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1. Rastogi A, Sharma P: Short-Segment Barrett's Esophagus and Adenocarcinoma. Gastroenterol Hepatol (N Y); 2006 Feb;2(2):134-139

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Short-Segment Barrett's Esophagus and Adenocarcinoma.
  • Barrett's esophagus is a known risk factor for the development of adenocarcinoma of the esophagus and esophagogastric junction.
  • The rapid rise in the incidence of esophageal adenocarcinoma has generated sustained research interest in this lesion.
  • Studies have shown that although the prevalence of short-segment Barrett's esophagus is higher than that of long-segment Barrett's esophagus, the risk of developing dysplasia and adenocarcinoma may actually be lower in those patients with short segment Barrett's esophagus.
  • Nonetheless, both dysplasia and esophageal adenocarcinoma have been reported in patients with short-segment Barrett's esophagus, making this arbitrary distinction clinically unimportant.
  • Another key issue is differentiating short-segment Barrett's esophagus from intestinal metaplasia of the gastric cardia.
  • The latter is distinct from esophageal intestinal metaplasia (ie, Barrett's esophagus) and probably does not warrant surveillance.

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  • (PMID = 28286441.001).
  • [ISSN] 1554-7914
  • [Journal-full-title] Gastroenterology & hepatology
  • [ISO-abbreviation] Gastroenterol Hepatol (N Y)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Barrett’s esophagus / adenocarcinoma / high-grade dysplasia / long-segment Barrett’s esophagus / low-grade dysplasia / short-segment Barrett’s esophagus
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2. 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
Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .

  • [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


3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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4. 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
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] 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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5. 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


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
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  • [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. 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.
  • 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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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
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  • [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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  • [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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  • [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
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  • [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. 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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14. 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
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  • [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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15. Abdo-Francis JM, Sobrino-Cossío S, Bernal-Sahagún F, Hernández-Guerrero A: [Prevalence of intestinal metaplasia of the gastric cardia and its relation with Helicobacter pylori strains cagA and vacA]. Cir Cir; 2010 Jul-Aug;78(4):315-21
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  • [Title] [Prevalence of intestinal metaplasia of the gastric cardia and its relation with Helicobacter pylori strains cagA and vacA].
  • [Transliterated title] Prevalencia de metaplasia intestinal en el cardias gástrico y su relación con cepas virulentas de Helicobacter pylori cagA y vacA.
  • BACKGROUND: Esophageal metaplasia progression is a consequence of chronic gastroesophageal reflux (CGR).
  • In addition, they present an increased risk for the development of gastric adenocarcinoma.
  • We undertook this study to establish a relationship between the presence of pathogenic Helicobacter pylori strains and the presence of metaplasia progression in patients with CGR.
  • Cardiac intestinal metaplasia was observed in 35% of the patients.
  • A marked tendency was observed to develop cardiac intestinal metaplasia in those patients diagnosed with high-pathogenicity strains infected in both anatomic areas.
  • CONCLUSIONS: These results suggest that infection with Helicobacter pylori can be considered a risk factor for developing gastric cardiac intestinal metaplasia.
  • [MeSH-minor] Adult. Aged. Biopsy. Cross-Sectional Studies. Female. Gastroesophageal Reflux / complications. Gastroscopy. Humans. Male. Metaplasia / epidemiology. Metaplasia / etiology. Middle Aged. Neutrophils / pathology. Precancerous Conditions / epidemiology. Precancerous Conditions / etiology. Precancerous Conditions / microbiology. Precancerous Conditions / pathology. Prospective Studies. Species Specificity. Virulence. Young Adult

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  • (PMID = 21167097.001).
  • [ISSN] 0009-7411
  • [Journal-full-title] Cirugía y cirujanos
  • [ISO-abbreviation] Cir Cir
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / VacA protein, Helicobacter pylori; 0 / cagA protein, Helicobacter pylori
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16. 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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  • [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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17. Mercer SJ, Toh SK, Somers SS: Esophageal adenocarcinoma developing above an Angelchik prosthesis. Dis Esophagus; 2007;20(6):546-8
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  • [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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18. Pellicano R, Fagoonee S, Palestro G, Rizzetto M, Ponzetto A: [Intestinal metaplasia, dysplasia, gastric cancer and Helicobacter pylori: epidemiological observations]. Minerva Med; 2005 Feb;96(1):1-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Intestinal metaplasia, dysplasia, gastric cancer and Helicobacter pylori: epidemiological observations].
  • [Transliterated title] Metaplasia intestinale, displasia, cancro gastrico e Helicobacter pylori: considerazioni epidemiologiche.
  • [MeSH-major] Adenocarcinoma / microbiology. Helicobacter Infections / complications. Helicobacter pylori. Stomach Neoplasms / microbiology
  • [MeSH-minor] Humans. Metaplasia / microbiology

