissues (n = 39) collected from 19 patients with Barrett's esophagus and 20 patients with esophageal adenocarcinoma.
  • CDX2 protein expression was assessed by immunohistochemistry in specimens of normal squamous esophagus (n = 13), IM (n = 10), dysplasia (n = 8,) and adenocarcinoma (n = 5).
  • RESULTS: The median relative CDX2 mRNA expression was approximately 200 times higher in Barrett's esophagus tissues (0.83) than in matching normal squamous esophagus (0.004) in the patients with Barrett's esophagus (P < .001).
  • The mRNA expression in cancer tissues (0.49) was also higher than in matching normal squamous esophagus specimens (0.009, P < .001).
  • There was no significant difference between the mRNA expression levels in Barrett's esophagus and adenocarcinoma.
  • There was no CDX2 protein expression in normal squamous esophagus, but moderate to strong protein expression was seen in all Barrett's tissues and in a majority of the dysplasia and adenocarcinoma cells.
  • Relative median PITX1 mRNA expression was decreased in Barrett's esophagus (8.02 for all specimens), compared with normal esophagus specimens (47.46 for all specimens, P < .001), and was further reduced in cancer specimens (2.21), compared with either Barrett's esophagus or normal esophagus (both P < .001).
  • CONCLUSIONS: CDX2 mRNA and CDX2 protein expression are upregulated in Barrett's IM tissues, compared with normal squamous esophagus, and remain elevated in dysplasia and adenocarcinoma tissues.
  • In contrast, PITX1 mRNA expression is decreased in Barrett's esophagus, compared with matching normal squamous esophagus specimens, and is further decreased in Barrett's-associated cancer.
  • These descriptive findings suggest a possible role for these genes in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Homeodomain Proteins / genetics. Paired Box Transcription Factors / genetics

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  • (PMID = 16291394.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Paired Box Transcription Factors; 0 / RNA, Messenger; 0 / homeobox protein PITX1
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13. Pohl H, Sonnenberg A, Strobel S, Eckardt A, Rösch T: Endoscopic versus surgical therapy for early cancer in Barrett's esophagus: a decision analysis. Gastrointest Endosc; 2009 Oct;70(4):623-31
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  • [Title] Endoscopic versus surgical therapy for early cancer in Barrett's esophagus: a decision analysis.
  • BACKGROUND: Esophagectomy for early esophageal adenocarcinoma is associated with increased operative mortality and morbidity, but possibly a decreased recurrence rate compared with endoscopic therapy when using EMR and radiofrequency ablation.
  • OBJECTIVE: To compare the cost-effectiveness of esophagectomy and endoscopic therapy in the treatment of early esophageal adenocarcinoma.
  • Varying the recurrence rates of cancer or Barrett's esophagus metaplasia after endoscopic therapy did not change the overall outcome.
  • CONCLUSIONS: Endoscopic therapy for early Barrett's esophagus adenocarcinoma is more effective and less expensive than esophagectomy.
  • Even in early esophageal adenocarcinoma with submucosal invasion, endoscopic therapy is a cost-effective alternative to esophagectomy, especially in patients with a high operative risk.
  • [MeSH-major] Adenocarcinoma / therapy. Barrett Esophagus / therapy. Decision Support Techniques. Esophageal Neoplasms / therapy. Esophagectomy / economics. Esophagoscopy / economics

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  • [CommentIn] Gastrointest Endosc. 2009 Oct;70(4):632-4 [19788980.001]
  • (PMID = 19394011.001).
  • [ISSN] 1097-6779
  • [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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14. Inci K, Edebo A, Olbe L, Casselbrant A: Expression of protease-activated-receptor 2 (PAR-2) in human esophageal mucosa. Scand J Gastroenterol; 2009;44(6):664-71
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  • [Title] Expression of protease-activated-receptor 2 (PAR-2) in human esophageal mucosa.
  • The aim of the present study was to examine the presence and the position of the PAR-2 receptor in human esophageal mucosa in different subgroups of GERD.
  • MATERIAL AND METHODS: Distal biopsies taken from healthy controls, patients with erosive reflux disease (ERD), patients with specialized intestinal metaplasia (SIM) and adenocarcinoma were analyzed for the PAR-2 receptor with reverse-transcription polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry.
  • Immunohistochemistry revealed distinct staining for the PAR-2 receptor in the luminal part of the esophageal epithelium.
  • CONCLUSIONS: The localization of the PAR-2 receptor indicates that the receptor can be cleaved and activated by trypsin in duodenogastric esophageal refluxate.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Esophagus / metabolism. Gastroesophageal Reflux / genetics. Mucous Membrane / metabolism. Receptor, PAR-2 / biosynthesis
  • [MeSH-minor] Female. Gene Expression. Humans. Male. Metaplasia / genetics. Metaplasia / pathology. Middle Aged

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  • (PMID = 19263271.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Receptor, PAR-2
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15. Baczewska-Mazurkiewicz D, Rydzewska G, Milewski J, Durlik M, Lao M, Rydzewski A: Magnification chromoendoscopy in comparison to standard chromoendoscopy for detection of intestinal metaplasia in renal transplant recipients. Adv Med Sci; 2006;51:115-8
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  • [Title] Magnification chromoendoscopy in comparison to standard chromoendoscopy for detection of intestinal metaplasia in renal transplant recipients.
  • Intestinal metaplasia is a feature of atrophic gastritis whereas the diagnosis of Barrett's esophagus is based on histological demonstration of specialized metaplasia.
  • Both conditions are associated with increased risk of adenocarcinoma.
  • The aim of the present study was to assess whether magnification endoscopy improves the diagnostic accuracy of intestinal metaplasia in stomach and in esophagus.
  • MATERIAL AND METHODS: In this non-randomized, feasibility study thirty one (12 women and 19 men) renal transplant recipients, with a mean age of 44.0 years were evaluated for the presence of intestinal metaplasia.
  • The presence of gastritis and intestinal metaplasia was classified according to modified updated Sydney classification.
  • RESULTS: Of 31 patients, 16 patients had endoscopic and histopathological evidence of gastric intestinal metaplasia, and standard endoscopy with methylene blue staining was sufficient for diagnosis (15 from 16).
  • Magnification endoscopy allowed identification of 6 patients with specialized intestinal metaplasia in Barrett's esophagus, which would be otherwise missed.
  • CONCLUSIONS: In this study diagnostic accuracy of standard endoscopy for identification of intestinal metaplasia in the stomach was not improved by the use of magnification endoscopy, but the latter was an accurate method of predicting specialized intestinal metaplasia in Barrett's esophagus.
  • [MeSH-major] Endoscopy, Gastrointestinal / methods. Intestinal Diseases / diagnosis. Intestines / pathology. Kidney Transplantation
  • [MeSH-minor] Adult. Barrett Esophagus / pathology. Feasibility Studies. Female. Humans. Intestinal Neoplasms / diagnosis. Male. Metaplasia / diagnosis. Middle Aged. Reproducibility of Results. Sensitivity and Specificity

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  • (PMID = 17357289.001).
  • [ISSN] 1896-1126
  • [Journal-full-title] Advances in medical sciences
  • [ISO-abbreviation] Adv Med Sci
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Poland
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16. Downs-Kelly E, Mendelin JE, Bennett AE, Castilla E, Henricks WH, Schoenfield L, Skacel M, Yerian L, Rice TW, Rybicki LA, Bronner MP, Goldblum JR: Poor interobserver agreement in the distinction of high-grade dysplasia and adenocarcinoma in pretreatment Barrett's esophagus biopsies. Am J Gastroenterol; 2008 Sep;103(9):2333-40; quiz 2341
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  • [Title] Poor interobserver agreement in the distinction of high-grade dysplasia and adenocarcinoma in pretreatment Barrett's esophagus biopsies.
  • OBJECTIVE: Grading Barrett's dysplasia at the lower end of the metaplasia-dysplasia spectrum (negative, indefinite, and low-grade dysplasia) suffers from poor interobserver agreement, even among gastrointestinal pathologists.
  • Data evaluating interobserver agreement in Barrett's mucosal biopsies with changes at the upper end of the dysplasia spectrum (high-grade dysplasia, intramucosal, and submucosal adenocarcinoma) have not been published.
  • METHODS: All study pathologists agreed upon the histologic criteria distinguishing four diagnostic categories, including high-grade dysplasia; high-grade dysplasia with marked distortion of glandular architecture, cannot exclude intramucosal adenocarcinoma; intramucosal adenocarcinoma; and submucosally invasive adenocarcinoma.
  • The histologic criteria were used to independently review preresection biopsies from 163 consecutive Barrett's esophagus patients with at least high-grade dysplasia who ultimately underwent esophagectomy.
  • Agreement for high-grade dysplasia was moderate (kappa= 0.47), while agreement for high-grade dysplasia with marked architectural distortion, cannot exclude intramucosal adenocarcinoma and intramucosal adenocarcinoma were only fair (kappa= 0.21 and 0.30, respectively) and agreement for submucosal adenocarcinoma was poor (kappa= 0.14).
  • CONCLUSIONS: The overall poor interobserver reproducibility among gastrointestinal pathologists who see a high volume of Barrett's cases calls into question treatment regimens based on the assumption that high-grade dysplasia, intramucosal adenocarcinoma, and submucosal adenocarcinoma can reliably be distinguished in biopsy specimens.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Precancerous Conditions / pathology


17. Béchade D, Blondon H, Sekkach Y, Desramé J, Algayres JP: [Review of the association between obesity and gastroesophageal reflux and its complications]. Gastroenterol Clin Biol; 2009 Mar;33(3):155-66
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  • Esophageal adenocarcinoma and its precursor Barrett's esophagus are increasing in incidence in western populations.
  • Studies about Barrett's esophagus in obese patients have emphasised the role of central adiposity as a stronger risk factor than BMI in the development of specialized intestinal metaplasia and subsequently esophagus adenocarcinoma.
  • Except cardiovascular diseases, type 2 diabetes and non alcoholic steatohepatitis, abdominal obesity and metabolic syndrome are responsible of an increase of prevalence of esophageal adenocarcinoma, but also other cancer sites.
  • [MeSH-minor] Adenocarcinoma / etiology. Esophageal Neoplasms / etiology. Esophagitis, Peptic / etiology. Humans

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  • (PMID = 19250782.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 143
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18. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • [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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19. Thomas T, Singh R, Ragunath K: Trimodal imaging-assisted endoscopic mucosal resection of early Barrett's neoplasia. Surg Endosc; 2009 Jul;23(7):1609-13
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  • Trimodal imaging endoscopy is useful in identifying early neoplasia in Barrett's esophagus.
  • RESULTS: Sixteen patients were included: 13 patients had high-grade intraepithelial neoplasia (HGIN); 3 patients had intramucosal carcinoma (IMC); (8 males, median age, 69.5 (range, 50-77) years with Barrett's esophagus (interquartile range (IQR), 2-5 cm; median length, 3 cm).
  • Four of 16 patients (18%; all with pre-EMR HGIN) were considered to have incomplete EMR (deep margins involved), but operative histology showed only Barrett's metaplasia in 2 (histological false positive) and IMC in 1.
  • CONCLUSIONS: Trimodal imaging endoscopy is a feasible alternative to chromoendoscopy to identify inconspicuous neoplasia and assist EMR of early neoplasia in Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / pathology. Carcinoma in Situ / surgery. Esophageal Neoplasms / surgery. Esophagoscopy / methods. Fluorometry / methods. Video-Assisted Surgery / methods

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  • (PMID = 19296171.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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20. Deviere J: Barrett's oesophagus: the new endoscopic modalities have a future. Gut; 2005 Mar;54 Suppl 1:i33-7
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  • Barrett's oesophagus is defined as the replacement of squamous oesophageal epithelium by intestinal metaplasia in the distal oesophagus.
  • GORD is essential for the development of Barrett's oesophagus.1 Intestinal metaplasia is a premalignant lesion that may further develop into dysplasia and lead to adenocarcinoma of the oesophagus.
  • Patients with Barrett's oesophagus have a 2-25% risk of developing mild to severe dysplasia and a 2-5% risk of having adenocarcinoma: 30-150 times higher than the risk in the general population.
  • Forty to fifty per cent of Barrett's oesophagus patients with severe dysplasia would present adenocarcinoma within 5 years.
  • [MeSH-major] Barrett Esophagus / surgery
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma / surgery. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagoscopy / methods. Esophagus / pathology. Esophagus / surgery. Humans. Metaplasia / surgery. Mucous Membrane / pathology. Mucous Membrane / surgery. Photochemotherapy / methods. Postoperative Complications / etiology. Precancerous Conditions / drug therapy. Precancerous Conditions / pathology. Precancerous Conditions / surgery

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  • (PMID = 15711006.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 50
  • [Other-IDs] NLM/ PMC1867791
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21. 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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22. Zhao J, Chang AC, Li C, Shedden KA, Thomas DG, Misek DE, Manoharan AP, Giordano TJ, Beer DG, Lubman DM: Comparative proteomics analysis of Barrett metaplasia and esophageal adenocarcinoma using two-dimensional liquid mass mapping. Mol Cell Proteomics; 2007 Jun;6(6):987-99
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  • [Title] Comparative proteomics analysis of Barrett metaplasia and esophageal adenocarcinoma using two-dimensional liquid mass mapping.
  • Esophageal adenocarcinoma, currently the seventh leading cause of cancer-related death, has been associated with the presence of Barrett metaplasia.
  • The malignant potential of Barrett metaplasia is evidenced by ultimate progression of this condition to invasive adenocarcinoma.
  • We utilized liquid phase separation of proteins with chromatofocusing in the first dimension and nonporous reverse phase HPLC in the second dimension followed by ESI-TOF mass spectrometry to identify proteins differentially expressed in six Barrett metaplasia samples as compared with six esophageal adenocarcinoma samples; all six Barrett samples were obtained from the identical six patients from whom we obtained the esophageal adenocarcinoma tissue.
  • Among the proteins that were identified, Rho GDP dissociation inhibitor 2, alpha-enolase, Lamin A/C, and nucleoside-diphosphate kinase A were demonstrated to be up-regulated in both mRNA and protein expression in esophageal adenocarcinomas relative to Barrett metaplasia.
  • The cellular expression patterns were verified in both esophageal adenocarcinomas and in Barrett metaplasia by immunohistochemistry.
  • These differentially expressed proteins may have utility as useful candidate markers of esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Proteomics. Spectrometry, Mass, Electrospray Ionization

