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1. Anderson LA, Johnston BT, Watson RG, Murphy SJ, Ferguson HR, Comber H, McGuigan J, Reynolds JV, Murray LJ: Nonsteroidal anti-inflammatory drugs and the esophageal inflammation-metaplasia-adenocarcinoma sequence. Cancer Res; 2006 May 1;66(9):4975-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonsteroidal anti-inflammatory drugs and the esophageal inflammation-metaplasia-adenocarcinoma sequence.
  • Observational studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of esophageal adenocarcinoma, but it is not known at what stage they may act in the esophageal inflammation-metaplasia-adenocarcinoma sequence.
  • In an all-Ireland case-control study, we investigated the relationship between the use of NSAIDs and risk of reflux esophagitis, Barrett's esophagus, and esophageal adenocarcinoma.
  • Patients with esophageal adenocarcinoma, long-segment Barrett's esophagus and population controls were recruited from throughout Ireland.
  • Data were collected on known and potential risk factors for esophageal adenocarcinoma and on the use of NSAIDs, including aspirin, at least 1 year before interview.
  • Associations between use of NSAIDs and the stages of the esophageal inflammation-metaplasia-adenocarcinoma sequence were estimated by multiple logistic regression.
  • In total, 230 reflux esophagitis, 224 Barrett's esophagus, and 227 esophageal adenocarcinoma and 260 population controls were recruited.
  • Use of aspirin and NSAIDs was associated with a reduced risk of Barrett's esophagus [odds ratio [OR; 95% confidence interval (95% CI)], 0.53 (0.31-0.90) and 0.40 (0.19-0.81), respectively] and esophageal adenocarcinoma [OR (95% CI), 0.57 (0.36-0.93) and 0.58 (0.31-1.08), respectively].
  • Barrett's esophagus and esophageal adenocarcinoma patients were less likely than controls to have used NSAIDs.
  • Selection or recall bias may explain these results and the results of previous observational studies indicating a protective effect of NSAIDs against esophageal adenocarcinoma.
  • If NSAIDs have a true protective effect on the esophageal inflammation-metaplasia-adenocarcinoma sequence, they may act early in the sequence.
  • [MeSH-major] Adenocarcinoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Barrett Esophagus / prevention & control. Esophageal Neoplasms / prevention & control. Esophagitis, Peptic / prevention & control
  • [MeSH-minor] Acetaminophen / administration & dosage. Aged. Aged, 80 and over. Aspirin / administration & dosage. Case-Control Studies. Esophagus / drug effects. Esophagus / pathology. Female. Humans. Male. Metaplasia. Middle Aged


2. Holmes K, Egan B, Swan N, O'Morain C: Genetic Mechanisms and Aberrant Gene Expression during the Development of Gastric Intestinal Metaplasia and Adenocarcinoma. Curr Genomics; 2007 Sep;8(6):379-97
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  • [Title] Genetic Mechanisms and Aberrant Gene Expression during the Development of Gastric Intestinal Metaplasia and Adenocarcinoma.
  • Gastric adenocarcinoma occurs via a sequence of molecular events known as the Correa's Cascade which often progresses over many years.
  • Despite recent antibiotic intervention of H. pylori infections, gastric adenocarcinoma remains the second most common cause of cancer deaths worldwide.
  • Intestinal metaplasia is the next step along the carcinogenic sequence after gastritis and is considered to be a precursor lesion for gastric cancer; however, not all patients with intestinal metaplasia develop adenocarcinoma and little is known about the molecular and genetic events that trigger the progression of intestinal metaplasia into adenocarcinoma.
  • This review aims to highlight the progress to date in the genetic events involved in intestinal-type gastric adenocarcinoma and its precursor lesion, intestinal metaplasia.
  • The use of technologies such as whole genome microarray analysis, immunohistochemical analysis and DNA methylation analysis has allowed an insight into some of the events which occur in intestinal metaplasia and may be involved in carcinogenesis.

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  • (PMID = 19412438.001).
  • [ISSN] 1389-2029
  • [Journal-full-title] Current genomics
  • [ISO-abbreviation] Curr. Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC2671722
  • [Keywords] NOTNLM ; Intestinal metaplasia / aberrant gene expression / gastric cancer / genetic markers.
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3. 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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4. Brundler MA, Harrison JA, de Saussure B, de Perrot M, Pepper MS: Lymphatic vessel density in the neoplastic progression of Barrett's oesophagus to adenocarcinoma. J Clin Pathol; 2006 Feb;59(2):191-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lymphatic vessel density in the neoplastic progression of Barrett's oesophagus to adenocarcinoma.
  • BACKGROUND: Oesophageal adenocarcinoma is an aggressive neoplasm with poor prognosis as a result of early lymph node metastasis.
  • AIMS: To measure lymphatic vessel density (LVD) in the neoplastic progression from Barrett's metaplasia to adenocarcinoma and determine whether LVD can predict the risk of cancer.
  • METHODS: LVD and microvascular density (MVD) were assessed after immunohistochemical staining of vessels in Barrett's metaplasia, dysplasia, and adenocarcinoma tissues and were correlated with clinicopathological features.
  • RESULTS: LVD was significantly reduced in adenocarcinoma, being half that seen in normal stomach/oesophagus or metaplasia/dysplasia.
  • MVD was also assessed as a prognostic marker; its increase appeared to be linked more with the development of Barrett's metaplasia than adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Lymphatic Vessels / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Esophagus / pathology. Female. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Metaplasia / pathology. Middle Aged. Neoplasm Staging. Prognosis. Survival Analysis