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  • (PMID = 15827537.001).
  • [ISSN] 0026-4806
  • [Journal-full-title] Minerva medica
  • [ISO-abbreviation] Minerva Med.
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 74
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19. 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
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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20. Wijnhoven BP, Hussey DJ, Watson DI, Tsykin A, Smith CM, Michael MZ, South Australian Oesophageal Research Group: MicroRNA profiling of Barrett's oesophagus and oesophageal adenocarcinoma. Br J Surg; 2010 Jun;97(6):853-61
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  • [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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21. Sánchez-Fayos P, Martín Relloso MJ, González Guirado A, Porres Cubero JC: [Gastric adenocarcinoma: approach to a complex biological reality]. Med Clin (Barc); 2007 Jan 13;128(1):21-30
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  • [Title] [Gastric adenocarcinoma: approach to a complex biological reality].
  • [Transliterated title] Adenocarcinoma gástrico: intento de aproximación a una realidad biológica compleja.
  • The authors review the complex biological reality of gastric adenocarcinoma from several viewpoints.
  • A good knowledge of this complex biological reality will allow the identification of better markers for an early diagnosis as well as vulnerable etiopathogenetic points for a useful prevention and therapy.
  • [MeSH-major] Adenocarcinoma. Stomach Neoplasms
  • [MeSH-minor] Achlorhydria / complications. Aged. Diet / adverse effects. Early Diagnosis. Epithelial Cells / cytology. Epithelial Cells / pathology. Female. Gastric Mucosa / pathology. Gastritis, Atrophic / complications. Helicobacter Infections / complications. Helicobacter pylori. Humans. Incidence. Male. Metaplasia. Middle Aged. Mitosis. Precancerous Conditions / chemically induced. Precancerous Conditions / pathology. Risk Factors. Stomach / pathology

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  • (PMID = 17266889.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 107
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22. 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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  • [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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23. Mader AM, Patrício FR, Rigueiro MP, Lourenço LG: [Analysis of clinicopathological, tumor cell proliferation and apoptosis parameters in adenocarcinoma of the gastric cardia]. Arq Gastroenterol; 2006 Jul-Sep;43(3):184-90
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  • [Title] [Analysis of clinicopathological, tumor cell proliferation and apoptosis parameters in adenocarcinoma of the gastric cardia].
  • [Transliterated title] Estudo clínico-patológico, da proliferação celular e da apoptose no adenocarcinoma gástrico da cárdia.
  • MATERIAL AND METHODS: Forty cases of adenocarcinoma of the cardia were studied between 1988 and 2001, with a minimum clinical follow-up of 3 years.
  • Gender; age, Laurén and Ming histological type, staging, and the presence or absence of intestinal metaplasia, epithelial dysplasia and Helicobacter pylori in the adjacent mucosa were analyzed.
  • For the survival analysis, cases with distant metastasis upon diagnosis were excluded.
  • There was no association with intestinal metaplasia and/or H. pylori.
  • CONCLUSIONS: Adenocarcinoma of the cardia predominated in male adults of mean age 61 years, and the predominant type was diffuse in more advanced stages.
  • Survival in cases of adenocarcinoma of the cardia is still low.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis. Cardia / pathology. Cell Proliferation. Stomach Neoplasms / pathology

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  • (PMID = 17160232.001).
  • [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 / Proliferating Cell Nuclear Antigen
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24. 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
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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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25. Chaves P, Cruz C, Dias Pereira A, Suspiro A, de Almeida JC, Leitão CN, Soares J: Gastric and intestinal differentiation in Barrett's metaplasia and associated adenocarcinoma. Dis Esophagus; 2005;18(6):383-7
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  • [Title] Gastric and intestinal differentiation in Barrett's metaplasia and associated adenocarcinoma.
  • Intestinal metaplasia is a prerequisite criterion for the diagnosis of Barrett's metaplasia and the sole columnar esophageal lining associated with malignancy.
  • The cellular heterogeneity of Barrett's metaplasia is well documented but the relationship between the distinct cell subtypes and neoplasia is unclear.
  • We studied 46 columnar-lined esophageal segments, 15 with associated adenocarcinoma.
  • In metaplasia there were no differences in MUC5AC and MUC6 immunoreactivity, between cases with and without associated neoplasia, except for goblet elements producing MUC6 that were exclusive of metaplasia adjacent to adenocarcinoma (P < 0.05).
  • In metaplasia it was restricted to Barrett's cases and was more frequent in areas with intestinal metaplasia.
  • Columnar-lined esophagus without intestinal metaplasia did not express MUC2.

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  • (PMID = 16336609.001).
  • [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 / Biomarkers, Tumor; 0 / Gastric Mucins; 0 / MUC6 protein, human; 0 / Mucin-6; 0 / Mucins; 0 / apomucin
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26. Colleypriest BJ, Ward SG, Tosh D: How does inflammation cause Barrett's metaplasia? Curr Opin Pharmacol; 2009 Dec;9(6):721-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How does inflammation cause Barrett's metaplasia?
  • Oesophageal adenocarcinoma conveys a poor prognosis and has a rapidly increasing incidence.
  • Similarly, Barrett's metaplasia (a precursor lesion for oesophageal adenocarcinoma) has an increasing incidence.
  • Both oesophageal adenocarcinoma and Barrett's metaplasia are more common in the context of inflammation as a result of acid and bile reflux.
  • The cytokine profile of Barrett's metaplasia is predominantly a T-helper 2 response that contrasts with the T-helper 1 response in normal and inflamed oesophagus and normal intestine.
  • A key transcription factor in the development of Barrett's metaplasia, CDX2, has recently been shown to be induced in response to inflammatory mediators.
  • Understanding the role of oesophageal inflammation will provide important insight into the development of Barrett's metaplasia and oesophageal cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / etiology. Barrett Esophagus / metabolism. Esophageal Neoplasms / metabolism. Esophagitis / complications
  • [MeSH-minor] Animals. Cyclooxygenase 2 / metabolism. Cytokines / metabolism. Humans. Metaplasia / metabolism. Metaplasia / pathology. Models, Immunological. NF-kappa B / metabolism. Precancerous Conditions / metabolism. Precancerous Conditions / pathology