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  • (PMID = 16829691.001).
  • [ISSN] 1535-9476
  • [Journal-full-title] Molecular & cellular proteomics : MCP
  • [ISO-abbreviation] Mol. Cell Proteomics
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA71606; United States / NCI NIH HHS / CA / R01CA10010; United States / NCI NIH HHS / CA / R01CA90503; United States / NIGMS NIH HHS / GM / R01GM49500
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger
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23. Segat D, Cassaro M, Dazzo E, Cavallini L, Romualdi C, Salvador R, Vitale MP, Vitiello L, Fassan M, Rugge M, Zaninotto G, Ancona E, Baroni MD: Pericentriolar material analyses in normal esophageal mucosa, Barrett's metaplasia and adenocarcinoma. Histol Histopathol; 2010 05;25(5):551-60
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  • [Title] Pericentriolar material analyses in normal esophageal mucosa, Barrett's metaplasia and adenocarcinoma.
  • Barrett's esophagus metaplasia is a pre-cancerous condition caused by chronic esophagitis.
  • Chromosomal instability (CIN) is common in Barrett's cells: therefore, we investigated the possible presence of centrosomal aberrations (a main cause of CIN) by centrosomal protein immunostaining in paraffined esophageal samples of patients who developed a Barrett's adenocarcinoma.
  • In most (55%) patients, alterations of the pericentriolar material (PCM) signals were evident and consistently marked the transition between normal epithelium to metaplasia.
  • The alterations could even be found in adjacent native squamous epithelium, Barrett's mucosa and submucosal gland cells, as well as in the basal/epibasal layers of the mucosa and submucosal gland duct, which are the regions hosting esophageal stem and progenitor cells.
  • These findings strongly support the hypothesis that the three esophageal histotypes (one being pathological) can have a common progenitor.
  • Importantly, PCM altered signals in Barrett's mucosa and their apparent evolution in successive histopathological steps were correlated to adenocarcinoma aggressiveness, suggesting PCM as a possible prognostic marker for tumor relapse.
  • Extending our observations in a prospective study might help in the development of new prevention protocols for adenocarcinoma patients.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Centrosome / metabolism. Esophageal Neoplasms / metabolism. Esophagus / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens / metabolism. Chromosomal Instability. Female. Humans. Immunohistochemistry. Male. Metaplasia. Middle Aged. Models, Biological. Mucous Membrane / anatomy & histology. Mucous Membrane / metabolism. Mucous Membrane / pathology. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Prognosis. Tubulin / metabolism

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  • (PMID = 20238294.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antigens; 0 / Tubulin; 0 / pericentrin
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24. Bobryshev YV, Freeman AK, Botelho NK, Tran D, Levert-Mignon AJ, Lord RV: Expression of the putative stem cell marker Musashi-1 in Barrett's esophagus and esophageal adenocarcinoma. Dis Esophagus; 2010 Sep;23(7):580-9
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  • [Title] Expression of the putative stem cell marker Musashi-1 in Barrett's esophagus and esophageal adenocarcinoma.
  • Cancer stem cells have been identified in several solid tumors, but stem cells in normal human esophagus or in Barrett's esophagus or adenocarcinoma have not been reported.
  • The present study investigated whether Musashi-1 is expressed in the esophagus and its relation to immune inflammation of the mucosa in Barrett's esophagus and esophageal adenocarcinoma.
  • A total of 41 esophageal tissue specimens from 41 patients were studied.
  • Of these, 15 were esophageal adenocarcinoma, 17 were Barrett's esophagus (10 intestinal metaplasia and 7 dysplasia), and 9 were normal squamous esophagus tissue specimens from patients without esophageal pathology.
  • Immunohistochemistry demonstrated the presence of small numbers of Musashi-1+ cells scattered in the connective tissue stroma and within the epithelium in cardiac-type glands in biopsies from patients without Barrett's esophagus.
  • Musashi-1 expression was present in Barrett's intestinal metaplasia and in dysplastic Barrett's in which the majority of epithelial cells in individual glands expressed this antigen.
  • Expression of Musashi-1 was highest in esophageal adenocarcinoma, where it was most intense in glands that displayed features of early stages of adenocarcinoma formation.
  • In contrast, Musashi-1 staining level was weaker in glands that displayed features of advanced adenocarcinoma.
  • Musashi-1 mRNA expression levels were significantly higher in esophageal adenocarcinoma than in normal esophagus or Barrett's esophagus tissues.
  • Dendritic cell-specific intercellular molecule-3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) mRNA expression levels were significantly increased in both Barrett's tissues and adenocarcinoma tissues.
  • Expression of the putative stem cell marker Musashi-1 is absent in normal squamous epithelium, weak in esophageal cardiac-type glands and Barrett's esophagus, and markedly increased in adenocarcinoma, especially in glands displaying features of early cancer development.
  • Musashi-1 expressing cells may be significant in the etiology of Barrett's esophagus and adenocarcinoma, and perhaps even a cell of origin for this disease.
  • We speculate that immune inflammation occurring in Barrett's esophagus alters the mucosal microenvironment in a manner which is favorable to the activation of dormant stem cells.

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  • [Copyright] © 2010 Copyright the Authors. Journal compilation © 2010, Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus.
  • (PMID = 20459440.001).
  • [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 / MSI1 protein, human; 0 / Nerve Tissue Proteins; 0 / RNA-Binding Proteins
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25. Rossi M, Barreca M, de Bortoli N, Renzi C, Santi S, Gennai A, Bellini M, Costa F, Conio M, Marchi S: Efficacy of Nissen fundoplication versus medical therapy in the regression of low-grade dysplasia in patients with Barrett esophagus: a prospective study. Ann Surg; 2006 Jan;243(1):58-63
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  • [Title] Efficacy of Nissen fundoplication versus medical therapy in the regression of low-grade dysplasia in patients with Barrett esophagus: a prospective study.
  • OBJECTIVE: The aim of this study is to compare the effect of medical and surgical treatment on the history of patients with Barrett esophagus (BE) and histologic evidence of low-grade dysplasia (LGD).
  • It is considered a major risk factor for esophageal adenocarcinoma, which may develop through stages from nondysplastic metaplasia to dysplasia (LGD and high-grade dysplasia).
  • CONCLUSION: The results of our study suggest that surgical treatment may be more effective than medical therapy to modify the natural history of LGD in patients with BE, perhaps because it not only controls acid but also biliopancreatic reflux into the esophagus.
  • [MeSH-major] Barrett Esophagus / pathology. Barrett Esophagus / therapy. Enzyme Inhibitors / therapeutic use. Fundoplication. Omeprazole / therapeutic use
  • [MeSH-minor] Adult. Aged. Disease Progression. Esophagus / pathology. Female. Humans. Laparoscopy. Male. Middle Aged. Prospective Studies. Proton Pump Inhibitors. Remission Induction. Treatment Outcome

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  • (PMID = 16371737.001).
  • [ISSN] 0003-4932
  • [Journal-full-title] Annals of surgery
  • [ISO-abbreviation] Ann. Surg.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Proton Pump Inhibitors; KG60484QX9 / Omeprazole
  • [Other-IDs] NLM/ PMC1449954
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26. Lopes CV, Pereira-Lima JC, Hartmann AA, Tonelotto E, Salgado K: [Does the criterium of positivity for the immunohistochemical analysis of p53 in the confirmation of Barrett's dysplasia make any difference?]. Arq Gastroenterol; 2005 Oct-Dec;42(4):233-8
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  • BACKGROUND: Barrett's esophagus is the most serious complication of the gastroesophageal reflux disease and presents a malignant potential.
  • The expression of the tumoral marker p53 increases with the dysplasia-adenocarcinoma sequence.
  • AIMS: To evaluate the p53 expression in Barrett's esophagus with or without dysplasia according to the two positive immunostaining criteria.
  • MATERIALS AND METHODS: The material was constituted by endoscopic biopsy specimens from 42 patients with Barrett's esophagus.
  • The diagnosis of dysplasia was confirmed by the agreement between three pathologists.
  • According to the two different p53 immunostaining criteria, the protein was detected in non-dysplastic Barrett's metaplasia, respectively, in 5 (13.9%) and 14 (38.9%) patients.
  • CONCLUSIONS: In this group, p53 immunohistochemical expression, regardless of positive criteria take into account, was not useful for detecting dysplasia in Barrett's esophagus.
  • [MeSH-major] Barrett Esophagus / pathology. Precancerous Conditions / pathology. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16444378.001).
  • [ISSN] 0004-2803
  • [Journal-full-title] Arquivos de gastroenterologia
  • [ISO-abbreviation] Arq Gastroenterol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Tumor Suppressor Protein p53
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27. Ingravallo G, Dall'Olmo L, Segat D, Fassan M, Mescoli C, Dazzo E, Castoro C, Polimeno L, Rizzetto C, Baroni MD, Zaninotto G, Ancona E, Rugge M: CDX2 hox gene product in a rat model of esophageal cancer. J Exp Clin Cancer Res; 2009;28:108
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  • [Title] CDX2 hox gene product in a rat model of esophageal cancer.
  • BACKGROUND: Barrett's mucosa is the precursor of esophageal adenocarcinoma.
  • Experimental models of longstanding esophageal reflux of duodenal-gastric contents may provide important information on the biological sequence of the Barrett's oncogenesis.
  • RESULTS: No Cdx2 expression was detected in either squamous epithelia of the proximal esophagus or squamous cell carcinomas.
  • De novo Cdx2 expression was consistently documented in the proliferative zone of the squamous epithelium close to reflux ulcers (Group A: 68%; Group B: 64%; Group C: 80%), multilayered epithelium and intestinal metaplasia (Group A: 9%; Group B: 41%; Group C: 60%), and esophageal adenocarcinomas (Group B: 36%; Group C: 35%).
  • CONCLUSION: De novo expression of Cdx2 is an early event in the spectrum of the lesions induced by experimental gastro-esophageal reflux and should be considered as a key step in the morphogenesis of esophageal adenocarcinoma.
  • [MeSH-major] Esophageal Neoplasms / genetics. Homeodomain Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. Barrett Esophagus / pathology. Disease Models, Animal. Esophagus / pathology. Gastroesophageal Reflux / pathology. Male. Rats. Rats, Wistar

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  • (PMID = 19664209.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cdx2 protein, rat; 0 / Homeodomain Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC3225830
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28. Sinn DH, Kim KM, Kim ER, Son HJ, Kim JJ, Rhee JC, Rhee PL: Development of Barrett's Esophagus Soon after Total Gastrectomy. Gut Liver; 2008 Jun;2(1):51-3
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  • [Title] Development of Barrett's Esophagus Soon after Total Gastrectomy.
  • The role of duodenal reflux and the time required for the development of Barrett's esophagus has remained controversial.
  • We report a case of Barrett's esophagus that developed 6 months after total gastrectomy.
  • A 76-year-old man diagnosed with gastric adenocarcinoma underwent a total gastrectomy and a Rouxen-Y esophagojejunostomy.
  • A biopsy specimen from the esophagus showed intestinal-type metaplasia of the columnar epithelium.
  • This case supports the development of Barrett's esophagus solely from duodenal reflux and after a relatively short time in this clinical setting.

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  • (PMID = 20485611.001).
  • [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/ PMC2871574
  • [Keywords] NOTNLM ; Barrett's esophagus / Gastrectomy
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29. Szentpáli K, Széll M, Paszt A, Wolfárd A, Dobozy A, Németh I, Tiszlavicz L, Iván L, Boros M: Simultaneous adeno- and squamous cell carcinoma with different phenotypic profiles in a rat model of chronic gastroesophageal reflux. Dis Esophagus; 2007;20(4):305-10
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  • The aim of our study was to investigate the incidence of duodeno-gastroesophageal reflux-induced malignant transformation in a series of duodeno-esophageal anastomosis operations in rats.
  • This surgical method provides a model for reflux-induced esophageal pathologies, without carcinogen administration.
  • Thirty weeks of duodeno-gastroesophageal reflux disease significantly increased the risk of the development of Barrett's esophagus, and reflux-induced esophageal adenocarcinoma formation was evident in four animals.
  • In one of these particular cases, a superficial squamous cell cancer was noted in close vicinity to the adenocarcinoma formation.
  • The specialized intestinal metaplasia and mucinous adenocarcinoma cells exhibited exclusively diffuse cox-2 positivity (90% of all glandular cells) and weak focal c-erbB2 (5%) staining, without cyclin D1 expression or p53 protein accumulation.
  • The most dramatic changes were observed in the level of expression of cyclin D1 (a 9.08-fold expression as compared with the non-treated esophagus samples), while the p53 and cox-2 gene expressions were increased by 1.61 and 2.45-fold, respectively, relative to the non-treated samples.


30. Lastraioli E, Taddei A, Messerini L, Comin CE, Festini M, Giannelli M, Tomezzoli A, Paglierani M, Mugnai G, De Manzoni G, Bechi P, Arcangeli A: hERG1 channels in human esophagus: evidence for their aberrant expression in the malignant progression of Barrett's esophagus. J Cell Physiol; 2006 Nov;209(2):398-404
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  • [Title] hERG1 channels in human esophagus: evidence for their aberrant expression in the malignant progression of Barrett's esophagus.
  • We investigated the expression of hERG1 K+ channels in the human upper gastrointestinal tract, focusing our attention on the lower esophagus.
  • In particular, we analyzed by both Reverse transcription and polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) endoscopic samples obtained from normal subjects, from patients suffering from gastroesophageal reflux, associated or not with esophagitis, and from patients affected by Barrett's esophagus (BE), that is, intestinal metaplasia.
  • None of the normal samples, nor those from patients with gastro-esophageal reflux symptoms and reflux esophagitis expressed the hERG1 protein.
  • Data here reported, support the hypothesis that hERG1 expression marks an early step of the progression of normality to cancer in the human esophagus through a metaplastic and dysplastic stage.
  • [MeSH-major] Barrett Esophagus / pathology. Esophagus / metabolism. Ether-A-Go-Go Potassium Channels / genetics. Ether-A-Go-Go Potassium Channels / metabolism
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Gene Expression Regulation. Humans. Male. Metaplasia. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16883575.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ether-A-Go-Go Potassium Channels; 0 / KCNH1 protein, human; 0 / RNA, Messenger
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31. Shaheen NJ, Peery AF, Overholt BF, Lightdale CJ, Chak A, Wang KK, Hawes RH, Fleischer DE, Goldblum JR, AIM Dysplasia Investigators: Biopsy depth after radiofrequency ablation of dysplastic Barrett's esophagus. Gastrointest Endosc; 2010 Sep;72(3):490-496.e1
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  • [Title] Biopsy depth after radiofrequency ablation of dysplastic Barrett's esophagus.
  • BACKGROUND: After endoscopic radiofrequency ablation (RFA) of dysplastic Barrett's esophagus (BE), endoscopic biopsy samples are obtained to assess response to therapy.
  • Almost 80% of all biopsy samples were adequate to evaluate for subsquamous intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Catheter Ablation / methods. Esophageal Neoplasms / pathology. Esophageal Neoplasms / surgery. Esophagoscopy. Postoperative Complications / pathology. Postoperative Complications / surgery. Precancerous Conditions / pathology. Precancerous Conditions / surgery
  • [MeSH-minor] Aged. Biopsy. Disease Progression. Esophagus / pathology. Female. Follow-Up Studies. Humans. Male. Metaplasia. Middle Aged. Predictive Value of Tests. Treatment Outcome

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  • [Copyright] Copyright 2010 American Society for Gastrointestinal Endoscopy. Published by Mosby, Inc. All rights reserved.
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  • (PMID = 20598302.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00282672
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007634-15; United States / NIDDK NIH HHS / DK / T32 DK 07634; United States / NIDDK NIH HHS / DK / P30 DK034987; United States / NIDDK NIH HHS / DK / IH P30 DK034987; United States / NIDDK NIH HHS / DK / T32 DK007634
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS289916; NLM/ PMC3093936
  • [Investigator] Shaheen NJ; Madanick RD; Galanko JA; Sharma P; Overholt BF; Wolfsen HC; Sampliner RE; Wang KK; Falk GW; Bronner MP; Goldblum JR; Bennett AE; Jobe BA; Eisen GM; Fennerty MB; Hunter JG; Fleischer DE; Sharma VK; Hawes RH; Hoffman BJ; Rothstein RI; Gordon SR; Mashimo H; Chang KJ; Muthusamy VR; Edmundowicz SA; Spechler SJ; Siddiqui AA; Souza RF; Infantolino A; Kimmey MB; Chak A; Lightdale CJ
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32. 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.