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  • (PMID = 16443737.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860317
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5. 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
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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.
  • 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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6. Wang XW, Gao HJ, Fang DC: Advances in gene chip technique in Barrett's metaplasia and adenocarcinoma. J Dig Dis; 2008 May;9(2):68-71
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advances in gene chip technique in Barrett's metaplasia and adenocarcinoma.
  • Many studies have applied this technology for Barrett's metaplasia and adenocarcinoma, and identified a number of candidate genes useful as biomarkers in cancer staging, prediction of recurrence, prognosis and treatment selection.
  • This review described the gene expression profile and molecular changes related to Barrett's metaplasia and adenocarcinoma of the esophagus, with emphasis on its prognostic value and possibilities for targeted therapy in a clinical setting.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Oligonucleotide Array Sequence Analysis / trends
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Metaplasia / diagnosis. Metaplasia / genetics. Metaplasia / pathology

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  • (PMID = 18419638.001).
  • [ISSN] 1751-2972
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 18
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7. Anderson LA, Murphy SJ, Johnston BT, Watson RG, Ferguson HR, Bamford KB, Ghazy A, McCarron P, McGuigan J, Reynolds JV, Comber H, Murray LJ: Relationship between Helicobacter pylori infection and gastric atrophy and the stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence: results from the FINBAR case-control study. Gut; 2008 Jun;57(6):734-9
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  • [Title] Relationship between Helicobacter pylori infection and gastric atrophy and the stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence: results from the FINBAR case-control study.
  • OBJECTIVE: A number of studies have shown an inverse association between infection with Helicobacter pylori and oesophageal adenocarcinoma (OAC).
  • The relationship between all stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence and H pylori infection and gastric atrophy was explored.
  • [MeSH-major] Adenocarcinoma / complications. Esophageal Neoplasms / complications. Gastritis, Atrophic / complications. Helicobacter Infections / complications. Helicobacter pylori / isolation & purification


8. Bansal A, Kahrilas PJ: Treatment of GERD complications (Barrett's, peptic stricture) and extra-oesophageal syndromes. Best Pract Res Clin Gastroenterol; 2010 Dec;24(6):961-8
MedlinePlus Health Information. consumer health - GERD.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Apart from typical reflux symptoms and oesophagitis, the clinical presentation of GERD can be dominated by mucosal complications of reflux (Barrett's oesophagus, oesophageal adenocarcinoma, Peptic structure) or by extra-oesophageal syndromes, most notably asthma, laryngitis, or chronic cough.
  • With respect to adenocarcinoma, metaplasia and dysplasia are recognised precursors, but the potential of these lesions to evolve to cancer has not been shown to lessen as a result of treatment, medical or surgical.

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  • [Copyright] Published by Elsevier Ltd.
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  • (PMID = 21126707.001).
  • [ISSN] 1532-1916
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK056033-09; United States / NIDDK NIH HHS / DK / R01 DK056033; United States / NIDDK NIH HHS / DK / R01 DK056033-09; United States / NIDDK NIH HHS / DK / R01 DK56033
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors
  • [Other-IDs] NLM/ NIHMS247533; NLM/ PMC3006235
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9. Ko S, Chu KM, Luk JM, Wong BW, Yuen ST, Leung SY, Wong J: CDX2 co-localizes with liver-intestine cadherin in intestinal metaplasia and adenocarcinoma of the stomach. J Pathol; 2005 Apr;205(5):615-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CDX2 co-localizes with liver-intestine cadherin in intestinal metaplasia and adenocarcinoma of the stomach.
  • Overexpression of CDX2 was significantly associated with CDH17 in gastric adenocarcinoma.
  • Furthermore, the expression of CDX2 and LI-cadherin proteins was strongly coupled in intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Cadherins / metabolism. Homeodomain Proteins / metabolism. Stomach Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Immunoenzyme Techniques. Lymphatic Metastasis. Male. Metaplasia / metabolism. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm Staging. Precancerous Conditions / metabolism. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Stomach / pathology. Up-Regulation