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  • (PMID = 19828375.001).
  • [ISSN] 1471-4973
  • [Journal-full-title] Current opinion in pharmacology
  • [ISO-abbreviation] Curr Opin Pharmacol
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300415
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / NF-kappa B; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 53
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27. Mukonoweshuro P, Oriowolo A: Stromal osseous metaplasia in a low-grade ovarian adenocarcinoma. Gynecol Oncol; 2005 Oct;99(1):222-4
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  • [Title] Stromal osseous metaplasia in a low-grade ovarian adenocarcinoma.
  • BACKGROUND: Stromal osseous metaplasia is a rare and curious finding in tumors of the ovary.
  • CASE REPORT: The patient, a 66-year-old P3 G3 white female, had a past history of stage 1c left ovarian, well-differentiated endometrioid adenocarcinoma removed in 1981.
  • The tumor recurred 21 years later with prominent stromal osseous metaplasia that had not been present in the primary.
  • DISCUSSION: The pathogenesis of osseous metaplasia in epithelial tumors of the ovary is unclear; however, it is probable that a metaplastic process involving multipotential stromal stem cells results in bone formation.
  • CONCLUSION: Benign osseous metaplasia in ovarian tumors is rare and its histogenesis remains unclear.
  • [MeSH-minor] Aged. Female. Humans. Metaplasia

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  • (PMID = 16023183.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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28. 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 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.
  • 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.
  • No correlation was identified when the c-Myc expression was compared with morphologic and histologic tumor features or endoscopic data.
  • 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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29. Pantanowitz L: Colonic adenoma with squamous metaplasia. Int J Surg Pathol; 2009 Aug;17(4):340-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Colonic adenoma with squamous metaplasia.
  • Squamous metaplasia arising within colon adenomas is a rare occurrence, with a 0.4% incidence noted predominantly in elderly males.
  • A case of squamous metaplasia arising in a tubulovillous adenoma of the cecum, associated with adenocarcinoma, is described.
  • Squamous metaplasia was immunoreactive for beta-catenin, but negative for cytokeratin 20, CDX2, p63, estrogen receptor, progesterone receptor, p16, and human papilloma virus.
  • [MeSH-minor] Adenocarcinoma / pathology. Aged. Biomarkers, Tumor / analysis. Colectomy. Female. Humans. Metaplasia / pathology. Metaplasia / surgery. Neoplasms, Second Primary / pathology. Precancerous Conditions / pathology. beta Catenin / analysis

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  • (PMID = 18701516.001).
  • [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] 0 / Biomarkers, Tumor; 0 / beta Catenin
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30. Sakurai T, Sakashita H, Honjo G, Kasyu I, Manabe T: Gastric foveolar metaplasia with dysplastic changes in Brunner gland hyperplasia: possible precursor lesions for Brunner gland adenocarcinoma. Am J Surg Pathol; 2005 Nov;29(11):1442-8
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  • [Title] Gastric foveolar metaplasia with dysplastic changes in Brunner gland hyperplasia: possible precursor lesions for Brunner gland adenocarcinoma.
  • Herein, we report the morphologic spectrum of hyperplastic changes culminating into dysplasia and carcinoma in 722 cases of BGH listed in our files.
  • Interestingly, hyperplastic glands around dysplastic foci were associated with gastric foveolar metaplasia and papillary configuration in 13 cases, 11 of which showed a gradual increase in nuclear atypism in the transition from metaplastic to dysplastic glands.
  • Immunohistochemical profiles also supported the concept of a continuous spectrum in carcinogenesis from gastric foveolar hyperplasia through atypical hyperplasia or dysplasia and eventually to frank adenocarcinoma.
  • The results of our study suggest, therefore, that dysplastic and/or carcinomatous change does occur in BGH, that they form the continuous morphologic spectrum, and that papillary foveolar metaplasia may be a precursor lesion in the process of carcinogenesis with a background of BGH.
  • [MeSH-major] Adenocarcinoma / pathology. Brunner Glands / pathology. Precancerous Conditions / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Transformation, Neoplastic. Disease Progression. Female. Humans. Hyperplasia. Male. Metaplasia. Middle Aged. Mucin 5AC. Mucins / biosynthesis

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  • (PMID = 16224210.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucins
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31. de Faria PC Jr, Andreollo NA, Trevisan MA, Lopes LR: [Relationship of the sialomucins (Tn and Stn antigens) with adenocarcinoma in Barrett's esophagus]. Rev Assoc Med Bras (1992); 2007 Jul-Aug;53(4):360-4
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  • [Title] [Relationship of the sialomucins (Tn and Stn antigens) with adenocarcinoma in Barrett's esophagus].
  • [Transliterated title] A inter-relação das sialomucinas (antígenos Tn e Stn) com o adenocarcinoma no esôfago de Barrett.
  • OBJECTIVE: Barrett's esophagus (BE) is a consequence of chronic gastroesophageal reflux and is considered a risk factor for adenocarcinoma.
  • The study of the mucus, especially acid mucins, such as the sialomucins in the goblet cells which characterize BE, showed that in intestinal metaplasia, frequent in the digestive tract, the organ's original epithelium could express Tn and Stn antigens.
  • This research aimed to analyze these antigens in patients with BE and in adenocarcinoma associated with BE.
  • METHODS: Utilizing immunohistochemistry tests, Tn and Stn antigens were studied in the endoscopic biopsies of 29 patients with BE and seven with adenocarcinoma in BE, as well as eight individuals with normal esophageal epithelium at upper digestive endoscopy.
  • However, in adenocarcinoma in BE, both antigens were 100% positive.
  • CONCLUSION: It is probable that the BE group in which the Tn antigens in the goblet cells are positive, similarly to the same antigen in the adenocarcinoma group, might indicate a higher susceptibility for potential occurrence of cancer.
  • In the future, trials with sialomucins could be used routinely, thereby contributing as a prognostic factor of adenocarcinoma in BE.
  • [MeSH-major] Adenocarcinoma / immunology. Barrett Esophagus / immunology. Esophageal Neoplasms / immunology. Sialomucins / analysis