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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
  •  go-up   go-down


33. Peters CJ, Fitzgerald RC: Systematic review: the application of molecular pathogenesis to prevention and treatment of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2007 Jun 01;25(11):1253-69
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  • [Title] Systematic review: the application of molecular pathogenesis to prevention and treatment of oesophageal adenocarcinoma.
  • BACKGROUND: Oesophageal adenocarcinoma is an increasingly common cancer with a poor prognosis.
  • It develops in a stepwise progression from Barrett's metaplasia to dysplasia, and then adenocarcinoma followed by metastasis.
  • AIM: To outline the key molecular changes in oesophageal adenocarcinoma and to summarize the chemopreventative and therapeutic strategies proposed.
  • Search terms included: Barrett's (o)esophagus, intestinal metaplasia, (o)esophageal adenocarcinoma, molecular changes, genetic changes, pathogenesis, chemoprevention, therapeutic strategies and treatment.
  • RESULTS: A large number of molecular changes have been identified in the progression from Barrett's oesophagus to oesophageal adenocarcinoma although there does not appear to be an obligate order of events.
  • In established adenocarcinoma, targeted treatments under evaluation include receptor tyrosine kinase inhibitors of EGFR and cyclin-dependent kinase inhibitors, which may benefit a subgroup of patients.
  • CONCLUSIONS: Advances in molecular methodology have led to a greater understanding of the oesophageal adenocarcinoma pathways, which provides opportunities for chemoprevention and therapeutic strategies with a mechanistic basis.
  • [MeSH-major] Adenocarcinoma / prevention & control. Angiogenesis Inhibitors / therapeutic use. Anti-Inflammatory Agents / therapeutic use. Antioxidants / therapeutic use. Esophageal Neoplasms / prevention & control

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  • (PMID = 17509094.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Anti-Inflammatory Agents; 0 / Antioxidants
  • [Number-of-references] 149
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34. Lurje G, Vallbohmer D, Collet PH, Xi H, Baldus SE, Brabender J, Metzger R, Heitmann M, Neiss S, Drebber U, Holscher AH, Schneider PM: COX-2 mRNA expression is significantly increased in acid-exposed compared to nonexposed squamous epithelium in gastroesophageal reflux disease. J Gastrointest Surg; 2007 Sep;11(9):1105-11
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  • BACKGROUND: Little is known about the role of cyclooxygenase (COX)-2 in gastroesophageal reflux disease (GERD) and the development of Barrett's metaplasia.
  • The objectives of this study were to further analyze COX-2 mRNA expression in patients with GERD compared to Barrett's esophagus (BE) and Barrett's cancer (BC).
  • Also, 24-h pH monitoring was performed in all patients of the GERD study group and the DeMeester composite score was used to match COX-2 mRNA expression with the severity of acid exposure in the lower esophagus.
  • RESULTS: COX-2 mRNA is progressively upregulated within the metaplasia-dysplasia-adenocarcinoma (MDA) sequence (p = 0.001).
  • COX-2 levels of the squamous epithelium in the distal esophagus from patients with GERD and a pathologic mean DeMeester score (>14.72) were significantly higher than in patients with normal DeMeester scores (p = 0.01).
  • CONCLUSION: In summary our findings suggest that alterations in COX-2 mRNA expression occur independently of endoscopic or histologic signs of GERD in the acid-exposed squamous epithelium of the distal esophagus.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Cyclooxygenase 2 / metabolism. Esophageal Neoplasms / metabolism. Gastroesophageal Reflux / metabolism

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  • (PMID = 17619937.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 2
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35. Piazuelo E, Cebrián C, Escartín A, Jiménez P, Soteras F, Ortego J, Lanas A: Superoxide dismutase prevents development of adenocarcinoma in a rat model of Barrett's esophagus. World J Gastroenterol; 2005 Dec 21;11(47):7436-43
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  • [Title] Superoxide dismutase prevents development of adenocarcinoma in a rat model of Barrett's esophagus.
  • AIM: To test whether antioxidant treatment could prevent the progression of Barrett's esophagus to adenocarcinoma.
  • Rat's esophagus was assessed by histological analysis, superoxide anion and peroxinitrite generation, SOD levels and DNA oxidative damage.
  • RESULTS: All rats undergoing esophagojejunostomy developed extensive esophageal mucosal ulceration and inflammation by mo 4.
  • The process was associated with a progressive presence of intestinal metaplasia beyond the anastomotic area (9% 1st mo and 50% 4th mo) (94% at the anastomotic level) and adenocarcinoma (11% 1st mo and 60% 4th mo).
  • Exogenous administration of SOD decreased mucosal superoxide levels, increased mucosal SOD levels and reduced the risk of developing intestinal metaplasia beyond the anastomotic area (odds ratio = 0.326; 95%CI: 0.108-0.981; P = 0.046), and esophageal adenocarcinoma (odds ratio = 0.243; 95%CI: 0.073-0.804; P = 0.021).
  • CONCLUSION: Superoxide dismutase prevents the progression of esophagitis to Barrett's esophagus and adenocarcinoma in this rat model of gastrointestinal reflux, supporting a role of antioxidants in the chemoprevention of esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / drug therapy. Esophageal Neoplasms / prevention & control. Free Radical Scavengers / pharmacology. Superoxide Dismutase / pharmacology

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  • (PMID = 16437713.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Free Radical Scavengers; EC 1.15.1.1 / Superoxide Dismutase
  • [Other-IDs] NLM/ PMC4725177
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36. Bîrlă R, Losif C, Gîndea C, Hoară P, Constantinoiu S: [Treatment of the esophago-gastric junction adenocarcinoma]. Chirurgia (Bucur); 2008 Mar-Apr;103(2):143-53
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  • [Title] [Treatment of the esophago-gastric junction adenocarcinoma].
  • The aim of the work paper is to present the treatment methods of the esophago-gastric junction adenocarcinoma, (AC) based on our experience and literature data.
  • The later reveal many novelties about AC prophylaxis through Barrett's esophagus (BE) treatment, using proton pomp inhibitors or antireflux surgical procedures, the progress of the endoluminal ablative methods for intestinal metaplasia, as well as a new surgical approach for advances tumors based on Siewert classification.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagogastric Junction. Stomach Neoplasms / surgery

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  • (PMID = 18457092.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Romania
  • [Number-of-references] 43
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37. Gatenby P, Ramus J, Caygill C, Shepherd N, Winslet M, Watson A: Routinely diagnosed low-grade dysplasia in Barrett's oesophagus: a population-based study of natural history. Histopathology; 2009 Jun;54(7):814-9
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  • AIMS: To examine the natural history of columnar-lined oesophagus with routinely diagnosed low-grade dysplasia and ascertain the risk of oesophageal adenocarcinoma development.
  • One hundred and forty-four patients had biopsies prior to low-grade dysplasia diagnosis and 217 had follow-up biopsies after index low-grade dysplasia diagnosis.
  • In these patients the incidence of high-grade dysplasia and adenocarcinoma combined was 4.6% per annum and of adenocarcinoma alone was 2.7% per annum.
  • When prevalent cases were excluded (those occurring within 1 year of index low-grade dysplasia diagnosis), the annual incidence of high-grade dysplasia and adenocarcinoma combined was 2.2% and of adenocarcinoma alone was 1.4%.
  • The relative risk for adenocarcinoma development in low-grade dysplasia compared with non-dysplastic columnar-lined oesophagus was 2.871 (P = 0.002).
  • [MeSH-major] Barrett Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / etiology. Cohort Studies. Epithelium / pathology. Esophageal Neoplasms / etiology. Esophagoscopy. Follow-Up Studies. Great Britain. Humans. Metaplasia. Retrospective Studies. Risk Factors. Time Factors

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  • (PMID = 19635100.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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38. Martin RC, Liu Q, Wo JM, Ray MB, Li Y: Chemoprevention of carcinogenic progression to esophageal adenocarcinoma by the manganese superoxide dismutase supplementation. Clin Cancer Res; 2007 Sep 1;13(17):5176-82
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  • [Title] Chemoprevention of carcinogenic progression to esophageal adenocarcinoma by the manganese superoxide dismutase supplementation.
  • PURPOSE: Oxidative stress is related to the carcinogenic pathway of reflux esophagitis to Barrett's metaplasia to esophageal adenocarcinoma (EAC).
  • Recent studies have shown that a decreased manganese superoxide dismutase (MnSOD) level is associated with the increased incidences of Barrett's esophagus (BE) and EAC.
  • RESULTS: Severe esophagitis was seen in 100% of the EDA rats, and morphologic transformation within the esophageal epithelium was observed with intestinal metaplasia (40% of animals) and cancer (40% of animals) identified after 3 months.
  • CONCLUSION: MnTBAP protected rat esophageal epithelium from oxidative injury induced by EDA, and it could prevent the transformation of esophageal epithelial cell to BE to EAC by preservation of antioxidants.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anticarcinogenic Agents / administration & dosage. Antioxidants / therapeutic use. Esophageal Neoplasms / prevention & control. Metalloporphyrins / therapeutic use. Superoxide Dismutase / administration & dosage
  • [MeSH-minor] Animals. Apoptosis. Cell Proliferation. Deoxyguanosine / analogs & derivatives. Deoxyguanosine / analysis. Esophagus / pathology. Rats. Rats, Sprague-Dawley

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  • (PMID = 17785574.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Metalloporphyrins; 0 / manganese(III)-tetrakis(4-benzoic acid)porphyrin; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; EC 1.15.1.1 / Superoxide Dismutase; G9481N71RO / Deoxyguanosine
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39. Weston AP, Sharma P, Banerjee S, Mitreva D, Mathur S: Visible endoscopic and histologic changes in the cardia, before and after complete Barrett's esophagus ablation. Gastrointest Endosc; 2005 Apr;61(4):515-21
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  • [Title] Visible endoscopic and histologic changes in the cardia, before and after complete Barrett's esophagus ablation.
  • BACKGROUND: Adverse events associated with the thermal ablation of Barrett's esophagus (BE) include the generation of gastric mucosa buried beneath the neosquamous regrowth, and unrecognized development and growth of adenocarcinomas.
  • RESULTS: Before ablation, cardia nodules were noted in 3, cardia intestinal metaplasia (IM) in 7 (8.5%), and none harbored cardia dysplasia.
  • CONCLUSIONS: The pathophysiology of the abnormal cardia histology and the endoscopic lesions (nodules) is unclear, but endoscopic surveillance of not only the neosquamous epithelium but also the cardia should be considered after ablation, especially in those high-grade dysplasia and early adenocarcinoma BE patients.
  • [MeSH-major] Barrett Esophagus / pathology. Barrett Esophagus / therapy. Cardia / pathology. Esophageal Neoplasms / pathology. Esophageal Neoplasms / therapy
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / therapy. Aged. Electrocoagulation. Endoscopy, Gastrointestinal. Female. Humans. Laser Coagulation. Male. Middle Aged. Photochemotherapy. Prospective Studies

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  • [CommentIn] Gastrointest Endosc. 2005 Nov;62(5):820; author reply 820 [16246712.001]
  • (PMID = 15812402.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Sampliner RE, Camargo E, Prasad AR: Association of ablation of Barrett's esophagus with high grade dysplasia and adenocarcinoma of the gastric cardia. Dis Esophagus; 2006;19(4):277-9
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  • [Title] Association of ablation of Barrett's esophagus with high grade dysplasia and adenocarcinoma of the gastric cardia.
  • There has been increasing application of endoscopic ablation therapy for patients with high-grade dysplasia (HGD) and Barrett's esophagus (BE).
  • Three cases are reported in which the patient developed adenocarcinoma of the gastric cardia after thermal ablation of HGD.
  • A definition of BE including endoscopic abnormality and intestinal metaplasia by biopsy was used.
  • Biopsies documented adenocarcinoma of the gastric cardia.
  • The development of adenocarcinoma of the cardia is unexpected.