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  • (PMID = 15732140.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDH17 protein, human; 0 / CDX2 protein, human; 0 / Cadherins; 0 / Homeodomain Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • [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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11. Miwa K, Oyama K, Fujimura T: [A COX-2 inhibitor suppresses esophageal inflammation-metaplasia-adenocarcinoma sequence in rats]. Nihon Rinsho; 2005 Aug;63(8):1387-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A COX-2 inhibitor suppresses esophageal inflammation-metaplasia-adenocarcinoma sequence in rats].
  • In the control group, esophagitis, columnar-lined epithelium (CLE) and adenocarcinoma (ADC) were first observed at the 10th, 20th, and 30th week, respectively, and their incidences sequentially increased and reached 100%, 89% and 47% at the 40th week, respectively.
  • [MeSH-major] Adenocarcinoma / prevention & control. Barrett Esophagus / prevention & control. Cyclooxygenase Inhibitors / therapeutic use. Duodenogastric Reflux / complications. Esophageal Neoplasms / prevention & control. Esophagus / pathology. Gastroesophageal Reflux / complications. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use
  • [MeSH-minor] Animals. Apoptosis. Celecoxib. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Dinoprostone / metabolism. Disease Models, Animal. Male. Metaplasia / pathology. Metaplasia / prevention & control. Prostaglandin-Endoperoxide Synthases / metabolism. Rats. Rats, Inbred F344

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  • (PMID = 16101227.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
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12. Oyama K, Fujimura T, Ninomiya I, Miyashita T, Kinami S, Fushida S, Ohta T, Koichi M: A COX-2 inhibitor prevents the esophageal inflammation-metaplasia-adenocarcinoma sequence in rats. Carcinogenesis; 2005 Mar;26(3):565-70
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A COX-2 inhibitor prevents the esophageal inflammation-metaplasia-adenocarcinoma sequence in rats.
  • Barrett's esophagus (BE) and esophageal adenocarcinoma (ADC) is associated with reflux of duodenal contents.
  • [MeSH-major] Adenocarcinoma / prevention & control. Cyclooxygenase Inhibitors / pharmacology. Esophageal Neoplasms / prevention & control. Esophagitis / prevention & control. Metaplasia / prevention & control. Prostaglandin-Endoperoxide Synthases / drug effects

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  • (PMID = 15564290.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / DNA Primers; 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
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13. Healy CF, Feeley L, Leen E, Walsh TN: Primary squamous cell carcinoma of the breast: value of positron emission tomography scanning in confirming the diagnosis. Clin Breast Cancer; 2006 Dec;7(5):413-5
MedlinePlus Health Information. consumer health - Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary squamous cell carcinoma of the breast: value of positron emission tomography scanning in confirming the diagnosis.
  • Controversy exists as to whether a pure form exists or whether described cases represent extreme squamous metaplasia within an adenocarcinoma.

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  • (PMID = 17239268.001).
  • [ISSN] 1526-8209
  • [Journal-full-title] Clinical breast cancer
  • [ISO-abbreviation] Clin. Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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14. Mercer SJ, Toh SK, Somers SS: Esophageal adenocarcinoma developing above an Angelchik prosthesis. Dis Esophagus; 2007;20(6):546-8
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Esophageal adenocarcinoma developing above an Angelchik prosthesis.
  • This article details the cases of three patients in our institution who underwent the insertion of an Angelchik prosthesis and who subsequently developed adenocarcinoma of the esophagus.
  • It is suggested that the Angelchik prosthesis does not effectively prevent acid reflux and thus has no effect in preventing the dysplasia-metaplasia-adenocarcinoma sequence in the lower esophagus.

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  • (PMID = 17958734.001).
  • [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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15. Gibson CJ, Parry NM, Jakowski RM, Cooper J: Adenomatous polyp with intestinal metaplasia of the esophagus (Barrett esophagus) in a dog. Vet Pathol; 2010 Jan;47(1):116-9
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenomatous polyp with intestinal metaplasia of the esophagus (Barrett esophagus) in a dog.
  • This article reports a case of spontaneous esophageal adenomatous polyp with intestinal metaplasia (Barrett esophagus) and reviews the pathogenesis of esophageal metaplasia and adenocarcinoma.
  • [MeSH-minor] Animals. Dogs. Esophagus / pathology. Goblet Cells / pathology. Male. Metaplasia / pathology. Metaplasia / veterinary

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  • (PMID = 20080491.001).
  • [ISSN] 1544-2217
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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16. Gil J, Błaszak A, Wojtuń S, Wojtkowiak M: [Endoscopic methods of gastro-esophageal reflux disease (GERD) treatment and their complications]. Pol Merkur Lekarski; 2007 May;22(131):429-33
MedlinePlus Health Information. consumer health - GERD.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Chronic character of GERD is associated with intestinal metaplasia and adenocarcinoma of the esophagus in its distal part.
  • [MeSH-minor] Animals. Barrett Esophagus / pathology. Barrett Esophagus / surgery. Esophagogastric Junction / pathology. Esophagogastric Junction / surgery. Fundoplication / methods. Humans. Laser Coagulation. Laser Therapy. Metaplasia. Monitoring, Ambulatory. Postoperative Complications. Proton Pump Inhibitors. Proton Pumps / drug effects