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  • (PMID = 17823742.001).
  • [ISSN] 0104-4230
  • [Journal-full-title] Revista da Associação Médica Brasileira (1992)
  • [ISO-abbreviation] Rev Assoc Med Bras (1992)
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Biomarkers, Tumor; 0 / Sialomucins; 0 / Tn antigen; 0 / sialosyl-Tn antigen
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32. Pera M, Grande L, Iglesias M, Ramón JM, Conio M: [New advances in the diagnosis and treatment of early onset dysplasia and adenocarcinoma in Barrett's oesophagus]. Cir Esp; 2009 Jun;85(6):331-40
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  • [Title] [New advances in the diagnosis and treatment of early onset dysplasia and adenocarcinoma in Barrett's oesophagus].
  • [Transliterated title] Nuevos avances en el diagnóstico y el tratamiento de la displasia y el adenocarcinoma precoz en el esófago de Barrett.
  • Periodic endoscopic follow-up is recommended after the diagnosis of Barrett's oesophagus, particularly in patients with dysplasia.
  • The new endoscopic techniques show promising results in identifying areas suspected of housing high grade dysplasia and adenocarcinoma.
  • Likewise, this technique may be the therapeutic option in patients with high grade dysplasia and adenocarcinoma, although its application must be complemented with ablation techniques such as radiofrequency to eliminate the residual Barrett's metaplasia.
  • Oesophagectomy associated with lymphadenectomy is the option of choice in patients with submucosal adenocarcinoma.
  • The diagnosis and treatment of patients with early onset high grade dysplasia and adenocarcinoma must be carried out with multidisciplinary teams who can evaluate each case individually.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / surgery. Barrett Esophagus / complications. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / surgery. Esophagus / pathology

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  • (PMID = 19463990.001).
  • [ISSN] 0009-739X
  • [Journal-full-title] Cirugía española
  • [ISO-abbreviation] Cir Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Number-of-references] 71
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33. 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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34. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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35. 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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  • [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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36. 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
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  • [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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37. Leys CM, Nomura S, Rudzinski E, Kaminishi M, Montgomery E, Washington MK, Goldenring JR: Expression of Pdx-1 in human gastric metaplasia and gastric adenocarcinoma. Hum Pathol; 2006 Sep;37(9):1162-8
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  • [Title] Expression of Pdx-1 in human gastric metaplasia and gastric adenocarcinoma.
  • Metaplastic lineages represent critical putative preneoplastic precursors for gastrointestinal metaplasia.
  • Two metaplastic processes are associated with gastric cancer: intestinal metaplasia (the presence of intestinal goblet cell containing lineages in the stomach) and spasmolytic polypeptide-expressing metaplasia (SPEM; antralization of the gastric fundus).
  • We have therefore sought to examine the presence of Pdx-1 expression in gastric metaplasias and gastric adenocarcinoma in humans.
  • Tissue microarrays containing gastric cancers from the fundus and antrum and samples of SPEM and intestinal metaplasia were immunostained for Pdx-1.
  • Although SPEM lineages did not show any staining for Pdx-1, intestinal metaplasia showed strong nuclear staining for Pdx-1.
  • Thus, Pdx-1 expression is not associated with antralizing metaplasia (SPEM) but is associated with intestinal metaplasia.
  • Given the pattern of normal Pdx-1 expression in the duodenum, goblet cell metaplasia in the stomach may reflect the adoption of a duodenal lineage paradigm.
  • [MeSH-major] Adenocarcinoma / metabolism. Homeodomain Proteins / biosynthesis. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism. Trans-Activators / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Female. Humans. Male. Metaplasia

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  • (PMID = 16938521.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P 50 CA95103; United States / NCI NIH HHS / CA / K12 CA090625
  • [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 / Homeodomain Proteins; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein
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38. 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.
  • 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-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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39. Friedrich-Rust M, Jaeger C, Gossner L, May A, Günter E, Stolte M, Ell C: [Early duodenal adenocarcinoma arising in gastric metaplasia treated by endoscopic resection]. Z Gastroenterol; 2006 Apr;44(4):323-8
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  • [Title] [Early duodenal adenocarcinoma arising in gastric metaplasia treated by endoscopic resection].
  • This report describes the case of a 59-year-old lady with an early duodenal adenocarcinoma diagnosed at check-up gastroduodenoscopy in an outpatient clinic who was referred to us for further investigation and management.
  • Histopathological examination revealed the rare entity of an early duodenal carcinoma arising from incomplete-type gastric metaplasia in the duodenum.
  • In summary, the presented paper describes a case of successful endoscopic treatment of an early duodenal carcinoma arising from incomplete gastric metaplasia.
  • [MeSH-major] Adenocarcinoma / surgery. Duodenal Neoplasms / surgery. Endoscopy, Gastrointestinal. Stomach / pathology
  • [MeSH-minor] Female. Humans. Metaplasia / complications. Metaplasia / pathology. Metaplasia / surgery. Middle Aged. Stomach Diseases / complications. Treatment Outcome