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  • (PMID = 16866860.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] United States
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41. Long KB, Hornick JL: SOX2 is highly expressed in squamous cell carcinomas of the gastrointestinal tract. Hum Pathol; 2009 Dec;40(12):1768-73
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  • SOX2 is a high-mobility group box embryonic stem cell transcription factor that is expressed in the developing foregut and normal gastric epithelium and is downregulated in intestinal metaplasia of the stomach and esophagus.
  • In addition, SOX2 colocalizes with p63 in the basal layer and plays a critical role in the maintenance of the stratified squamous epithelium of the esophagus.
  • The purpose of this study was to determine whether SOX2 is differentially expressed in squamous cell carcinomas versus adenocarcinomas of the esophagus and rectum/anal canal and to compare its expression to p63, cytokeratin 5/6, and CDX2.
  • In total, 93 tumors were evaluated: 26 esophageal squamous cell carcinomas, 23 esophageal adenocarcinomas, 21 squamous cell carcinomas of the anal canal, and 23 rectal adenocarcinomas.
  • SOX2 was expressed in 81% of esophageal squamous cell carcinomas and 91% of anal canal squamous cell carcinomas, compared to 13% and 17% of esophageal and rectal adenocarcinomas, respectively. p63 was expressed in 96% of esophageal squamous cell carcinomas and 100% of anal canal squamous cell carcinomas; the single squamous cell carcinoma negative for p63 was strongly positive for SOX2.
  • Cytokeratin 5/6 was expressed in most esophageal and anal canal squamous cell carcinomas, but was also positive in 43% of esophageal adenocarcinomas and 13% of rectal adenocarcinomas.
  • In summary, SOX2 is preferentially expressed in squamous cell carcinomas of the esophagus and anal canal compared to adenocarcinomas from these sites.
  • [MeSH-minor] Adenocarcinoma / metabolism. Diagnosis, Differential. Homeodomain Proteins / biosynthesis. Humans. Immunohistochemistry. Keratin-5 / biosynthesis. Keratin-6 / biosynthesis. Membrane Proteins / biosynthesis

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  • (PMID = 19716157.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / CKAP4 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-5; 0 / Keratin-6; 0 / Membrane Proteins; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors
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42. 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.
  • Recent advances in endoscopic diagnostic and therapeutic modalities demand additional proficiency in diagnosis and grading of dysplasia.
  • (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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43. Martinek J, Benes M, Brandtl P, Hucl T, Vasicek M, Voska L, Lanska V, Nosek V, Spicak J: Low incidence of adenocarcinoma and high-grade intraepithelial neoplasia in patients with Barrett's esophagus: a prospective cohort study. Endoscopy; 2008 Sep;40(9):711-6
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  • [Title] Low incidence of adenocarcinoma and high-grade intraepithelial neoplasia in patients with Barrett's esophagus: a prospective cohort study.
  • BACKGROUND AND STUDY AIMS: Barrett's esophagus is a premalignant condition.
  • The risk of developing high grade intraepithelial neoplasia (HGIN) or adenocarcinoma is currently a matter of debate.
  • The main aim of our study was to investigate the incidence of HGD and adenocarcinoma in a cohort of patients with Barrett's esophagus.
  • PATIENTS AND METHODS: In a prospective, cohort study, all patients had intestinal metaplasia and macroscopic evidence of short- or long-segment (< 3 cm or > or = 3 cm) Barrett's esophagus.
  • Simultaneous HGIN and adenocarcinoma were detected in two patients with long-segment Barrett's esophagus (1.5%; 2 and 6 years after the index endoscopy).
  • Our study shows an incidence of HGIN/adenocarcinoma of 1/350 patient-years.
  • Endoscopic regression of Barrett's esophagus was seen in 20.7% of patients.
  • CONCLUSION: The incidence of HGIN/adenocarcinoma is low in patients with adequately treated Barrett's esophagus.
  • The annual risk of developing HGIN/adenocarcinoma is 0.21% (1.6% in long-segment Barrett's esophagus).
  • [MeSH-major] Adenocarcinoma / epidemiology. Barrett Esophagus / epidemiology. Carcinoma in Situ / epidemiology

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  • (PMID = 18698534.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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44. Fouad YM, Makhlouf MM, Tawfik HM, el-Amin H, Ghany WA, el-Khayat HR: Barrett's esophagus: prevalence and risk factors in patients with chronic GERD in Upper Egypt. World J Gastroenterol; 2009 Jul 28;15(28):3511-5
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  • [Title] Barrett's esophagus: prevalence and risk factors in patients with chronic GERD in Upper Egypt.
  • AIM: To determine the prevalence and possible risk factors of Barrett's esophagus (BE) in patients with chronic gastroesophageal reflux disease (GERD) in El Minya and Assuit, Upper Egypt.
  • Endoscopic signs suggestive of columnar-lined esophagus (CLE) were defined as mucosal tongues or an upward shift of the squamocolumnar junction.
  • BE was diagnosed by pathological examination when specialized intestinal metaplasia was detected histologically in suspected CLE. pH was monitored in 40 patients.
  • Adenocarcinoma was detected in eight cases (0.8%), six of them in BE patients.
  • Patients with BE had significantly longer esophageal acid exposure time in the supine position, measured by pH monitoring.
  • [MeSH-major] Barrett Esophagus. Gastroesophageal Reflux
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Adult. Egypt / epidemiology. Esophageal Neoplasms / pathology. Esophageal Neoplasms / physiopathology. Female. Humans. Male. Middle Aged. Risk Factors. Young Adult

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  • (PMID = 19630106.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2715977
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45. Anandasabapathy S, Jhamb J, Davila M, Wei C, Morris J, Bresalier R: Clinical and endoscopic factors predict higher pathologic grades of Barrett dysplasia. Cancer; 2007 Feb 15;109(4):668-74
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  • BACKGROUND: Barrett esophagus is highly prevalent in the Western world; however, only a minority of affected individuals progress to esophageal adenocarcinoma.
  • Whereas many studies have examined risk factors for development of Barrett metaplasia, few data are available on risk factors for progression to neoplasia.
  • Identifying simple, reliable, clinical, and endoscopic predictors of high-grade dysplasia and adenocarcinoma would be helpful for risk stratification in screening and surveillance programs.
  • METHODS: Clinical, endoscopic, and histologic data were reviewed for patients with a new Barrett diagnosis between 2002 and 2005.
  • Patients were classified, by an expert gastrointestinal pathologist, as having intestinal metaplasia, indefinite-for-dysplasia, low-grade dysplasia, high-grade dysplasia, and esophageal adenocarcinoma.
  • RESULTS: In all, 109 patients (26 women, 83 men, mean age: 58.8) were newly diagnosed with Barrett metaplasia (n = 39), indefinite/low-grade dysplasia (n = 35), and high-grade dysplasia/esophageal adenocarcinoma (n = 35) over a 3-year period.
  • CONCLUSIONS: Male gender, longstanding gastroesophageal reflux disease, hiatal hernia size, and segment length are strongly associated with higher grades of dysplasia at index diagnosis.
  • These factors along with H. pylori status warrant further prospective evaluation as predictors of risk for development of high-grade dysplasia and esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagoscopy. Hernia, Hiatal / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Esophagus / pathology. Female. Gastroesophageal Reflux / epidemiology. Gastroesophageal Reflux / pathology. Humans. Male. Metaplasia / epidemiology. Metaplasia / pathology. Middle Aged. Precancerous Conditions / epidemiology. Precancerous Conditions / pathology. Prognosis. Risk Assessment

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  • (PMID = 17211862.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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46. Woodall CE, Li Y, Liu QH, Wo J, Martin RC: Chemoprevention of metaplasia initiation and carcinogenic progression to esophageal adenocarcinoma by resveratrol supplementation. Anticancer Drugs; 2009 Jul;20(6):437-43
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  • [Title] Chemoprevention of metaplasia initiation and carcinogenic progression to esophageal adenocarcinoma by resveratrol supplementation.
  • The effects of resveratrol on the initiation of Barrett's metaplasia and the carcinogenic progression to esophageal adenocarcinoma have not been evaluated.
  • The aim of this study was to evaluate the effects of resveratrol on the transition from reflux esophagitis to Barrett's metaplasia to dysplasia to esophageal adenocarcinoma in an established rat model.
  • The distal esophagus was preserved for blinded histopathological examination at the time of harvest.
  • Thirty-one animals in the 5-month resveratrol group showed a decreased severity of esophagitis (P<0.0001), incidence of intestinal metaplasia (P = 0.3567), and incidence of carcinoma (P = 0.4590) as compared with both the saline and nonoperated control groups.
  • In conclusion, morphological characteristics consistent with decreased esophagitis and incidences of metaplasia and esophageal adenocarcinoma were seen on histopathology in the resveratrol group.
  • Resveratrol resulted in a small diminution of the carcinogenic effects and progression to metaplasia, and further human studies are designed to explore the potential anticarcinogenic mechanism.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Esophageal Neoplasms / prevention & control. Esophagus / drug effects. Stilbenes / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Catalase / metabolism. Disease Models, Animal. Disease Progression. Glutathione / metabolism. Immunohistochemistry. In Situ Nick-End Labeling. Male. Metaplasia. Oxidative Stress / drug effects. Rats. Rats, Sprague-Dawley. Superoxide Dismutase / metabolism. Thiobarbituric Acid Reactive Substances / metabolism

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  • (PMID = 19398904.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Stilbenes; 0 / Thiobarbituric Acid Reactive Substances; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione; Q369O8926L / resveratrol
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47. Vakoc BJ, Shishko M, Yun SH, Oh WY, Suter MJ, Desjardins AE, Evans JA, Nishioka NS, Tearney GJ, Bouma BE: Comprehensive esophageal microscopy by using optical frequency-domain imaging (with video). Gastrointest Endosc; 2007 May;65(6):898-905
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  • [Title] Comprehensive esophageal microscopy by using optical frequency-domain imaging (with video).
  • BACKGROUND: Optical coherence tomography (OCT) has been used for high-resolution endoscopic imaging and diagnosis of specialized intestinal metaplasia, dysplasia, and intramucosal carcinoma of the esophagus.
  • However, the relatively slow image-acquisition rate of the present OCT systems inhibits wide-field imaging and limits the clinical utility of OCT for diagnostic imaging in patients with Barrett's esophagus.
  • OBJECTIVE: This study describes a new optical imaging technology, optical frequency-domain imaging (OFDI), derived from OCT, that enables comprehensive imaging of large esophageal segments with microscopic resolution.
  • The system was used in combination with a balloon-centering catheter to comprehensively image the distal esophagus in swine.
  • The 3-dimensional data sets were used to create cross-sectional microscopic images, as well as vascular maps of the esophagus.
  • CONCLUSIONS: Comprehensive microscopic imaging of the distal esophagus in vivo by using OFDI is feasible.
  • The unique capabilities of this technology for obtaining detailed information of tissue microstructure over large mucosal areas may open up new possibilities for improving the management of patients with Barrett's esophagus.

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  • (PMID = 17383652.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / R01 RR019768-03; United States / NCI NIH HHS / CA / R01 CA103769-03; United States / NCRR NIH HHS / RR / RR019768-03; United States / NCI NIH HHS / CA / CA103769-03; United States / NCI NIH HHS / CA / R33 CA110130-02; United States / NCI NIH HHS / CA / R33 CA110130; United States / NCI NIH HHS / CA / R01 CA103769; United States / NCRR NIH HHS / RR / R01 RR0119768; United States / NCI NIH HHS / CA / CA110130-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS118155; NLM/ PMC2705339
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48. Kimchi ET, Posner MC, Park JO, Darga TE, Kocherginsky M, Karrison T, Hart J, Smith KD, Mezhir JJ, Weichselbaum RR, Khodarev NN: Progression of Barrett's metaplasia to adenocarcinoma is associated with the suppression of the transcriptional programs of epidermal differentiation. Cancer Res; 2005 Apr 15;65(8):3146-54
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  • [Title] Progression of Barrett's metaplasia to adenocarcinoma is associated with the suppression of the transcriptional programs of epidermal differentiation.
  • We did expressional profiling on 24 paired samples of normal esophageal epithelium, Barrett's metaplasia, and esophageal adenocarcinomas.
  • Matching tissue samples representing the three different histologic types were obtained from each patient undergoing esophagectomy for adenocarcinoma.
  • Our analysis compared the molecular changes accompanying the transformation of normal squamous epithelium with Barrett's esophagus and adenocarcinoma in individual patients rather than in a random cohort.
  • We tested the hypothesis that expressional profiling may reveal gene sets that can be used as molecular markers of progression from normal esophageal epithelium to Barrett's esophagus and adenocarcinoma.
  • The final selection of 214 genes permitted the discrimination of differential gene expression of normal esophageal squamous epithelium, Barrett's esophagus, and adenocarcinoma using two-dimensional hierarchical clustering of selected genes.
  • These data indicate that transformation of Barrett's esophagus to adenocarcinoma is associated with suppression of the genes involved in epidermal differentiation, including genes in 1q21 loci and corresponding to the epidermal differentiation complex.
  • Correlation analysis of genes concordantly expressed in Barrett's esophagus and adenocarcinoma revealed 21 genes that represent potential genetic markers of disease progression and pharmacologic targets for treatment intervention.
  • PCR analysis of genes selected based on DNA array experiments revealed that estimation of the ratios of GATA6 to SPRR3 allows discrimination among normal esophageal epithelium, Barrett's dysplasia, and adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Cell Transformation, Neoplastic / genetics. Esophageal Neoplasms / genetics

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  • (PMID = 15833844.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 71933
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cornified Envelope Proline-Rich Proteins; 0 / DNA-Binding Proteins; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Proteins; 0 / SPRR3 protein, human; 0 / Transcription Factors
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49. Gatenby PA, Ramus JR, Caygill CP, Fitzgerald RC, Charlett A, Winslet MC, Watson A: The influence of symptom type and duration on the fate of the metaplastic columnar-lined Barrett's oesophagus. Aliment Pharmacol Ther; 2009 May 15;29(10):1096-105
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  • BACKGROUND: Prolonged gastro-oesophageal reflux resulting in columnar metaplasia of the oesophagus is the main risk factor for oesophageal adenocarcinoma.
  • AIM: To examine the duration of symptoms and associations of different symptoms with the development of columnar-lined oesophagus, dysplasia and adenocarcinoma.
  • High-grade dysplasia and adenocarcinoma were associated with dysphagia/odynophagia and weight loss.
  • Median duration from symptom onset to detection of columnar-lined oesophagus without intestinal metaplasia: 2.6 years, columnar-lined oesophagus with intestinal metaplasia: 5.0 years, indefinite changes for dysplasia: 19.3 years and low-grade dysplasia: 30.0 years.
  • One tenth of patients had developed high-grade dysplasia at 9.6 years and one tenth had developed adenocarcinoma at 13.8 years from symptom onset.
  • CONCLUSIONS: In patients with columnar-lined oesophagus, symptoms of dysphagia/odynophagia and nausea/vomiting were associated with a higher risk of development of dysplasia and adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / pathology. Deglutition Disorders / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Cohort Studies. Esophagus / pathology. Humans. Metaplasia / pathology. Risk Factors. Time Factors

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  • (PMID = 19222408.001).
  • [ISSN] 1365-2036
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105365007
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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50. Basseri B, Conklin JL, Mertens RB, Lo SK, Bellack GS, Shaye OA: Heterotopic gastric mucosa (inlet patch) in a patient with laryngopharyngeal reflux (LPR) and laryngeal carcinoma: a case report and review of literature. Dis Esophagus; 2009;22(4):E1-5
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  • The inlet patch is an area of heterotopic gastric mucosa most commonly located in the postcricoid portion of the esophagus at, or just below, the level of the upper esophageal sphincter.
  • Esophageal and supraesophageal symptoms are commonly associated with inlet patch, while esophageal adenocarcinoma rarely complicates it.
  • Laryngeal adenocarcinoma associated with inlet patch is not described in the literature.
  • Upper endoscopy at our institution revealed an upper esophageal stricture and a 1 cm inlet patch.
  • Biopsies showed columnar mucosa (predominantly gastric cardiac/fundic type) consistent with inlet patch, with focal intestinal metaplasia.
  • Dysphagia and regurgitation were improved by serial dilatations of the upper esophageal stricture.