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  • (PMID = 17679388.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors; 0 / Proton Pumps
  • [Number-of-references] 25
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17. Wijnhoven BP, Hussey DJ, Watson DI, Tsykin A, Smith CM, Michael MZ, South Australian Oesophageal Research Group: MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma. Br J Surg; 2010 Jun;97(6):853-61
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma.
  • BACKGROUND: The genetic changes that drive metaplastic progression from squamous oesophageal mucosa toward intestinal metaplasia and adenocarcinoma are unclear.
  • This study examined whether miRNAs play a role in the development of oesophageal adenocarcinoma.
  • METHODS: RNA was extracted from mucosa of normal oesophageal squamous epithelium, normal gastric epithelium, Barrett's oesophagus with intestinal metaplasia and oesophageal adenocarcinoma obtained from 16 individuals.
  • Expression of miR-143, miR-145 and miR-215 was lower in oesophageal adenocarcinoma than in Barrett's oesophagus.
  • MiR-205 levels were lower in gastric epithelium than in both Barrett's oesophagus and adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. MicroRNAs / analysis. RNA, Messenger / analysis

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  • (PMID = 20301167.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Messenger
  • [Investigator] Wijnhoven BP; Hussey DJ; Watson DI; Smith CM; Mayne GC; Michael MZ; Astill D; Van der Hoek MB; Tsykin A; Tilanus HW; Wijnhoven BP
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18. Mabrut JY, Collard JM, Baulieux J: [Duodenogastric and gastroesophageal bile reflux]. J Chir (Paris); 2006 Nov-Dec;143(6):355-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study reviews current data regarding duodenogastric and gastroesophageal bile reflux-pathophysiology, clinical presentation, methods of diagnosis (namely, 24-hour intraluminal bile monitoring) and therapeutic management.
  • In patients with concomitant gastroesophageal reflux, the backwash of duodenal content into the lower esophagus can cause mixed (alkaline and acid) reflux esophagitis, and lead, in turn, to esophageal mucosal damage such as Barrett's metaplasia and adenocarcinoma.

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  • (PMID = 17285081.001).
  • [ISSN] 0021-7697
  • [Journal-full-title] Journal de chirurgie
  • [ISO-abbreviation] J Chir (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anion Exchange Resins; 0 / Anti-Ulcer Agents; 0 / Bile Acids and Salts; 0 / Gastrointestinal Agents; 0 / Proton Pump Inhibitors; 11041-12-6 / Cholestyramine Resin; 54182-58-0 / Sucralfate; UVL329170W / Cisapride
  • [Number-of-references] 182
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19. Murphy JO, Ravi N, Byrne PJ, McDonald GS, Reynolds JV: Neither antioxidants nor COX-2 inhibition protect against esophageal inflammation in an experimental model of severe reflux. J Surg Res; 2007 Sep;142(1):20-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Reflux-induced injury and oxidative stress result in esophageal inflammation and the potential for progression to intestinal metaplasia and adenocarcinoma.
  • No animal developed metaplasia or tumor.

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  • (PMID = 17543990.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cyclooxygenase 2 Inhibitors; 0 / Lactones; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; PQ6CK8PD0R / Ascorbic Acid
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20. 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
MedlinePlus Health Information. consumer health - GERD.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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21. Murphy JO, Ravi N, Byrne PJ, McDonald GS, Reynolds JV: Neither antioxidants nor COX-2 inhibition protect against esophageal inflammation in an experimental model of severe reflux. J Surg Res; 2008 Mar;145(1):33-40
Hazardous Substances Data Bank. L-Ascorbic Acid .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Reflux-induced injury and oxidative stress result in esophageal inflammation and the potential for progression to intestinal metaplasia and adenocarcinoma.
  • No animal developed metaplasia or tumor.

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  • (PMID = 17727884.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cyclooxygenase 2 Inhibitors; 0 / Lactones; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; PQ6CK8PD0R / Ascorbic Acid
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22. Park KJ, Soslow RA, Sonoda Y, Barakat RR, Abu-Rustum NR: Frozen-section evaluation of cervical adenocarcinoma at time of radical trachelectomy: pathologic pitfalls and the application of an objective scoring system. Gynecol Oncol; 2008 Sep;110(3):316-23
International Agency for Research on Cancer - Screening Group. diagnostics - A practical manual on visual screening for cervical neoplasia .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frozen-section evaluation of cervical adenocarcinoma at time of radical trachelectomy: pathologic pitfalls and the application of an objective scoring system.
  • OBJECTIVE: To analyze the incidence of diagnostic discrepancy between frozen-section and final diagnosis of the endocervical margin at time of radical trachelectomy and to apply an objective scoring system to non-invasive endocervical glandular atypia to determine its utility in distinguishing benign from malignant lesions.
  • METHODS: Histologic slides from 19 cases of radical trachelectomy performed for invasive endocervical adenocarcinoma were evaluated for correlation between the frozen and permanent sections of the endocervical margin.
  • An objective scoring system for grading non-invasive endocervical glandular lesions proposed by Ioffe et al. was also applied to the frozen and permanent section slides and compared to the final diagnosis.
  • RESULTS: There was 84% concordance between the frozen-section and final diagnosis using histology alone, vs. 95% concordance using the Ioffe scoring system.
  • One trachelectomy was converted to completion hysterectomy for what was presumed to be adenocarcinoma in situ at the margin, which in retrospect, was a benign lesion and was correctly classified using the Ioffe system.
  • Most of the discrepancies were due to misinterpretation of tubal metaplasia, tubo-endometrioid metaplasia, and atypical tubal metaplasia as adenocarcinoma in situ.
  • CONCLUSION: Benign mimics of endocervical adenocarcinoma in situ can be difficult to distinguish from malignant lesions, especially during frozen-section evaluation of the trachelectomy.
  • Correctly diagnosing the margin status intraoperatively has great clinical impact and the application of an objective scoring system, like that proposed by Ioffe et al., can increase diagnostic accuracy when applied to frozen-section slides and better correlates with final diagnosis when compared to histology alone.
  • [MeSH-major] Adenocarcinoma / pathology. Uterine Cervical Neoplasms / pathology