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  • (PMID = 16625461.001).
  • [ISSN] 0044-2771
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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40. Sharma P, Wani S, Bansal A: The quest for intestinal metaplasia--is it worth the effort? Am J Gastroenterol; 2007 Jun;102(6):1162-5
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  • [Title] The quest for intestinal metaplasia--is it worth the effort?
  • Starting with the basics, the definition and diagnosis of Barrett's esophagus (BE) continues to be a point of major debate globally leading to definitions that have been restrictive (requiring histologically confirmed intestinal metaplasia) or all-encompassing (simply the presence of CLE at endoscopy).
  • The interest in intestinal metaplasia stems from studies that have consistently demonstrated intestinal metaplasia and dysplasia both adjacent to and remote from esophageal adenocarcinoma.
  • The proponents of not requiring histology suggest that if a sufficient number of biopsies is obtained over an adequate period of time, intestinal metaplasia can usually be demonstrated in such cases and that the true neoplastic potential of the cardiac and fundic-type mucosa detected in the CLE has not been delineated.
  • The optimal number of biopsies required to detect intestinal metaplasia is largely unknown, and in this issue of The American Journal of Gastroenterology, Harrison et al. add to the limited data on this subject.
  • There is ample evidence that once a diagnosis of BE is made, it has significant implications on the financial, psychosocial, and insurance status of the patients.
  • We feel that an optimal, practical definition of BE requires clear, accepted, reproducible, and clinically relevant criteria with evidence of an increased risk of cancer--the most crucial consequence of the lesion--and discuss the pros and cons of the need for documenting intestinal metaplasia in the CLE.
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Biopsy. Diagnostic Imaging. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology. Gastric Mucosa / pathology. Humans. Metaplasia. Precancerous Conditions / pathology

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  • [CommentOn] Am J Gastroenterol. 2007 Jun;102(6):1154-61 [17433019.001]
  • (PMID = 17531009.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] United States
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41. 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
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  • [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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  • (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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42. Griffiths EA, Pritchard SA, McGrath SM, Valentine HR, Price PM, Welch IM, West CM: Increasing expression of hypoxia-inducible proteins in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence. Br J Cancer; 2007 May 7;96(9):1377-83
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  • [Title] Increasing expression of hypoxia-inducible proteins in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
  • Our aim was to assess the immunohistochemical expression of hypoxia-inducible factor (HIF)-1alpha, HIF-2alpha, erythropoietin (Epo), Epo receptor (Epo-R), Glut-1 and vascular endothelial growth factor (VEGF) along with Ki67/MIB-1 in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
  • Endoscopic biopsies of normal squamous epithelium (NSE) (n=20), columnar-lined oesophagus (CLO) (n=15), CLO with intestinal metaplasia (n=20), dysplasia (n=17) and Barrett's type adenocarcinoma (n=20) were obtained.
  • Significant increases in the expression of HIF-2alpha (P=0.014), VEGF (P<0.0001), Epo-R (P<0.0001) and Ki67 (P<0.0001) were found as tissue progressed from NSE to adenocarcinoma.
  • HIF-2alpha was expressed late in the sequence and was only seen in dysplasia and adenocarcinoma.
  • High HIF-2alpha expression was seen in 12 out of 20 Barrett's type adenocarcinoma.
  • The late expression of HIF-2alpha in the Barrett's carcinogenesis sequence and its high expression in adenocarcinoma suggest that it is worth further investigation as a marker of disease progression and therapeutic target.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Basic Helix-Loop-Helix Transcription Factors / metabolism. Esophageal Neoplasms / pathology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • [MeSH-minor] Biopsy. Disease Progression. Epithelial Cells / cytology. Epithelial Cells / pathology. Esophageal Diseases / pathology. Esophagus / cytology. Esophagus / pathology. Immunohistochemistry. Ki-67 Antigen / metabolism. Metaplasia. Receptors, Erythropoietin / metabolism. Reference Values. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 17437013.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Ki-67 Antigen; 0 / Receptors, Erythropoietin; 0 / Vascular Endothelial Growth Factor A; 0 / endothelial PAS domain-containing protein 1
  • [Other-IDs] NLM/ PMC2360174
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43. 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.
  • [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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44. Colleypriest BJ, Farrant JM, Slack JM, Tosh D: The role of Cdx2 in Barrett's metaplasia. Biochem Soc Trans; 2010 Apr;38(2):364-9
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  • [Title] The role of Cdx2 in Barrett's metaplasia.
  • Metaplasia (or transdifferentiation) is defined as the transformation of one tissue type to another.
  • Clues to the molecular mechanisms that control the development of metaplasia are implied from knowledge of the transcription factors that specify tissue identity during normal embryonic development.
  • Barrett's metaplasia describes the development of a columnar/intestinal phenotype in the squamous oesophageal epithelium and is the major risk factor for oesophageal adenocarcinoma.
  • The homoeotic transcription factor Cdx2 (Caudal-type homeobox 2) has been implicated as a master switch gene for intestine and therefore for Barrett's metaplasia.
  • In addition, Cdx2 is sufficient to provoke intestinal metaplasia in the stomach.
  • In the present paper, we review the evidence for the role of Cdx2 in the development of Barrett's metaplasia.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. CDX2 Transcription Factor. Esophageal Neoplasms / genetics. Esophageal Neoplasms / pathology. Humans. Metaplasia / genetics. Models, Biological

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  • (PMID = 20298184.001).
  • [ISSN] 1470-8752
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300415; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins
  • [Number-of-references] 72
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45. 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
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  • [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