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  • (PMID = 19473208.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 30
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51. Berndt U, Philipsen L, Bartsch S, Hu Y, Röcken C, Bertram W, Hämmerle M, Rösch T, Sturm A: Comparative Multi-Epitope-Ligand-Cartography reveals essential immunological alterations in Barrett's metaplasia and esophageal adenocarcinoma. Mol Cancer; 2010;9:177
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  • [Title] Comparative Multi-Epitope-Ligand-Cartography reveals essential immunological alterations in Barrett's metaplasia and esophageal adenocarcinoma.
  • BACKGROUND: Barrett's esophagus (BE) is caused by gastroesophageal reflux with consecutive mucosal inflammation, predisposing patients to the development of esophageal adenocarcinoma (EAC).
  • CONCLUSION: Proteomic analysis showed for the first time that proteins, which are critically involved in the mucosal immune system of the esophagus, are distinctly expressed in BE and EAC, whereas others are comparably altered in both diseases, suggesting that many pathogenic events might be shared by both diseases.
  • [MeSH-major] Adenocarcinoma / immunology. Barrett Esophagus / immunology. Epitopes / analysis. Esophageal Neoplasms / immunology

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  • (PMID = 20604962.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Epitopes; 0 / Ligands
  • [Other-IDs] NLM/ PMC2909181
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52. Li Y, Woodall C, Wo JM, Zheng H, Ng CK, Ray MB, Martin RC: The use of dynamic positron emission tomography imaging for evaluating the carcinogenic progression of intestinal metaplasia to esophageal adenocarcinoma. Cancer Invest; 2008 Apr-May;26(3):278-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The use of dynamic positron emission tomography imaging for evaluating the carcinogenic progression of intestinal metaplasia to esophageal adenocarcinoma.
  • BACKGROUND: In this study, we investigate the use of PET scanning in the carcinogenic progression of reflux esophagitis to Barrett's esophagus to high grade dysplasia to esophageal adenocarcinoma, and correlate the uptake levels of 18F-FDG related to histological changes, and the rates of proliferation and apoptosis.
  • The higher level of 18F-FDG uptake within esophageal epithelium was identified in intestinal metaplastic transformation and esophagoduodenal adenocarcinoma by histological examination.
  • CONCLUSIONS: Dynamic PET scanning represents a powerful tool in analyzing morphological carcinogenic transformation non-invasively in the esophagus.
  • 18F- FDG accumulation was a sensitive marker in reflux esophageal injury carcinogenic progression from intestinal metaplasia to EAC.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Cell Transformation, Neoplastic / pathology. Esophageal Neoplasms / pathology. Positron-Emission Tomography. Precancerous Conditions / pathology
  • [MeSH-minor] Animals. Disease Progression. Fluorodeoxyglucose F18. Immunohistochemistry. Metaplasia / pathology. Proliferating Cell Nuclear Antigen / biosynthesis. Rats. Rats, Sprague-Dawley

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  • (PMID = 18317969.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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53. 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.
  • In contrast, in those who have gastric metaplasia, tumor markers were negative.
  • [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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54. McElholm AR, McKnight AJ, Patterson CC, Johnston BT, Hardie LJ, Murray LJ, Finbar Group: A population-based study of IGF axis polymorphisms and the esophageal inflammation, metaplasia, adenocarcinoma sequence. Gastroenterology; 2010 Jul;139(1):204-12.e3
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  • [Title] A population-based study of IGF axis polymorphisms and the esophageal inflammation, metaplasia, adenocarcinoma sequence.
  • Few studies have examined the relationship between genetic variation of this axis and esophageal adenocarcinoma (EAC) or its precursors.
  • METHODS: In a population-based case-control study, we investigated the association of common polymorphisms of IGF-1, IGF-2, IGF-1 receptor, IGF binding protein-3, growth hormones (GH) 1 and GH2, and GH receptor with reflux esophagitis (RE), Barrett esophagus (BE), and EAC.
  • [MeSH-major] Adenocarcinoma / genetics. Esophageal Neoplasms / genetics. Esophagitis / genetics. Esophagus / pathology. Polymorphism, Single Nucleotide
  • [MeSH-minor] Female. Humans. Insulin-Like Growth Factor I / genetics. Male. Metaplasia. Middle Aged

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20403354.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I
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55. Bîrla R, Iosif C, Gîndea C, Hoară P, Constantinoiu S: [Clinical diagnosis of adenocarcinoma of the esophago-gastric junction]. Chirurgia (Bucur); 2007 Sep-Oct;102(5):511-20
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  • [Title] [Clinical diagnosis of adenocarcinoma of the esophago-gastric junction].
  • The aim of the work paper is to present the diagnosis methods of the esophago-gastric junction adenocarcinoma, based on our experience and literature data.
  • The later reveal many novelties about diagnosis means in Barrett's esophagus (BE), the definition and classification of BE, as well as the progress of the endoscopical, immunohistochemical and molecular methods in surveillance of the dysplasia arising in BE and in detection of intraepithelial neoplasia.
  • Early esophago-gastric junction (EGJ) adenocarcinoma (AC) is asymptomatic and its detection may be possible only through endoscopical surveillance.
  • For this reason is necessary to use some more precise methods for identifying intestinal metaplasia on distal esophagus, in patients with gastro-esophageal reflux disease, as well as for risk stratification in patients with dysplasia and for detection of intraepithelial neoplasia.
  • Applying modern methods of immunohistochemical and molecular diagnosis on endoscopical biopsy or esophageal brushing samples, the diagnosis rate for BE, dysplasia and early AC is improved and using the imaging means permits to obtain preoperative TNM staging and tumoral type (Siewert), with implications in therapeutical management.
  • [MeSH-major] Adenocarcinoma / diagnosis. Esophageal Neoplasms / diagnosis. Esophagogastric Junction. Stomach Neoplasms / diagnosis
  • [MeSH-minor] Barrett Esophagus / complications. Barrett Esophagus / pathology. Diagnosis, Differential. Humans. Neoplasm Staging. Risk Factors

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  • (PMID = 18018349.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Romania
  • [Number-of-references] 47
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56. Dumot JA, Vargo JJ 2nd, Falk GW, Frey L, Lopez R, Rice TW: An open-label, prospective trial of cryospray ablation for Barrett's esophagus high-grade dysplasia and early esophageal cancer in high-risk patients. Gastrointest Endosc; 2009 Oct;70(4):635-44
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  • [Title] An open-label, prospective trial of cryospray ablation for Barrett's esophagus high-grade dysplasia and early esophageal cancer in high-risk patients.
  • BACKGROUND: Endoscopic ablation of Barrett's esophagus (BE) is a treatment option for patients with high-grade dysplasia (HGD) and intramucosal carcinoma (IMCA).
  • MAIN OUTCOME MEASUREMENTS: Histologic response was defined by the worst pathology obtained at any level of the esophagus or gastric cardia in 1 of 3 categories:.
  • (1) incremental = absence of HGD and IMCA in all biopsy specimens, (2) partial = residual IMCA with absence of any dysplasia, and (3) complete = absence of any intestinal metaplasia or dysplasia.
  • [MeSH-major] Adenocarcinoma / therapy. Barrett Esophagus / therapy. Carcinoma, Squamous Cell / therapy. Cryosurgery / methods. Esophageal Neoplasms / therapy


57. 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.
  • 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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58. Musana AK, Resnick JM, Torbey CF, Mukesh BN, Greenlee RT: Barrett's esophagus: incidence and prevalence estimates in a rural Mid-Western population. Am J Gastroenterol; 2008 Mar;103(3):516-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Barrett's esophagus: incidence and prevalence estimates in a rural Mid-Western population.
  • BACKGROUND AND AIMS: Barrett's esophagus (BE) predisposes to adenocarcinoma of the esophagus and survival in esophageal adenocarcinoma is low.
  • Our objectives were to estimate the prevalence of diagnosed BE, estimate the annual incidence of initial diagnosis of BE, and characterize the demographics of patients diagnosed with BE.
  • All slides were retrieved and reviewed by a gastrointestinal pathologist to establish the presence of intestinal metaplasia and dysplasia.
  • Median age at diagnosis was 65.5 yr (range 17-94).
  • The incidence of an initial diagnosis of BE between 1996 and 2002 was 32.7 per 100,000 person-years (95% CI 27.1-38.2) and did not change significantly over the study period despite an increase in EGD rates.
  • At the initial diagnosis, 41.7% of the patients were on proton pump inhibitors.
  • CONCLUSION: The incidence of initial diagnosis of BE in a stable white population did not change significantly over a 7-yr period, despite an increase in EGD rates.
  • [MeSH-major] Barrett Esophagus / epidemiology

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  • (PMID = 17970839.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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59. Micev M, Cosić-Micev M: [Pathology and pathobiology of the oesophageal carcinoma]. Acta Chir Iugosl; 2010;57(2):15-26
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  • Although Barrett's esophagus is a precursor to esophageal adenocarcinoma and have a well described sequence of carcinogenesis: the Barrett's metaplasia-dysplasia-adenocarcinoma sequence, not all patients with this disorder require intensive surveillance.
  • [MeSH-major] Esophageal Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Barrett Esophagus / complications. Barrett Esophagus / pathology. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / pathology. Humans

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  • (PMID = 20954310.001).
  • [ISSN] 0354-950X
  • [Journal-full-title] Acta chirurgica Iugoslavica
  • [ISO-abbreviation] Acta Chir Iugosl
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Serbia
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60. Sharma P: Narrow band imaging in Barrett's esophagus. Clin Gastroenterol Hepatol; 2005 Jul;3(7 Suppl 1):S21-2
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  • [Title] Narrow band imaging in Barrett's esophagus.
  • Barrett's esophagus is the premalignant lesion for esophageal and esophagogastric junction adenocarcinoma.
  • Progression of Barrett's esophagus to dysplasia and cancer can occur, thus requiring endoscopy with random biopsy examinations.
  • Currently, the diagnosis of metaplastic and dysplastic mucosa within the esophagus requires endoscopy with biopsy examination of abnormal-appearing tissue.
  • The presence of intestinal metaplasia and dysplasia within the esophagus often is patchy, and our current practices of performing standard endoscopy with random biopsy examinations are inaccurate.
  • Narrow band imaging is among several tools used in the esophagus to improve detection of Barrett's esophagus and associated dysplasia.
  • [MeSH-major] Barrett Esophagus / pathology. Diagnostic Imaging. Endoscopy, Gastrointestinal / methods
  • [MeSH-minor] Equipment Design. Esophagus / pathology. Humans. Intestinal Mucosa / pathology. Video Recording

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  • (PMID = 16012989.001).
  • [ISSN] 1542-3565
  • [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; Review
  • [Publication-country] United States
  • [Number-of-references] 9
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61. 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.
  • 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).

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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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62. Vallböhmer D, Peters JH, Kuramochi H, Oh D, Yang D, Shimizu D, DeMeester SR, Hagen JA, Chandrasoma PT, Danenberg KD, Danenberg PV, DeMeester TR: Molecular determinants in targeted therapy for esophageal adenocarcinoma. Arch Surg; 2006 May;141(5):476-81; discussion 481-2
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  • [Title] Molecular determinants in targeted therapy for esophageal adenocarcinoma.
  • HYPOTHESIS: Cyclooxygenase 2 (COX-2), vascular endothelial growth factor (VEGF), and epidermal growth factor receptor (EGFR) are useful biological determinants in targeted therapy for esophageal adenocarcinoma.
  • PATIENTS: Sixteen patients with squamous mucosa and normal results of a pH study without mucosal injury (control group), 15 with Barrett esophagus (metaplasia group), and 44 with adenocarcinoma (carcinoma group).
  • After laser-capture microdissection, quantitative real-time polymerase chain reaction was used to measure gene expression across the spectrum of the metaplasia-dysplasia-carcinoma sequence.
  • RESULTS: Expression of both COX-2 and VEGF was significantly up-regulated in patients with metaplasia, dysplasia, and cancer compared with controls (P<.01).
  • Expression levels of both were significantly higher in cancer than in the metaplasia group (P<.05) and increased sequentially from metaplasia to dysplasia to cancer.
  • No change in expression levels of EGFR was seen in the histologic progression to esophageal adenocarcinoma.
  • CONCLUSION: Gene expression data suggest that pharmacologic inhibition of COX-2 and VEGF may be useful adjuncts in targeted therapy for esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Antineoplastic Agents / therapeutic use. Cyclooxygenase 2 / metabolism. Esophageal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Receptor, Epidermal Growth Factor / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16702519.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA84424-02
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / RNA, Neoplasm; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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63. Zhang T, Zhang F, Han Y, Gu Z, Zhou Y, Cheng Q, Zhu Y, Zhang C, Wang Y: A rat surgical model of esophageal metaplasia and adenocarcinoma-induced by mixed reflux of gastric acid and duodenal contents. Dig Dis Sci; 2007 Nov;52(11):3202-8
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  • [Title] A rat surgical model of esophageal metaplasia and adenocarcinoma-induced by mixed reflux of gastric acid and duodenal contents.
  • Herein we report a novel rat surgical model in which esophageal metaplasia and adenocarcinoma develop as complications of MR.
  • Severe inflammatory and proliferative changes, high prevalence of esophageal metaplasia (78%), and adenocarcinoma (50%) were observed in the lower part of the esophagus of rats 20 weeks after surgery.
  • The resulting esophageal lesions resembled those described in humans and supported a progression from intestinal metaplasia to dysplasia and, ultimately, esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / surgery. Duodenostomy / methods. Esophageal Neoplasms / surgery. Esophagostomy / methods. Esophagus / pathology. Gastroesophageal Reflux / complications. Jejunostomy / methods
  • [MeSH-minor] Animals. Disease Models, Animal. Disease Progression. Duodenum / secretion. Gastric Acid / secretion. Male. Metaplasia / etiology. Metaplasia / pathology. Metaplasia / surgery. Models, Anatomic. Rats. Rats, Sprague-Dawley