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  • (PMID = 18635252.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA008748
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS809092; NLM/ PMC4996344
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23. Oyama K, Fujimura T, Ninomiya I, Miyashita T, Kinami S, Fushida S, Ohta T: [Cyclooxygenase (COX)-2 expression in a rat duodenoesophageal reflux model and chemoprevention of adenocarcinoma by the selective COX-2 inhibitor nimesulide]. Nihon Shokakibyo Gakkai Zasshi; 2007 Aug;104(8):1183-91
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  • [Title] [Cyclooxygenase (COX)-2 expression in a rat duodenoesophageal reflux model and chemoprevention of adenocarcinoma by the selective COX-2 inhibitor nimesulide].
  • In the control group, esophagitis, Barrett's esophagus (BE) and adenocarcinoma (EAC) were observed, and the frequency of these conditions increased with time.
  • COX-2 may play an important role in esophageal carcinogenesis through the activation of the inflammation-metaplasia-adenocarcinoma sequence.
  • [MeSH-major] Adenocarcinoma / prevention & control. Cyclooxygenase 2 / biosynthesis. Cyclooxygenase 2 Inhibitors / therapeutic use. Duodenogastric Reflux / metabolism. Esophageal Neoplasms / prevention & control. Sulfonamides / therapeutic use
  • [MeSH-minor] Animals. Barrett Esophagus / pathology. Dinoprostone / biosynthesis. Disease Models, Animal. Esophagus / metabolism. Gastric Mucosa / pathology. Metaplasia. RNA, Messenger / biosynthesis. Rats

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  • (PMID = 17675820.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / RNA, Messenger; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone; V4TKW1454M / nimesulide
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24. Stewart CJ, Little L: Diagnostic value and implications of vimentin expression in normal, reactive and neoplastic endocervical epithelium. Pathology; 2010 Apr;42(3):217-23
International Agency for Research on Cancer - Screening Group. diagnostics - Histopathology and cytopathology of the uterine cervix - digital atlas .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Sixty-two cervical biopsy specimens including normal endocervical epithelium, tubo-endometrioid metaplasia, adenocarcinoma in situ, stratified mucin producing intraepithelial lesions (SMILE), and invasive adenocarcinomas were stained immunohistochemically for vimentin and for p16 protein, Ki-67 and bcl-2.
  • RESULTS: Normal endocervical epithelium usually showed subtle but distinct sub-nuclear and delicate lateral cell border vimentin expression while tubo-endometrioid metaplasia exhibited more diffuse cytoplasmic immunoreactivity.
  • Usually adenocarcinoma in situ was completely negative and therefore vimentin staining sharply distinguished the benign and neoplastic epithelial elements.
  • CONCLUSIONS: Normal endocervical cells often exhibit vimentin staining, and this is increased in reactive and metaplastic situations, whereas adenocarcinoma in situ is usually completely negative.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / analysis. Uterine Cervical Neoplasms / metabolism. Vimentin / biosynthesis

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  • (PMID = 20350213.001).
  • [ISSN] 1465-3931
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vimentin
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25. Leys CM, Nomura S, LaFleur BJ, Ferrone S, Kaminishi M, Montgomery E, Goldenring JR: Expression and prognostic significance of prothymosin-alpha and ERp57 in human gastric cancer. Surgery; 2007 Jan;141(1):41-50
The Lens. Cited by Patents in .

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  • PURPOSE: Prothymosin-alpha and ERp57 were previously identified as markers for gastric metaplasia in a mouse model of Helicobacter-induced gastric metaplasia and neoplasia.
  • In this paper we assess whether the expression of these putative biomarkers in humans is correlated with gastric metaplasia and adenocarcinoma and clinical outcomes.
  • CONCLUSIONS: These results suggest that although prothymosin-alpha is overexpressed in gastric adenocarcinoma, it is not associated with alterations in survival.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / mortality. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Down-Regulation. Endoplasmic Reticulum / metabolism. Humans. Immunohistochemistry. Metaplasia / metabolism. Molecular Chaperones / metabolism. Prognosis. Protein Array Analysis. Retrospective Studies. Stomach / metabolism. Stomach / pathology. Survival Rate

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  • (PMID = 17188166.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P50 CA95103; United States / NCI NIH HHS / CA / CA67108; United States / NCI NIH HHS / CA / K12 CA090625; United States / NCI NIH HHS / CA / P50 CA62924
  • [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 / Biomarkers, Tumor; 0 / Molecular Chaperones; 0 / Protein Precursors; 0 / prothymosin alpha; 61512-21-8 / Thymosin; EC 5.3.4.1 / Protein Disulfide-Isomerases; EC 5.3.4.1. / PDIA3 protein, human
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26. Combet E, Paterson S, Iijima K, Winter J, Mullen W, Crozier A, Preston T, McColl KE: Fat transforms ascorbic acid from inhibiting to promoting acid-catalysed N-nitrosation. Gut; 2007 Dec;56(12):1678-84
Hazardous Substances Data Bank. OXYGEN .