46. Elfvin A, Bölin I, Von Bothmer C, Stolte M, Watanabe H, Fändriks L, Vieth M: Helicobacter pylori induces gastritis and intestinal metaplasia but no gastric adenocarcinoma in Mongolian gerbils. Scand J Gastroenterol; 2005 Nov;40(11):1313-20
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  • [Title] Helicobacter pylori induces gastritis and intestinal metaplasia but no gastric adenocarcinoma in Mongolian gerbils.
  • OBJECTIVE: The Mongolian gerbil is considered as the model of choice when studying adenocarcinoma related to Helicobacter pylori infection.
  • Intestinal metaplasia was found in both the infected groups.
  • Glands buried in the submucusal layer, changes that might be misinterpreted as adenocarcinoma, were found in 10% of the SS1 and in 65% of the TN2GF4 animals.
  • Adenocarcinoma was not found in any of the gerbils.
  • It is suggested that atypical glands in the muscularis layer are not enough as a diagnostic criterion for gastric adenocarcinoma.
  • It is concluded that adenocarcinoma has not yet been shown convincingly to develop in Mongolian gerbils infected with H. pylori.
  • Nevertheless, it is a model well suited for studying gastritis, gastric ulcer and premalignant changes such as metaplasia.
  • [MeSH-minor] Adenocarcinoma / microbiology. Adenocarcinoma / pathology. Animals. Biopsy, Needle. Disease Models, Animal. Gastric Mucosa / microbiology. Gastric Mucosa / pathology. Gerbillinae. Immunohistochemistry. Intestinal Mucosa / microbiology. Intestinal Mucosa / pathology. Male. Random Allocation. Reference Values. Risk Factors. Sensitivity and Specificity. Stomach Neoplasms / microbiology. Stomach Neoplasms / pathology

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  • (PMID = 16334441.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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47. Izzo JG, Luthra R, Wu TT, Correa AM, Luthra M, Anandasabapathy S, Chao KS, Hung MC, Aggarwal B, Hittelman WN, Ajani JA: Molecular mechanisms in Barrett's metaplasia and its progression. Semin Oncol; 2007 Apr;34(2 Suppl 1):S2-6
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  • [Title] Molecular mechanisms in Barrett's metaplasia and its progression.
  • The dramatic increase in the incidence and poor overall survival rates of esophageal/gastroesophageal junction adenocarcinoma underscore the necessity to discover molecular markers that can be used for risk assessment, early diagnosis, and targeted therapeutic intervention.
  • Barrett's esophagus (BE) is proposed to represent a precursor of esophageal/gastroesophageal junction adenocarcinoma.
  • BE progression to invasive cancer is defined by a metaplasia-dysplasia-carcinoma progression characterized by an increasing accumulation of genetic changes associated with alterations in molecular gatekeepers of cell circuitries and tissue homeostasis.
  • [MeSH-minor] Adenocarcinoma / pathology. Cell Transformation, Neoplastic / pathology. Chemoprevention. Cyclin D1 / physiology. Disease Progression. Early Diagnosis. Humans. Metaplasia. NF-kappa B / physiology. Risk Assessment. Signal Transduction / physiology. Treatment Outcome

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  • (PMID = 17449347.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 86390; United States / NIDCR NIH HHS / DE / R01 DE 13157-04
  • [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 / Biomarkers, Tumor; 0 / NF-kappa B; 136601-57-5 / Cyclin D1
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48. Joo M, Kim H, Kim MK, Yu HJ, Kim JP: Expression of Ep-CAM in intestinal metaplasia, gastric epithelial dysplasia and gastric adenocarcinoma. J Gastroenterol Hepatol; 2005 Jul;20(7):1039-45
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  • [Title] Expression of Ep-CAM in intestinal metaplasia, gastric epithelial dysplasia and gastric adenocarcinoma.
  • METHOD: We examined the expression of Ep-CAM in 99 cases of gastric adenocarcinoma and associated uninvolved gastric mucosa, 39 cases of gastric biopsy specimens with chronic gastritis (CG) with or without intestinal metaplasia (IM) (25 cases) and gastric epithelial dysplasia (GED) (14 cases) by immunohistochemical staining.
  • In gastric adenocarcinoma, we correlated the results with established prognostic factors, and in IM and GED, with Hepatocyte paraffin 1 (Hep Par 1) expression, introduced as a marker of IM.
  • RESULTS: Ep-CAM overexpression was noted in 0% of normal epithelia, 93.9% of IM, 42.9% of GED and 34.3% of adenocarcinoma.
  • The average immunostaining score of normal epithelia, IM, GED and gastric adenocarcinoma was 0.14 (+/- 0.26), 7.18 (+/- 1.93), 5.67 (+/- 2.29) and 4.09 (+/- 1.89), respectively.
  • Ep-CAM overexpression in adenocarcinoma correlated with Lauren classification and histologic grade, but not with tumor stage, lymph node metastasis and p53 expression.
  • [MeSH-major] Adenocarcinoma / metabolism. Antigens, Neoplasm / biosynthesis. Cell Adhesion Molecules / biosynthesis. Gastric Mucosa / metabolism. Intestines / pathology. Stomach Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Female. Humans. Immunohistochemistry. In Vitro Techniques. Male. Metaplasia / metabolism. Metaplasia / pathology. Middle Aged. Neoplasm Staging

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  • (PMID = 15955212.001).
  • [ISSN] 0815-9319
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / EPCAM protein, human
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49. 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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  • [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.
  • 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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50. Hannachi Sassi S, Dhouib R, Abbes I, Braham E, Mrad K, Driss M, Ben Hamida N, Ben Romdhane K: [Endometrial atypical complex hyperplasia with extensive squamous metaplasia: two cases]. Ann Pathol; 2008 Jun;28(3):233-6