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  • (PMID = 17393326.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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64. Broder IA, Moroshek AA, Sigal EI, Burmistrov MV: [An integrated approach to diagnosis and treatment of Barrett's esophagus]. Eksp Klin Gastroenterol; 2009;(4):48-51
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  • [Title] [An integrated approach to diagnosis and treatment of Barrett's esophagus].
  • Barrett's oesophagus is a condition when the oesophagus adenocarcinoma risk increases.
  • [MeSH-major] Barrett Esophagus / diagnosis. Barrett Esophagus / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Algorithms. Biopsy. Combined Modality Therapy. Esophagoscopy. Esophagus / pathology. Esophagus / surgery. Female. Fundoplication. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / epidemiology. Gastroesophageal Reflux / pathology. Humans. Intestines / pathology. Laparoscopy. Laser Coagulation. Male. Metaplasia / epidemiology. Metaplasia / pathology. Middle Aged. Stomach / pathology. Treatment Outcome. Vagotomy, Proximal Gastric. Young Adult

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  • (PMID = 19960995.001).
  • [ISSN] 1682-8658
  • [Journal-full-title] Ėksperimental'nai︠a︡ i klinicheskai︠a︡ gastroėnterologii︠a︡ = Experimental & clinical gastroenterology
  • [ISO-abbreviation] Eksp Klin Gastroenterol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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65. Quaroni L, Casson AG: Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy. Analyst; 2009 Jun;134(6):1240-6
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  • [Title] Characterization of Barrett esophagus and esophageal adenocarcinoma by Fourier-transform infrared microscopy.
  • The objective of this exploratory study was to evaluate the feasibility of using Fourier-Transform Infrared (FTIR) spectromicroscopy to characterize formalin-fixed, paraffin-embedded human esophageal tissues.
  • Matched histologically normal esophageal squamous epithelium (NS), premalignant Barrett esophagus (BE), and primary esophageal adenocarcinoma (EADC) tissues, each defined according to strict clinicopathologic criteria, were obtained from patients who underwent esophageal resection.
  • Normal esophageal epithelia were characterized by a few well defined regions, mostly of large size (tens of contiguous pixels), which correlated with tissue histology, specifically the basal cell layer.
  • The technical feasibility of using FTIR to characterize formalin-fixed, paraffin-embedded human esophageal tissues demonstrates the potential of this technique to study archival human BE tissue specimens via automated screening techniques.
  • [MeSH-major] Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Spectroscopy, Fourier Transform Infrared / methods
  • [MeSH-minor] Adenocarcinoma / pathology. Cluster Analysis. Goblet Cells / cytology. Goblet Cells / pathology. Humans. Intestines / pathology. Light. Metaplasia / pathology. Microscopy. Synchrotrons

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  • (PMID = 19475154.001).
  • [ISSN] 1364-5528
  • [Journal-full-title] The Analyst
  • [ISO-abbreviation] Analyst
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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66. Helm J, Enkemann SA, Coppola D, Barthel JS, Kelley ST, Yeatman TJ: Dedifferentiation precedes invasion in the progression from Barrett's metaplasia to esophageal adenocarcinoma. Clin Cancer Res; 2005 Apr 1;11(7):2478-85
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  • [Title] Dedifferentiation precedes invasion in the progression from Barrett's metaplasia to esophageal adenocarcinoma.
  • PURPOSE: Adenocarcinoma arises in Barrett's esophagus by progression from metaplasia to cancer through grades of dysplasia.
  • EXPERIMENTAL DESIGN: Microarray analysis was used to obtain individual gene expression profiles from endoscopic biopsies of nine esophageal adenocarcinomas and the Barrett's epithelia from which three of the cancers had arisen.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Gene Expression Profiling
  • [MeSH-minor] Cell Differentiation / genetics. Cluster Analysis. Disease Progression. Epithelium / metabolism. Epithelium / pathology. Gene Expression Regulation, Neoplastic / genetics. Humans. Metaplasia / genetics. Models, Biological. Neoplasm Invasiveness / genetics. Oligonucleotide Array Sequence Analysis. Prognosis

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  • (PMID = 15814623.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24-CA85429-04; United States / NCI NIH HHS / CA / R01-CA098522-01; United States / NCI NIH HHS / CA / RZ1-CA101355-01-A1; United States / NCI NIH HHS / CA / U01-CA85052-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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67. Modiano N, Gerson LB: Barrett's esophagus: Incidence, etiology, pathophysiology, prevention and treatment. Ther Clin Risk Manag; 2007 Dec;3(6):1035-145
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  • [Title] Barrett's esophagus: Incidence, etiology, pathophysiology, prevention and treatment.
  • Barrett's esophagus is a metaplastic alteration of the normal esophageal epithelium that is detected on endoscopic examination and pathologically confirmed by the presence of intestinal metaplasia on biopsy.
  • Its major significance is as a predisposing factor for esophageal adenocarcinoma, which carries a high mortality rate and a rapidly growing incidence in the United States.
  • Detection of Barrett's esophagus allows for endoscopic surveillance in order to detect the potential development of dysplasia and early cancer before symptoms develop, and thereby significantly increases treatment options and may lower mortality from esophageal adenocarcinoma.
  • Much current work in the field is aimed at reducing the risk of progression from Barrett's esophagus to cancer, and in the identification of biomarkers that may predict progression towards cancer.
  • Barrett's esophagus is present in 10%-20% of patients with gastroesophageal reflux disease (GERD) and has also been detected in patients who deny classic GERD symptoms and are undergoing endoscopy for other indications.
  • We used an evidence-based approach to describe treatment options for patients with Barrett's esophagus.

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  • (PMID = 18516262.001).
  • [ISSN] 1176-6336
  • [Journal-full-title] Therapeutics and clinical risk management
  • [ISO-abbreviation] Ther Clin Risk Manag
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2387291
  • [Keywords] NOTNLM ; Barrett’s esophagus / endoscopic surveillance / esophageal adenocarcinoma / evidence-based approach
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68. Mehta S, Johnson IT, Rhodes M: Systematic review: the chemoprevention of oesophageal adenocarcinoma. Aliment Pharmacol Ther; 2005 Nov 1;22(9):759-68
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  • [Title] Systematic review: the chemoprevention of oesophageal adenocarcinoma.
  • The incidence of oesophageal adenocarcinoma is increasing in the UK faster than any other malignancy.
  • Despite its relatively poor prognosis and the limited success of existing treatments, there is enthusiasm that chemopreventive agents might be able to stem the transition from normal squamous epithelium to adenocarcinoma.
  • We discuss gastro-oesophageal reflux as the main risk factor for the development of Barrett's metaplasia, the only known precursor of oesophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / prevention & control. Esophageal Neoplasms / prevention & control
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Arachidonic Acid / metabolism. Barrett Esophagus / complications. Diet. Disease Progression. Fatty Acids, Omega-3 / metabolism. Gastroesophageal Reflux / complications. Gastroesophageal Reflux / drug therapy. Humans. Nitric Oxide / metabolism. Oxidative Stress / physiology. Proton Pump Inhibitors

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  • (PMID = 16225483.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Fatty Acids, Omega-3; 0 / Proton Pump Inhibitors; 27YG812J1I / Arachidonic Acid; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 96
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69. Maru DM, Singh RR, Hannah C, Albarracin CT, Li YX, Abraham R, Romans AM, Yao H, Luthra MG, Anandasabapathy S, Swisher SG, Hofstetter WL, Rashid A, Luthra R: MicroRNA-196a is a potential marker of progression during Barrett's metaplasia-dysplasia-invasive adenocarcinoma sequence in esophagus. Am J Pathol; 2009 May;174(5):1940-8
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  • [Title] MicroRNA-196a is a potential marker of progression during Barrett's metaplasia-dysplasia-invasive adenocarcinoma sequence in esophagus.
  • Barrett's esophagus (BE)/Barrett's metaplasia (BM) is a recognized precursor of esophageal adenocarcinoma (EA) with an intermediary stage of dysplasia.
  • The low yield and high cost of endoscopic screening of patients with BE underscores the need for novel biomarkers, such as microRNA (miRNA), which have emerged as important players in neoplastic progression for risk assessment of developing dysplasia/adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Esophagus / pathology. MicroRNAs / genetics
  • [MeSH-minor] Adult. Aged. Calgranulin B / genetics. Calgranulin B / metabolism. Cornified Envelope Proline-Rich Proteins / genetics. Cornified Envelope Proline-Rich Proteins / metabolism. DNA Primers / chemistry. Disease Progression. Female. Humans. Keratin-5 / genetics. Keratin-5 / metabolism. Male. Metaplasia. Middle Aged. Neoplasm Invasiveness. RNA, Messenger / genetics. RNA, Messenger / metabolism. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19342367.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calgranulin B; 0 / Cornified Envelope Proline-Rich Proteins; 0 / DNA Primers; 0 / KRT5 protein, human; 0 / Keratin-5; 0 / MIRN196 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / SPRR2C protein, human
  • [Other-IDs] NLM/ PMC2671281
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70. Hermann B, Li Y, Ray MB, Wo JM, Martin RC 2nd: Association of manganese superoxide dismutase expression with progression of carcinogenesis in Barrett esophagus. Arch Surg; 2005 Dec;140(12):1204-9; discussion 1209
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of manganese superoxide dismutase expression with progression of carcinogenesis in Barrett esophagus.
  • HYPOTHESIS: The down-regulation of manganese superoxide dismutase (MnSOD) expression plays a role in the progression of Barrett esophagus (BE).
  • DESIGN: An evaluation of 92 esophageal samples, including 17 patients with normal esophagus, 22 with intestinal metaplasia, 22 with indefinite/low-grade dysplasia, 16 with high-grade dysplasia (HGD), and 15 with esophageal adenocarcinoma were evaluated for MnSOD expression.
  • SETTING: Study subjects were recruited from the Barrett's Esophageal Registry at the University of Louisville, Louisville, KY.
  • The expression of MnSOD was found to be significantly reduced in samples with specialized intestinal metaplasia (mean score, 1.8), low-grade dysplasia (mean, 2.2), high-grade dysplasia (mean, 2.4), and esophageal adenocarcinoma (mean, 2.4) when compared with normal esophagus (mean, 3.9; P = .002).
  • Manganese superoxide dismutase expression was similar for esophageal adenocarcinoma and high-grade dysplasia.
  • CONCLUSIONS: Manganese superoxide dismutase expression is significantly reduced in patients with BE with high-grade dysplasia and esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Precancerous Conditions / metabolism. Superoxide Dismutase / metabolism

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  • (PMID = 16365243.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.15.1.1 / Superoxide Dismutase
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71. Schmidt MK, Meurer L, Volkweis BS, Edelweiss MI, Schirmer CC, Kruel CD, Gurski RR: c-Myc overexpression is strongly associated with metaplasia-dysplasia-adenocarcinoma sequence in the esophagus. Dis Esophagus; 2007;20(3):212-6
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  • [Title] c-Myc overexpression is strongly associated with metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.
  • We aim to determine the expression of the proto-oncogene c-Myc in patients with Barrett's esophagus (BE) and esophageal adenocarcinoma, and to evaluate the prevalence of such expression in relation to the metaplasia-dysplasia-adenocarcinoma sequence.
  • BE develops as a result of a severe esophageal mucosa injury from gastroesophageal reflux.
  • BE is a premalignant lesion and plays an important role in the development of esophageal adenocarcinoma.
  • The c-Myc protein expression was determined by immunohistochemical analysis in four different groups: 31 patients with normal tissue, 43 patients with BE without dysplasia, 11 patients with dysplasia in BE and 37 patients with esophageal adenocarcinoma.
  • The material was obtained from esophageal biopsies or the dissection of patient esophagectomy specimens.
  • Demographic and endoscopic data (sex, age, race and intestinal metaplasia extension), and morphologic and histopathologic tumor characteristics (deep tumor invasion, lymph node status, and tumor differentiation) were analyzed.
  • Overexpression of c-Myc was found in only 9.6% of normal tissue specimens, 37.2% of Barrett's esophagus, 45.5% of BE patients with dysplasia and 73% of adenocarcinoma samples, with significant statistical difference among these groups.
  • However, linear correlation of c-Myc overexpression along the metaplasia-dysplasia-adenocarcinoma sequence was observed.
  • This study demonstrates a significant increase in the expression of c-Myc in Barrett's esophagus, dysplasia and adenocarcinoma in relation to the control group, as well as a linear progression of this gene expression in this sequence.
  • These results point out the importance of this marker in the development of esophageal adenocarcinoma from BE.

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  • (PMID = 17509117.001).
  • [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
  • [Chemical-registry-number] 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc
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72. Guo M, House MG, Suzuki H, Ye Y, Brock MV, Lu F, Liu Z, Rustgi AK, Herman JG: Epigenetic silencing of CDX2 is a feature of squamous esophageal cancer. Int J Cancer; 2007 Sep 15;121(6):1219-26
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  • [Title] Epigenetic silencing of CDX2 is a feature of squamous esophageal cancer.
  • Mice heterozygously disrupted for CDX2 develop disorganized polypoid hamartomas with glandular epithelium and stratified squamous metaplasia resembling foregut mucosa.
  • Eleven of 17 squamous esophageal cancer cell lines lacked expression of CDX2 that was restored following treatment with 5-aza-2'-deoxycytidine, while all colorectal cancer cell lines expressed CDX2.
  • Methylation of CDX2 was rare in primary colorectal (1 of 44 tumors, 2%) and esophageal adenocarcinoma neoplasms (2 of 43 tumors, 5%), but was common in esophageal squamous carcinoma (24 of 45 tumors, 49%).
  • Using semi-quantitative RT-PCR, expression of CDX2 was found in low level in normal esophagus, at higher levels in primary adenocarcinoma of the esophagus, but not in primary squamous cancers of the esophagus.
  • Our results suggest that the inactivation of CDX2 in esophageal cancer associated with DNA methylation may be an important determinant of the squamous or non-adenomatous phenotype.
  • [MeSH-major] Adenocarcinoma / genetics. Cell Transformation, Neoplastic / genetics. Esophageal Neoplasms / genetics. Gene Silencing. Homeodomain Proteins / genetics. Neoplasms, Squamous Cell / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17534889.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84986
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / DNA, Neoplasm; 0 / Homeodomain Proteins; 0 / MUC2 protein, human; 0 / Muc2 protein, mouse; 0 / Mucin-2; 0 / Mucins; 0 / RNA, Small Interfering
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73. Yu C, Zhang X, Huang Q, Klein M, Goyal RK: High-fidelity DNA histograms in neoplastic progression in Barrett's esophagus. Lab Invest; 2007 May;87(5):466-72
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  • [Title] High-fidelity DNA histograms in neoplastic progression in Barrett's esophagus.
  • This study describes the high-fidelity DNA histograms in different stages of neoplastic progression to Barrett's adenocarcinoma (BAC).
  • One hundred and eighty-seven cases, including 34 normal gastrointestinal mucosa (control), 66 Barrett's-specialized intestinal metaplasia (SIM), 22 low-grade dysplasia (LGD), 22 high-grade dysplasia (HGD) and 43 BAC were investigated.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. DNA, Neoplasm / analysis. Esophageal Neoplasms / genetics. Ploidies. Precancerous Conditions / genetics