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  • BACKGROUND: The major potential site of acid nitrosation is the proximal stomach, an anatomical site prone to a rising incidence of metaplasia and adenocarcinoma.

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  • (PMID = 17785370.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lipids; 0 / Nitrosamines; 31C4KY9ESH / Nitric Oxide; PQ6CK8PD0R / Ascorbic Acid; QTT17582CB / Hydrochloric Acid; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2095705
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27. Babar M, Abdel-Latif MM, Ravi N, Murphy A, Byrne PJ, Kelleher D, Reynolds JV: Pilot translational study of dietary vitamin C supplementation in Barrett's esophagus. Dis Esophagus; 2010 Apr;23(3):271-6
Hazardous Substances Data Bank. L-Ascorbic Acid .

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  • In the esophagus, NF-kappaB is progressively activated from inflammation to Barrett's metaplasia and adenocarcinoma.
  • Twenty-five patients with long-segment Barrett's and specialized intestinal metaplasia received dietary vitamin C (1000 mg/day) orally for four weeks, and had pre- and post-vitamin C endoscopic biopsies.

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  • (PMID = 19930402.001).
  • [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] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cytokines; 0 / NF-kappa B; PQ6CK8PD0R / Ascorbic Acid
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28. Yoshizawa N, Takenaka Y, Yamaguchi H, Tetsuya T, Tanaka H, Tatematsu M, Nomura S, Goldenring JR, Kaminishi M: Emergence of spasmolytic polypeptide-expressing metaplasia in Mongolian gerbils infected with Helicobacter pylori. Lab Invest; 2007 Dec;87(12):1265-76
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  • [Title] Emergence of spasmolytic polypeptide-expressing metaplasia in Mongolian gerbils infected with Helicobacter pylori.
  • Spasmolytic polypeptide (TFF2)-expressing metaplasia (SPEM) is observed in mucosa adjacent to human gastric cancer and in fundic glands showing oxyntic atrophy in Helicobacter felis-infected mice.
  • Mongolian gerbils infected with Helicobacter pylori (Hp) develop goblet cell intestinal metaplasia and adenocarcinoma, but the presence of SPEM has not been studied in gerbils.
  • In uninfected animals, no SPEM or intestinal metaplasia was observed.
  • Goblet cell intestinal metaplasia developed only late in the infection.
  • Dual staining for TFF2 and MUC2 showed glands containing both SPEM- and MUC2-positive goblet cell intestinal metaplasia.
  • SPEM develops early in Hp infection in Mongolian gerbils, and alterations in gland morphology arise from SPEM glands during the course of gastric infection with goblet cell intestinal metaplasia developing subsequent to SPEM.
  • [MeSH-minor] Animals. Gastric Mucosa / metabolism. Gastric Mucosa / pathology. Gerbillinae. Goblet Cells / metabolism. Goblet Cells / pathology. Male. Metaplasia


29. Allameh A, Rasmi Y, Nasseri-Moghaddam S, Tavangar SM, Sharifi R, Sadreddini M: Immunohistochemical analysis of selected molecular markers in esophagus precancerous, adenocarcinoma and squamous cell carcinoma in Iranian subjects. Cancer Epidemiol; 2009 Jul;33(1):79-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical analysis of selected molecular markers in esophagus precancerous, adenocarcinoma and squamous cell carcinoma in Iranian subjects.
  • SUBJECTS: Formalin-fixed, paraffin-embedded esophageal specimens (n=87) from patients with gastroesophageal reflux disease (GERD), Barrett's metaplasia, adenocarcinoma (ADC) and squamous cells carcinoma (SCC) were collected based on their pathological diagnosis.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Precancerous Conditions / metabolism. Precancerous Conditions / pathology


30. Boult J, Roberts K, Brookes MJ, Hughes S, Bury JP, Cross SS, Anderson GJ, Spychal R, Iqbal T, Tselepis C: Overexpression of cellular iron import proteins is associated with malignant progression of esophageal adenocarcinoma. Clin Cancer Res; 2008 Jan 15;14(2):379-87
Hazardous Substances Data Bank. IRON, ELEMENTAL .