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  • [Title] [Endometrial atypical complex hyperplasia with extensive squamous metaplasia: two cases].
  • The histological study showed an increase in the gland to stroma ratio with a false crowding aspect due to an extensive area of squamous metaplasia; some metaplastic areas were centered by necrosis.
  • Histologic examination is necessary to confirm the diagnosis and to definitively rule out adenocarcinoma.
  • [MeSH-major] Endometrial Hyperplasia / pathology. Endometrium / pathology. Hyperplasia / pathology. Metaplasia / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Diabetes Mellitus, Type 2 / complications. Diabetes Mellitus, Type 2 / pathology. Diagnosis, Differential. Endometrial Neoplasms / pathology. Female. Humans. Middle Aged. Necrosis. Obesity / complications. Obesity / pathology

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  • (PMID = 18706369.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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51. Cai JC, Liu D, Liu KH, Zhang HP, Zhong S, Xia NS: Microsatellite alterations in phenotypically normal esophageal squamous epithelium and metaplasia-dysplasia-adenocarcinoma sequence. World J Gastroenterol; 2008 Jul 7;14(25):4070-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Microsatellite alterations in phenotypically normal esophageal squamous epithelium and metaplasia-dysplasia-adenocarcinoma sequence.
  • AIM: To investigate the microsatellite alterations in phenotypically normal esophageal squamous epithelium and metaplasia-dysplasia-adenocarcinoma sequence.
  • Histopathological assessment identified 23 squamous cell carcinomas (SCC) and 18 adenocarcinomas (ADC), including only 8 ADC with Barrett esophageal columnar epithelium (metaplasia) and dysplasia adjacent to ADC.
  • Paraffin-embedded normal squamous epithelium, Barrett esophageal columnar epithelium (metaplasia), dysplasia and esophageal tumor tissues were dissected from the surrounding tissues under microscopic guidance.
  • The levels of MSI and LOH were high in the metaplasia-dysplasia-adenocarcinoma sequence of diluted DNA.
  • CONCLUSION: The sequence of metaplasia-dysplasia-adenocarcinoma is associated with microsatellite alterations, including MSI and LOH.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Carcinoma, Squamous Cell / genetics. Cell Transformation, Neoplastic / genetics. Esophageal Neoplasms / genetics. Esophagus / pathology. Gene Expression Regulation, Neoplastic. Microsatellite Instability. Precancerous Conditions / genetics
  • [MeSH-minor] Genetic Markers. Genotype. Humans. Loss of Heterozygosity. Metaplasia. Paraffin Embedding. Phenotype. Polymerase Chain Reaction

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  • (PMID = 18609693.001).
  • [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 / Genetic Markers
  • [Other-IDs] NLM/ PMC2725348
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52. Hirschowitz L, Sen C, Murdoch J: Primary endometrioid adenocarcinoma of the cervix with widespread squamous metaplasia--a potential diagnostic pitfall. Diagn Pathol; 2007;2:40

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary endometrioid adenocarcinoma of the cervix with widespread squamous metaplasia--a potential diagnostic pitfall.
  • BACKGROUND: Uterine or endocervical biopsies that contain endometrioid adenocarcinoma with widespread squamous metaplasia are usually of endometrial origin.
  • The presence of squamous metaplasia is said to be helpful in distinguishing endocervical from endometrial adenocarcinomas in small biopsy samples.
  • Biopsy of a friable lesion in the proximal endocervical canal revealed an endocervical adenocarcinoma of endometrioid type with widespread squamous metaplasia.
  • The latter feature initially raised the possible diagnosis of a primary endometrial adenocarcinoma.
  • However, immunohistochemical marker studies indicated a diagnosis of primary endocervical adenocarcinoma of endometrioid type and this was confirmed at hysterectomy.

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  • (PMID = 17961245.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2116996
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53. Mokrowiecka A, Wierzchniewska-Ławska A, Smolarz B, Romanowicz-Makowska H, Malecka-Panas E: [Polymorphism/loss of heterozygosity of APC gene in GERD-Barrett's metaplasia-dysplasia-adenocarcinoma sequence]. Pol Merkur Lekarski; 2009 May;26(155):385-9
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  • [Title] [Polymorphism/loss of heterozygosity of APC gene in GERD-Barrett's metaplasia-dysplasia-adenocarcinoma sequence].
  • The incidence of esophageal adenocarcinoma (ADC) has been increasing rapidly over the past few decades.
  • There is a great need to find molecular biomarkers predicting increased progression risk in GERD-Barrett's metaplasia-dysplasia-adenocarcinoma sequence to improve risk assessment and stratification of patients to surveillance program.
  • AIM OF THE STUDY: To evaluate the polymorphism and prevalence of loss of heterozygosity (LOH) of APC tumor suppressor gene in mataplasia, dysplasia and adenocarcinoma.
  • CONCLUSIONS: APC gene inactivation concerns minority of patients with esophageal adenocarcinoma, however, its detection indicates higher risk of progression to ADC.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adult. Aged. Biomarkers, Tumor / analysis. Disease Progression. Esophagus / pathology. Female. Gastric Mucosa / pathology. Heterozygote. Humans. Hyperplasia. Male. Metaplasia. Middle Aged