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  • (PMID = 17310216.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK62867
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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74. Sharma VK, Kim HJ, Das A, Dean P, DePetris G, Fleischer DE: A prospective pilot trial of ablation of Barrett's esophagus with low-grade dysplasia using stepwise circumferential and focal ablation (HALO system). Endoscopy; 2008 May;40(5):380-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A prospective pilot trial of ablation of Barrett's esophagus with low-grade dysplasia using stepwise circumferential and focal ablation (HALO system).
  • BACKGROUND AND STUDY AIMS: Yearly surveillance endoscopy is carried out for Barrett's esophagus with low-grade dysplasia (LGD) so that progression to high-grade dysplasia and adenocarcinoma can be detected at the earliest stage.
  • The aim of the study was to assess the long-term safety and effectiveness of circumferential ablation followed by focal ablation (HALO system) for eliminating Barrett's esophagus and LGD.
  • PATIENTS AND METHODS: Patients with 2 - 6 cm of Barrett's esophagus with histology demonstrating LGD on their last two sequential endoscopies over the previous 2 years and confirmed by two pathologists were enrolled in this prospective, single-center trial.
  • Circumferential ablation was carried out at baseline and at 4 months (if residual Barrett's esophagus present).
  • After 1 year, focal ablation was applied to any visible Barrett's esophagus or irregularity of the squamocolumnar junction.
  • Complete responses for dysplasia (CR-dysplasia) and intestinal metaplasia (CR-IM) at 2-year follow-up, with complete response defined as "all biopsies negative for dysplasia or intestinal metaplasia" were the main outcomes.
  • There were no strictures or buried intestinal metaplasia at follow-up.
  • CONCLUSION: A stepwise regimen of circumferential ablation followed by focal ablation appears to eradicate intestinal metaplasia (90 % CR-IM) and dysplasia (100 % CR-dysplasia) at 2-year follow-up in this trial, without stricture formation or buried intestinal metaplasia.
  • [MeSH-major] Barrett Esophagus / surgery. Catheter Ablation / instrumentation. Endoscopes, Gastrointestinal. Endoscopy, Digestive System

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  • (PMID = 18459074.001).
  • [ISSN] 1438-8812
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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75. Burjonrappa SC, Reddimasu S, Nawaz Z, Gao X, Sharma P, Loggie B: Mucin expression profile in Barrett's, dysplasia, adenocarcinoma sequence in the esophagus. Indian J Cancer; 2007 Jan-Mar;44(1):1-5
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  • [Title] Mucin expression profile in Barrett's, dysplasia, adenocarcinoma sequence in the esophagus.
  • BACKGROUND: The molecular events that accompany the progression to adenocarcinoma (ADC) of the esophagus are poorly understood.
  • AIM: The aim of this study was to establish a pattern for mucin (MUC) gene expression in the esophageal mucosa under normal and pathological conditions.
  • MATERIALS AND METHODS: Tissue samples were obtained from the archives of patients with histological evidence of Barrett's esophagus (BE) progressing to ADC.
  • MUC1 expression was upregulated (7/7) in progression to adenocarcinoma (P=0.008).
  • Upregulation of MUC2 reflects intestinal metaplasia in BE.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Esophagus / metabolism. Mucins / metabolism. Precancerous Conditions / metabolism
  • [MeSH-minor] Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Gene Expression Regulation, Neoplastic. Humans. Intestinal Neoplasms / metabolism. Intestinal Neoplasms / pathology. Metaplasia / metabolism. Metaplasia / pathology. Mucin 5AC. Mucin-1. Mucin-2. Mucin-6. Retrospective Studies

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  • (PMID = 17401217.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / MUC1 protein, human; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / MUC6 protein, human; 0 / Muc2 protein, mouse; 0 / Muc5ac protein, mouse; 0 / Muc6 protein, mouse; 0 / Mucin 5AC; 0 / Mucin-1; 0 / Mucin-2; 0 / Mucin-6; 0 / Mucins
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76. Modena SF, Meirelles LR, Araújo MR, Lopes LR, Andreollo NA: Role of nitrites in the genesis of adenocarcinoma associated with Barrett's esophagus. In Vivo; 2009 Nov-Dec;23(6):919-23
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  • [Title] Role of nitrites in the genesis of adenocarcinoma associated with Barrett's esophagus.
  • BACKGROUND: Barrett's esophagus (BE) is one of the complications of gastroesophageal reflux disease (GERD) and a premalignant condition.
  • It consists of a process of replacement of the squamous epithelium of the esophagus by intestinal columnar epithelium containing goblet cells, known as specialized intestinal metaplasia with goblet cells, and several factors have been related to its pathogenesis.
  • The objective of this study was to evaluate an experimental model of duodenogastroesophageal reflux and the effect of ingestion of sodium nitrite solution on the genesis of adenocarcinoma associated with Barrett's esophagus.
  • The Vienna classification for dysplasia and adenocarcinoma was used in the analysis of results.
  • RESULTS: After 42 weeks of observation, Barrett's esophagus was found in 26.3% (5/19) of the animals submitted to surgery that had not ingested nitrites compared to 72.3% (13/18) of the animals in the group submitted to surgery and given nitrites.
  • Six cases of adenocarcinoma (33.3%) were also found in this latter group.
  • Barrett's esophagus was not found in any of the animals that were not submitted to surgery.
  • CONCLUSION: The ingestion of sodium nitrite associated with duodenogastroesophageal reflux plays an important role in the genesis of adenocarcinoma associated with Barrett's esophagus.
  • [MeSH-major] Adenocarcinoma / chemically induced. Barrett Esophagus / chemically induced. Food Preservatives / toxicity. Sodium Nitrite / toxicity

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  • (PMID = 20023233.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Food Preservatives; M0KG633D4F / Sodium Nitrite
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77. Force SD, Miller DL: Esophageal radiofrequency ablation for the treatment of intestinal metaplasia, low grade dysplasia, and high grade dysplasia. Semin Thorac Cardiovasc Surg; 2008;20(4):305-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Esophageal radiofrequency ablation for the treatment of intestinal metaplasia, low grade dysplasia, and high grade dysplasia.
  • The presence of intestinal metaplasia (IM) of the esophagus is associated with an elevated risk for developing high-grade dysplasia and invasive adenocarcinoma.
  • Radiofrequency ablation (RFA) has more recently been studied to eradicate IM and dysplasia of the esophagus.
  • [MeSH-major] Barrett Esophagus / surgery. Catheter Ablation / methods. Precancerous Conditions / surgery
  • [MeSH-minor] Animals. Equipment Design. Esophagoscopy. Humans. Hyperplasia / pathology. Hyperplasia / surgery. Metaplasia / pathology. Metaplasia / surgery

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  • (PMID = 19251169.001).
  • [ISSN] 1043-0679
  • [Journal-full-title] Seminars in thoracic and cardiovascular surgery
  • [ISO-abbreviation] Semin. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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78. Ponsot P: [Barrett's oesophagus: endoscopic diagnosis and follow-up]. Ann Chir; 2006 Jan;131(1):3-6
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  • [Title] [Barrett's oesophagus: endoscopic diagnosis and follow-up].
  • Barrett's oesophagus (BO), or replacement of the squamous mucosa by a specialized intestinal metaplasia due to gastro-oesophageal reflux disease (GORD), predisposes to adenocarcinoma.
  • Macroscopic diagnosis of BO is sometimes difficult and, in case of doubt, endoscopy should be redone after a period of efficient anti-secretory treatment.
  • Diagnosis of BO is histological and should be confirmed by biopsies.
  • The incidence of adenocarcinoma is globally estimated at 0.5% patient by year of follow-up, and exists for both short and long BO.
  • Due to this low incidence, screening for BO is only justified in patients at high risk for adenocarcinoma (male gender, age > 50 ans, old GORD in a young patient).
  • Low-grade dysplasia (LGD) then high-grade dysplasia (HGD) precedes adenocarcinoma.
  • Histological diagnosis of LGD is difficult: the main cause of confusion is inflammation so diagnosis of LGD must be confirmed after a 3-month high-dose anti-secretory treatment.
  • Diagnosis of HGD is easier but multiple biopsies are needed to determine the focal or multifocal disposition of HGD.
  • [MeSH-major] Adenocarcinoma / etiology. Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal. Esophageal Neoplasms / etiology
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Gastroesophageal Reflux / complications. Humans. Prognosis. Risk Factors

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  • (PMID = 16376849.001).
  • [ISSN] 0003-3944
  • [Journal-full-title] Annales de chirurgie
  • [ISO-abbreviation] Ann Chir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 16
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79. Mabrut JY, Baulieux J: [Barrett's oesophagus: place of antireflux surgery]. Ann Chir; 2006 Mar;131(3):177-82
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  • The aim of this study was to review the literature about the effect of antireflux surgery on the metaplasia-dysplasia-adenocarcinoma sequence in patients with Barrett's oesophagus.
  • However, ineffective antireflux surgery expose to histologic progression to high-grade dysplasia or adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / surgery. Digestive System Surgical Procedures. Esophageal Neoplasms / prevention & control

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  • (PMID = 16527242.001).
  • [ISSN] 0003-3944
  • [Journal-full-title] Annales de chirurgie
  • [ISO-abbreviation] Ann Chir
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 40
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80. Ajumobi A, Bahjri K, Jackson C, Griffin R: Surveillance in Barrett's esophagus: an audit of practice. Dig Dis Sci; 2010 Jun;55(6):1615-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surveillance in Barrett's esophagus: an audit of practice.
  • GOALS: Determine the rates of follow-up, incident rate of cancer during surveillance, and changes in pathologic grade of patients with Barrett's esophagus during surveillance in a gastroenterology practice without a formal surveillance program.
  • BACKGROUND: Barrett's esophagus is a pre-malignant condition.
  • Surveillance endoscopy (SE) is recommended in order to detect and treat high-grade dysplasia and esophageal adenocarcinoma early and prevent deaths.
  • Most gastroenterology practices do not have a surveillance program for Barrett's esophagus.
  • Little information exists on outcomes in patients with Barrett's esophagus outside of these well-structured surveillance programs.
  • STUDY: A retrospective analysis of a cohort of patients with Barrett's esophagus diagnosed and surveyed between 1995 and 2005 at a Veterans Affairs medical center.
  • RESULTS: A total of 472 patients were diagnosed with Barrett's esophagus or had SE between 1995 and 2005.
  • Two patients were excluded from the final analysis: one had an esophagectomy after an index diagnosis of high-grade dysplasia, and one had a diagnosis of esophageal adenocarcinoma 2 days after an initial impression of Barrett's esophagus.
  • There were 165 patients with Barrett's metaplasia or dysplasia who had SE more than once and were included in the final analysis.
  • None (0/165, 0%) progressed to esophageal adenocarcinoma; 3.6% (6/165) progressed to high-grade dysplasia and 11.5% (19/165) regressed to normal mucosa.
  • Four patients regressed to normal mucosa, one progressed to high-grade dysplasia and none progressed to esophageal adenocarcinoma.
  • None progressed to esophageal adenocarcinoma or high-grade dysplasia but three regressed to normal mucosa.
  • CONCLUSIONS: Most veteran patients with Barrett's esophagus do not undergo surveillance endoscopies.
  • Veteran patients with Barrett's esophagus undergoing SE rarely progress to high-grade dysplasia or esophageal adenocarcinoma.
  • Veteran patients with Barrett's esophagus who have longer SE up to twice the recommended intervals because they missed their scheduled SE did not have a worse outcome when compared to the general Barrett's esophagus surveillance group.
  • [MeSH-major] Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Esophagoscopy. Mass Screening / methods. Precancerous Conditions / diagnosis


81. Binato M, Gurski RR, Fagundes RB, Meurer L, Edelweiss MI: P53 and Ki-67 overexpression in gastroesophageal reflux disease--Barrett's esophagus and adenocarcinoma sequence. Dis Esophagus; 2009;22(7):588-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P53 and Ki-67 overexpression in gastroesophageal reflux disease--Barrett's esophagus and adenocarcinoma sequence.
  • Gastroesophageal reflux disease (GERD) is a major risk factor for the development of esophageal adenocarcinoma (ACE).
  • Many molecular alterations occur in esophageal carcinogenesis, yet the exact mechanism of ACE development remains unknown.
  • This study aims to determine p53 protein and Ki-67 expression in esophageal mucosa of patients with GERD and study the correlation between these markers and the progression from normal squamous epithelium to esophagitis, columnar epithelium with or without intestinal metaplasia and ACE.
  • (iii) G3 columnar epitheliums without intestinal metaplasia (30);.
  • (iv) G4, columnar epitheliums with intestinal metaplasia (32); and (v) G5 ACEs (35).


82. von Rahden BH, Stein HJ, Weber A, Vieth M, Stolte M, Rösch T, Schmid RM, Sarbia M, Meining A: Critical reappraisal of current surveillance strategies for Barrett's esophagus: analysis of a large German Barrett's database. Dis Esophagus; 2008;21(8):685-9
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  • [Title] Critical reappraisal of current surveillance strategies for Barrett's esophagus: analysis of a large German Barrett's database.
  • Endoscopic surveillance is recommended for patients with Barrett's esophagus (BE).
  • Detection of 'malignant Barrett' (either high-grade intra-epithelial neoplasia or invasive adenocarcinoma) was considered as study end-point.