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  • [Title] Overexpression of cellular iron import proteins is associated with malignant progression of esophageal adenocarcinoma.
  • PURPOSE: There is growing evidence that iron is important in esophageal adenocarcinoma, a cancer whose incidence is rising faster than any other in the Western world.
  • In this study, we investigated the expression of iron transport proteins involved in cellular iron import, export, and storage in the premalignant lesion Barrett's metaplasia and esophageal adenocarcinoma.
  • EXPERIMENTAL DESIGN: Perls' staining was used to examine iron deposition in tissue. mRNA expression in samples of Barrett's metaplasia matched with esophageal adenocarcinoma and samples of Barrett's metaplasia without evidence of adenocarcinoma were examined by real-time PCR.
  • RESULTS: In the progression of Barrett's metaplasia to adenocarcinoma, there was overexpression of divalent metal transporter 1 (DMT1), transferrin receptor 1, duodenal cytochrome b, ferroportin, and H-ferritin, and these changes were associated with increased iron deposition.
  • Overexpression of DMT1 was further associated with metastatic adenocarcinoma.
  • CONCLUSIONS: Progression to adenocarcinoma is associated with increased expression of iron import proteins.
  • [MeSH-major] Adenocarcinoma / physiopathology. Barrett Esophagus / physiopathology. Cation Transport Proteins / metabolism. Esophageal Neoplasms / physiopathology. Iron / metabolism

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  • (PMID = 18223212.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD71 antigen; 0 / Cation Transport Proteins; 0 / Cytochrome b Group; 0 / Receptors, Transferrin; 0 / metal transporting protein 1; 0 / solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2; 9013-31-4 / Apoferritins; E1UOL152H7 / Iron; EC 1.- / Oxidoreductases; EC 1.6.99.- / CYBRD1 protein, human
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31. Zhang HY, Spechler SJ, Souza RF: Esophageal adenocarcinoma arising in Barrett esophagus. Cancer Lett; 2009 Mar 18;275(2):170-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Esophageal adenocarcinoma arising in Barrett esophagus.
  • The major risk factors for esophageal adenocarcinoma are gastroesophageal reflux disease (GERD) and Barrett esophagus, a squamous-to-columnar cell metaplasia that predisposes to malignancy.
  • The cell that gives rise to Barrett metaplasia is not known.
  • It has been proposed that the metaplasia may arise from a change in the differentiation pattern of stem cells that either reside in the esophagus or are recruited to the esophagus from the bone marrow.
  • Alternatively, it is possible that Barrett metaplasia develops through the conversion of one differentiated cell type into another.
  • Regardless of the cell of origin, Barrett metaplasia ultimately must be sustained by stem cells, which might be identified by intestinal stem cell markers.
  • If Barrett cancers develop from Barrett stem cells, then a therapy targeted at those stem cells might prevent esophageal adenocarcinoma.
  • This report reviews the risk factors for Barrett esophagus and esophageal adenocarcinoma, the mechanisms by which genetic alterations might contribute to carcinogenesis in Barrett esophagus, and the role of stem cells in the development of Barrett metaplasia and adenocarcinoma.

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  • (PMID = 18703277.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK063621-06A2; United States / NIDDK NIH HHS / DK / R01 DK063621; United States / NIDDK NIH HHS / DK / DK 63621; United States / NIDDK NIH HHS / DK / R01 DK063621-06A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Ireland
  • [Number-of-references] 71
  • [Other-IDs] NLM/ NIHMS98405; NLM/ PMC2673195
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32. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • [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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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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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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33. Hes O, Curík R, Mainer K, Michal M: Urothelial signet-ring cell carcinoma of the renal pelvis with collagenous spherulosis: a case report. Int J Surg Pathol; 2005 Oct;13(4):375-8
MedlinePlus Health Information. consumer health - Kidney Cancer.

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  • No signs of intestinal type of metaplasia and adenocarcinoma, changes similar to the cystitis cystica or cystitis glandularis, were found in the tumor or in its vicinity.
  • [MeSH-major] Carcinoma, Signet Ring Cell / diagnosis. Carcinoma, Signet Ring Cell / pathology. Collagen / analysis. Kidney Neoplasms / diagnosis. Kidney Neoplasms / pathology

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  • (PMID = 16273199.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 68238-35-7 / Keratins; 9007-34-5 / Collagen
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34. Abdel-Latif MM, O'Riordan JM, Ravi N, Kelleher D, Reynolds JV: Activated nuclear factor-kappa B and cytokine profiles in the esophagus parallel tumor regression following neoadjuvant chemoradiotherapy. Dis Esophagus; 2005;18(4):246-52
Hazardous Substances Data Bank. FLUOROURACIL .

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  • Esophageal adenocarcinoma is increasing in incidence; it relates to chronic gastroesophageal reflux, it is difficult to cure, and treatment modalities increasingly use chemotherapy and radiation therapy prior to resectional surgery.
  • Nuclear factor-kappa B (NF-kappaB) is a pleiotropic transcription factor that regulates several genes for cytokines and enzymes involved in inflammation and immunity, and we have previously described sequential expression of NF-kappaB from the normal esophagus through Barrett's metaplasia to adenocarcinoma.
  • The aim of this exploratory study was to assess the NF-kappaB status and cytokine profiles pre- and post-chemoradiotherapy for esophageal adenocarcinoma.
  • Fresh biopsy specimens obtained from 20 patients with esophageal adenocarcinoma and normal adjacent squamous epithelium were obtained pre-, during and post-chemoradiotherapy, and NF-kappaB expression was analyzed by electrophoretic mobility shift assay.
  • NF-kappaB was constitutively activated in tumor tissues from esophageal adenocarcinoma but was not detected in adjacent normal esophageal mucosa.