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  • (PMID = 18847456.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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83. 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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  • 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.
  • 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.
  • [MeSH-major] Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal / contraindications. Mass Screening / methods. Population Surveillance / methods
  • [MeSH-minor] Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / prevention & control. Humans. Prognosis. Risk Factors

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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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84. Tischoff I, Tannapfel A: Barrett's esophagus: can biomarkers predict progression to malignancy? Expert Rev Gastroenterol Hepatol; 2008 Oct;2(5):653-63
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  • [Title] Barrett's esophagus: can biomarkers predict progression to malignancy?
  • Barrett's esophagus (BE) is one of the most common premalignant lesions and can progress to esophageal adenocarcinoma.
  • It is characterized histologically by a specialized intestinal metaplasia that replaces the squamous epithelium of the distal esophagus, and is associated with chronic gastroesophageal reflux disease and obesity.
  • Similar to the adenoma-carcinoma sequence of colorectal carcinomas, esophageal adenocarcinoma develops through progression from BE to low- and high-grade dysplasia, then to adenocarcinoma with accumulation of genetic and epigenetic abnormalities.
  • Dysplasia is the most predictive marker for risk of esophageal adenocarcinoma, whereas endoscopic and histological diagnoses are still the gold standard for surveillance of patients with BE.
  • Several studies have identified candidate biomarkers that may have predictive value and may serve as additional factors for the risk assessment of esophageal adenocarcinoma.
  • This review discusses the role of biomarkers in the progression from BE to adenocarcinoma, focusing on clinical and molecular markers.
  • [MeSH-major] Barrett Esophagus / metabolism. Biomarkers, Tumor / metabolism. Esophageal Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Disease Progression. Humans. Predictive Value of Tests

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  • (PMID = 19072343.001).
  • [ISSN] 1747-4132
  • [Journal-full-title] Expert review of gastroenterology & hepatology
  • [ISO-abbreviation] Expert Rev Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 97
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85. Leers JM, DeMeester SR, Chan N, Ayazi S, Oezcelik A, Abate E, Banki F, Lipham JC, Hagen JA, DeMeester TR: Clinical characteristics, biologic behavior, and survival after esophagectomy are similar for adenocarcinoma of the gastroesophageal junction and the distal esophagus. J Thorac Cardiovasc Surg; 2009 Sep;138(3):594-602; discussion 601-2
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  • [Title] Clinical characteristics, biologic behavior, and survival after esophagectomy are similar for adenocarcinoma of the gastroesophageal junction and the distal esophagus.
  • OBJECTIVE: The Siewert classification system differentiates between adenocarcinoma of the gastroesophageal junction and that of the distal esophagus.
  • METHODS: Records of all patients who underwent resection for adenocarcinoma of the distal esophagus or gastroesophageal junction from 1987 to 2007 were retrospectively reviewed.
  • Based on the endoscopic location of the epicenter of the tumor in relation to the gastroesophageal junction, tumors were categorized in 301 patients as being of the distal esophagus and in 208 as being of the gastroesophageal junction.
  • RESULTS: There were no significant differences in age, sex, or body mass index between patients with adenocarcinoma of the distal esophagus or gastroesophageal junction.
  • Patients with adenocarcinoma of the distal esophagus were more likely to have reflux symptoms (75% vs 53%, P < .0001) and peritumoral intestinal metaplasia (73% vs 51%, P < .0001) and be in a surveillance program (54% vs 9%, P = .0005) compared with patients with adenocarcinoma of the gastroesophageal junction.
  • However, the prevalence and location of nodal metastases was similar, and in node-positive patients mediastinal node involvement was present in more than 40% of the patients in each group (distal esophageal adenocarcinoma, 47%; gastroesophageal junction adenocarcinoma, 41%).
  • Survival was similar (5 years: distal esophageal adenocarcinoma, 45%; gastroesophageal junction adenocarcinoma, 38%; P = .14), as was the prevalence and type of recurrence.
  • CONCLUSION: The prevalence and distribution of lymph node metastases in patients with adenocarcinoma of the distal esophagus and gastroesophageal junction were similar, and after esophagectomy, there was no difference in overall survival or recurrence.
  • [MeSH-major] Adenocarcinoma / mortality. Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagectomy / mortality. Esophagogastric Junction / surgery. Neoplasm Recurrence, Local / classification

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  • (PMID = 19698841.001).
  • [ISSN] 1097-685X
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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86. Jaiswal KR, Morales CP, Feagins LA, Gandia KG, Zhang X, Zhang HY, Hormi-Carver K, Shen Y, Elder F, Ramirez RD, Sarosi GA Jr, Spechler SJ, Souza RF: Characterization of telomerase-immortalized, non-neoplastic, human Barrett's cell line (BAR-T). Dis Esophagus; 2007;20(3):256-64
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  • Barrett's esophagus, a metaplasia predisposed to malignant transformation, has been studied in vitro using esophageal adenocarcinoma cell lines.
  • However, findings in such transformed cells may not be applicable to the non-neoplastic cells of benign Barrett's esophagus.
  • This cell line should be a useful model for the study of the early events in carcinogenesis in Barrett's esophagus.

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  • (PMID = 17509124.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / 5T32DK-07745; 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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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87. Looby E, Abdel-Latif MM, Athié-Morales V, Duggan S, Long A, Kelleher D: Deoxycholate induces COX-2 expression via Erk1/2-, p38-MAPK and AP-1-dependent mechanisms in esophageal cancer cells. BMC Cancer; 2009;9:190
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  • [Title] Deoxycholate induces COX-2 expression via Erk1/2-, p38-MAPK and AP-1-dependent mechanisms in esophageal cancer cells.
  • BACKGROUND: The progression from Barrett's metaplasia to adenocarcinoma is associated with the acquirement of an apoptosis-resistant phenotype.
  • The bile acid deoxycholate (DCA) has been proposed to play an important role in the development of esophageal adenocarcinoma, but the precise molecular mechanisms remain undefined.
  • The aim of this study was to investigate DCA-stimulated COX-2 signaling pathways and their possible contribution to deregulated cell survival and apoptosis in esophageal adenocarcinoma cells.
  • CONCLUSION: DCA regulates both apoptosis and COX-2-regulated cell survival in esophageal cells suggesting that the balance between these two opposing signals may determine the transformation potential of DCA as a component of the refluxate.
  • [MeSH-major] Cyclooxygenase 2 / biosynthesis. Deoxycholic Acid / pharmacology. Esophageal Neoplasms / metabolism. Mitogen-Activated Protein Kinases / metabolism. Transcription Factor AP-1 / biosynthesis
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Apoptosis / drug effects. Barrett Esophagus / enzymology. Barrett Esophagus / metabolism. Barrett Esophagus / pathology. Cell Growth Processes / drug effects. Cell Line, Tumor. Collagen Type XI / metabolism. DNA, Neoplasm / metabolism. Enzyme Induction / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proto-Oncogene Proteins c-fos / metabolism. Proto-Oncogene Proteins c-jun / metabolism. Signal Transduction / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19534809.001).
  • [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] 0 / COL11A2 protein, human; 0 / Collagen Type XI; 0 / DNA, Neoplasm; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-jun; 0 / Transcription Factor AP-1; 0 / fos-related antigen 1; 005990WHZZ / Deoxycholic Acid; EC 1.14.99.1 / Cyclooxygenase 2; 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 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2704223
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88. Lee OJ, Schneider-Stock R, McChesney PA, Kuester D, Roessner A, Vieth M, Moskaluk CA, El-Rifai W: Hypermethylation and loss of expression of glutathione peroxidase-3 in Barrett's tumorigenesis. Neoplasia; 2005 Sep;7(9):854-61
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  • Chronic gastroesophageal reflux disease is a known risk factor for Barrett's esophagus (BE), which induces oxidative mucosal damage.
  • GPx3 promoter hypermethylation was detected in 62% of Barrett's metaplasia, 82% of dysplasia, and 88% of BA samples.
  • Immunohistochemical staining of GPx3 in matching tissue sections (normal, BE, Barrett's dysplasia, and BA) revealed strong immunostaining for GPx3 in normal esophageal and gastric tissues.
  • However, weak to absent GPx3 staining was observed in Barrett's dysplasia and adenocarcinoma samples where the promoter was hypermethylated.

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  • (PMID = 16229808.001).
  • [ISSN] 1522-8002
  • [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 / R01CA106176
  • [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 / RNA, Messenger; EC 1.11.1.- / GPX3 protein, human; EC 1.11.1.9 / Glutathione Peroxidase
  • [Other-IDs] NLM/ PMC1501938
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89. Lanuti M, Liu G, Goodwin JM, Zhai R, Fuchs BC, Asomaning K, Su L, Nishioka NS, Tanabe KK, Christiani DC: A functional epidermal growth factor (EGF) polymorphism, EGF serum levels, and esophageal adenocarcinoma risk and outcome. Clin Cancer Res; 2008 May 15;14(10):3216-22
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  • [Title] A functional epidermal growth factor (EGF) polymorphism, EGF serum levels, and esophageal adenocarcinoma risk and outcome.
  • PURPOSE: The epidermal growth factor (EGF) pathway is important in esophageal adenocarcinoma (EAC) tumorigenesis.
  • RESULTS: The EGF A61G G/G genotype conferred increased EAC risk, with an adjusted odds ratio of 1.81 (95% confidence interval, 1.2-2.7), and was even higher in the subgroup of EAC patients with concurrent Barrett's esophagus (adjusted odds ratio, 2.18; 95% confidence interval, 1.3-3.7).
  • EGF genotyping can potentially identify high-risk patients with GERD and Barrett's metaplasia who might benefit from increased surveillance.

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  • (PMID = 18483390.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P20 CA090578; United States / NCI NIH HHS / CA / R01 CA092824; United States / NCI NIH HHS / CA / R01 CA092824-06; United States / NCI NIH HHS / CA / P50 CA090578-067601; United States / NCI NIH HHS / CA / R01 CA109193-05; United States / NCI NIH HHS / CA / R03 CA110822; United States / NCI NIH HHS / CA / R01 CA074386; United States / NCI NIH HHS / CA / CA109193-05; United States / NCI NIH HHS / CA / R01 CA109193; United States / NCI NIH HHS / CA / CA110822-02; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / CA090578-067601; United States / NCI NIH HHS / CA / R01 CA 092824; United States / NCI NIH HHS / CA / CA092824-06; United States / NCI NIH HHS / CA / R01 CA090578; United States / NCI NIH HHS / CA / R03 CA110822-02; United States / NCI NIH HHS / CA / R01 CA074386-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 62229-50-9 / Epidermal Growth Factor
  • [Other-IDs] NLM/ NIHMS71521; NLM/ PMC2572712
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90. Moretó M: Diagnosis of esophagogastric tumors. Endoscopy; 2005 Jan;37(1):26-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis of esophagogastric tumors.
  • With regard to esophageal tumors, important reports on several topics have been published recently.
  • 1) The place of endoscopic ultrasonography (EUS) as the best locoregional staging technique for cancer of the esophagus has been further consolidated.
  • 4) The incidence of hypopharyngeal cancer increases after resection for esophageal carcinoma.
  • 6) Patients with Barrett's esophagus with a length of over 3 cm had a significantly greater prevalence of dysplasia in comparison with those in the whom the Barrett's segment was shorter than 3 cm (23 % vs. 9 %, P = 0.0001).
  • 2) Intestinal metaplasia types II and III have been shown to have a higher rate of progression to low-grade dysplasia than type I.
  • 4) In patients who have undergone esophagectomy for esophageal cancer, annual follow-up endoscopies are vital for detecting early secondary gastric cancer and ulcerations in which curative treatment is possible.
  • 5) High-resolution endoscopy allows more precise diagnosis of early gastric cancer.
  • 7) Gastric adenocarcinoma was found to show specific changes in the fluorescence spectra emitted, in comparison with normal gastric mucosa.
  • [MeSH-major] Endoscopy, Digestive System. Esophageal Neoplasms / diagnosis. Stomach Neoplasms / diagnosis

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  • (PMID = 15657854.001).
  • [ISSN] 0013-726X
  • [Journal-full-title] Endoscopy
  • [ISO-abbreviation] Endoscopy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 40
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91. Botelho NK, Schneiders FI, Lord SJ, Freeman AK, Tyagi S, Nancarrow DJ, Hayward NK, Whiteman DC, Lord RV: Gene expression alterations in formalin-fixed, paraffin-embedded Barrett esophagus and esophageal adenocarcinoma tissues. Cancer Biol Ther; 2010 Jul 15;10(2):172-9
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  • [Title] Gene expression alterations in formalin-fixed, paraffin-embedded Barrett esophagus and esophageal adenocarcinoma tissues.
  • BACKGROUND AND AIM: Widespread applicability of tissue-based mRNA expression screening for Barrett esophagus (BE) is likely to require (1) accurate methods for assaying archival formalin-fixed, paraffin-embedded (FFPE) histopathology specimens taken at endoscopy, and (2) validation studies of promising biomarkers in different patient cohorts.
  • METHODS: mRNA was isolated from 54 FFPE small endoscopic biopsies from patients with Barrett intestinal metaplasia (BE), esophageal adenocarcinoma (EAC), or control patients with a normal squamous-lined esophagus.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Gene Expression Profiling / methods. Polymerase Chain Reaction / methods

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  • (PMID = 20543560.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 1HG84L3525 / Formaldehyde
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92. Martins FP, Artigiani Neto R, Oshima CT, Costa PP, N M F, Ferrari AP: Over-expression of cyclooxygenase-2 in endoscopic biopsies of ectopic gastric mucosa. Braz J Med Biol Res; 2007 Nov;40(11):1447-54
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  • Rare cases of adenocarcinoma have been described.
  • The aim of this prospective study was to evaluate COX-2 expression in EGM and compare it with normal tissue and Barrett's esophagus.
  • Biopsies taken from normal esophageal, gastric antrum and body mucosa and Barrett's esophagus were retrieved from a tissue bank.
  • Expression of COX-2 was negative in normal distal esophagus, normal gastric antrum and normal gastric body specimens (10 each).
  • In contrast, EGM presented over-expression of COX-2 in 41.7% of cases and Barrett's esophagus in 90% of cases (P = 0.04 and 0.03, respectively).
  • COX-2 immunoexpression in EGM was not related to gender, age, epithelium type, presence of inflammation or intestinal metaplasia, H. pylori infection, or any endoscopic finding.

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  • (PMID = 17934641.001).
  • [ISSN] 1414-431X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] EC 1.14.99.1 / Cyclooxygenase 2
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93. Gomes LI, Esteves GH, Carvalho AF, Cristo EB, Hirata R Jr, Martins WK, Marques SM, Camargo LP, Brentani H, Pelosof A, Zitron C, Sallum RA, Montagnini A, Soares FA, Neves EJ, Reis LF: Expression profile of malignant and nonmalignant lesions of esophagus and stomach: differential activity of functional modules related to inflammation and lipid metabolism. Cancer Res; 2005 Aug 15;65(16):7127-36
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  • [Title] Expression profile of malignant and nonmalignant lesions of esophagus and stomach: differential activity of functional modules related to inflammation and lipid metabolism.
  • Adenocarcinomas of stomach and esophagus are frequently associated with preceding inflammatory alterations of the normal mucosa.
  • Whereas intestinal metaplasia of the gastric mucosa is associated with higher risk of malignization, Barrett's disease is a risk factor for adenocarcinoma of the esophagus.
  • Barrett's disease is characterized by the substitution of the squamous mucosa of the esophagus by a columnar tissue classified histopathologically as intestinal metapl