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  • (PMID = 16128781.001).
  • [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] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Interleukin-1; 0 / Interleukin-8; 0 / NF-kappa B; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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35. Castilloux J, Bouron-Dal Soglio D, Faure C: Endoscopic assessment of children with esophageal atresia: Lack of relationship of esophagitis and esophageal metaplasia to symptomatology. Can J Gastroenterol; 2010 May;24(5):312-6
MedlinePlus Health Information. consumer health - Swallowing Disorders.

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  • [Title] Endoscopic assessment of children with esophageal atresia: Lack of relationship of esophagitis and esophageal metaplasia to symptomatology.
  • Endoscopy was considered normal if no esophagitis, intestinal metaplasia or gastric metaplasia (GM) was discerned.
  • No intestinal metaplasia or adenocarcinoma was detected.
  • [MeSH-major] Deglutition Disorders / etiology. Endoscopy, Gastrointestinal / methods. Esophageal Atresia / diagnosis. Esophagitis / diagnosis. Esophagus / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cross-Sectional Studies. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Infant. Male. Metaplasia / complications. Metaplasia / diagnosis. Retrospective Studies

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  • (PMID = 20485706.001).
  • [ISSN] 0835-7900
  • [Journal-full-title] Canadian journal of gastroenterology = Journal canadien de gastroenterologie
  • [ISO-abbreviation] Can. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC2886573
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36. Bobryshev YV, Lu J, Lord RV: Expression of C1q complement component in Barrett's esophagus and esophageal adenocarcinoma. J Gastrointest Surg; 2010 Aug;14(8):1207-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of C1q complement component in Barrett's esophagus and esophageal adenocarcinoma.
  • The present study investigated whether C1q is expressed in Barrett's esophagus and esophageal adenocarcinoma and, if so, whether its expression is associated with dendritic cells.
  • MATERIAL AND METHODS: Endoscopic biopsy or operative surgical specimens were obtained from 15 patients with Barrett's esophagus, 13 patients with esophageal adenocarcinoma and 12 patients whose biopsy specimens did not show the presence of specialized intestinal metaplasia or adenocarcinoma.
  • Barrett's esophagus was diagnosed by the presence of a macroscopic area of columnar-lined esophagus as well as microscopic intestinal metaplasia with goblet cells.
  • A computerized quantitative analysis showed that C1q expression was significantly higher in tissue specimens without specialized intestinal-type metaplasia than in Barrett's esophagus specimens and specimens with adenocarcinoma.
  • CONCLUSION: The findings suggest that reduced levels of the expression of C1q by dendritic cells and macrophages in the esophagus may play a role in the formation of immune responses associated with the formation of specialized intestinal metaplasia and the development of adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Complement C1q / genetics. Esophageal Neoplasms / genetics. Gene Expression Regulation, Neoplastic. Precancerous Conditions / genetics. RNA, Neoplasm / genetics

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  • (PMID = 20496011.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Neoplasm; 80295-33-6 / Complement C1q
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37. Anderson MR, Harrison R, Atherfold PA, Campbell MJ, Darnton SJ, Obszynska J, Jankowski JA: Met receptor signaling: a key effector in esophageal adenocarcinoma. Clin Cancer Res; 2006 Oct 15;12(20 Pt 1):5936-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Met receptor signaling: a key effector in esophageal adenocarcinoma.
  • PURPOSE: The incidence of esophageal adenocarcinoma is rising, and survival rates remain poor.
  • We assessed the prognostic significance of Met expression in esophageal adenocarcinoma.
  • RESULTS: An increased expression of Met was seen along the metaplasia- adenocarcinoma sequence.
  • Inhibitors of Met may be effective treatment for esophageal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / physiopathology. Esophageal Neoplasms / physiopathology. Proto-Oncogene Proteins / genetics. Receptors, Growth Factor / genetics

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  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 17062664.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / DNA Primers; 0 / HGF protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Growth Factor; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
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38. Flaig TW, La Rosa FG, McKinney K, Maroni P, Wilson S: A man with changes in the urinary bladder: benign metaplasia or adenocarcinoma? Oncology (Williston Park); 2009 Feb;23(2):177-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A man with changes in the urinary bladder: benign metaplasia or adenocarcinoma?
  • [MeSH-major] Adenocarcinoma / diagnosis. Cystitis / diagnosis. Kidney Neoplasms / diagnosis. Lymphatic Diseases / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Male. Metaplasia. Nephrolithiasis / complications. Referral and Consultation

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  • MedlinePlus Health Information. consumer health - Lymphatic Diseases.
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  • (PMID = 19323300.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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