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  • (PMID = 19606680.001).
  • [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
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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54. Nambiar PR, Kirchain S, Fox JG: Gastritis-associated adenocarcinoma and intestinal metaplasia in a Syrian hamster naturally infected with Helicobacter species. Vet Pathol; 2005 May;42(3):386-90
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  • [Title] Gastritis-associated adenocarcinoma and intestinal metaplasia in a Syrian hamster naturally infected with Helicobacter species.
  • A previous report on 7- to 12-month-old Syrian hamsters described chronic gastritis and intestinal metaplasia, a putative preneoplastic lesion in the stomach, without cancer.
  • This report describes an invasive adenocarcinoma at the pyloric-duodenal junction in one of nine hamsters at a site of helicobacter-associated inflammation and marked intestinal metaplasia.
  • However, argyrophilic bacteria were demonstrated only within the stomach of the hamster with gastric adenocarcinoma.
  • This is a first report of gastric adenocarcinoma in helicobacter-infected hamsters.
  • [MeSH-major] Adenocarcinoma / veterinary. Gastritis / veterinary. Helicobacter / genetics. Helicobacter Infections / veterinary. Rodent Diseases / microbiology. Rodent Diseases / pathology. Stomach Neoplasms / veterinary
  • [MeSH-minor] Animals. Cricetinae. Immunohistochemistry / veterinary. Mesocricetus. Metaplasia / complications. Metaplasia / pathology. Metaplasia / veterinary. Polymerase Chain Reaction / veterinary

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  • (PMID = 15872391.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Grant] United States / PHS HHS / / R01A137750; United States / NCRR NIH HHS / RR / RR07036
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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55. Hartmann A, Junker K, Dietmaier W, Schröder S, Lopez D, Hofstädter F, Blaszyk H: Molecular evidence for progression of nephrogenic metaplasia of the urinary bladder to clear cell adenocarcinoma. Hum Pathol; 2006 Jan;37(1):117-20
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  • [Title] Molecular evidence for progression of nephrogenic metaplasia of the urinary bladder to clear cell adenocarcinoma.
  • Nephrogenic metaplasia or nephrogenic adenoma of the urinary tract may present a diagnostic challenge in surgical pathology practice.
  • Previous case reports suggest the possibility of nephrogenic metaplasia progressing to clear cell adenocarcinoma, but a malignant potential of nephrogenic metaplasia is generally not acknowledged.
  • A case of a 70-year-old female patient with multiple recurrences of nephrogenic metaplasia of the urinary bladder and subsequent development of clear cell adenocarcinoma is described.
  • Results of molecular studies, particularly comparative genomic hybridization analysis, suggest clonal evolution of nephrogenic metaplasia to clear cell adenocarcinoma in this case.
  • [MeSH-major] Adenocarcinoma, Clear Cell / pathology. Adenoma / pathology. Precancerous Conditions / pathology. Urinary Bladder / pathology. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Clone Cells. Cystectomy. DNA, Neoplasm / analysis. Disease Progression. Disease-Free Survival. Female. Humans. Loss of Heterozygosity. Metaplasia / genetics. Metaplasia / metabolism. Metaplasia / pathology. Neoplasm Recurrence, Local. Nucleic Acid Hybridization. Urethra / surgery

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  • (PMID = 16360424.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
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56. Quinlan JM, Colleypriest BJ, Farrant M, Tosh D: Epithelial metaplasia and the development of cancer. Biochim Biophys Acta; 2007 Sep;1776(1):10-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epithelial metaplasia and the development of cancer.
  • Metaplasia means the conversion, in postnatal life, of one cell type to another.
  • Understanding the steps leading to metaplasia is important for two reasons.
  • Secondly, metaplasia predisposes to certain forms of neoplasia.
  • So understanding the molecular and cellular mechanisms underlying metaplasia will provide insights into clinical diagnosis and potential therapies.
  • One of the best-described examples of metaplasia is Barrett's metaplasia or the appearance of intestinal-like columnar tissue in the oesophagus.
  • Barrett's metaplasia develops as a result of gastro-oesophageal reflux and is considered the precursor lesion for oesophageal adenocarcinoma.
  • While we know quite a bit about the molecular events associated with the development of oesophageal adenocarcinoma, our understanding of the initial events leading to Barrett's metaplasia is lacking.
  • In the present review we will focus on examples of metaplasia that lead to neoplasia and discuss some of the underlying molecular and cellular mechanisms.
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / pathology. Humans. Metaplasia

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  • (PMID = 17618050.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300415; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 137
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57. Wang DH, Clemons NJ, Miyashita T, Dupuy AJ, Zhang W, Szczepny A, Corcoran-Schwartz IM, Wilburn DL, Montgomery EA, Wang JS, Jenkins NA, Copeland NA, Harmon JW, Phillips WA, Watkins DN: Aberrant epithelial-mesenchymal Hedgehog signaling characterizes Barrett's metaplasia. Gastroenterology; 2010 May;138(5):1810-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant epithelial-mesenchymal Hedgehog signaling characterizes Barrett's metaplasia.
  • BACKGROUND & AIMS: The molecular mechanism underlying epithelial metaplasia in Barrett's esophagus remains unknown.
  • Human esophageal squamous epithelial (HET-1A) and adenocarcinoma (OE33) cells were subjected to acid treatment and used in transfection experiments.

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 20138038.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA123945-03; United States / NCI NIH HHS / CA / F32 CA123945-03; United States / NCI NIH HHS / CA / F32 CA123945-02; United States / NCI NIH HHS / CA / F32 CA123945-01; United States / NIDDK NIH HHS / DK / 1K23DK068149; United States / NIDDK NIH HHS / DK / K23 DK068149; United States / NCI NIH HHS / CA / CA123945-01; United States / NCI NIH HHS / CA / F32CA-123945; United States / NCI NIH HHS / CA / F32 CA123945; United States / NCI NIH HHS / CA / CA123945-02
  • [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 / BMP4 protein, human; 0 / Bmp4 protein, mouse; 0 / Bone Morphogenetic Protein 4; 0 / DMBT1 protein, human; 0 / Hedgehog Proteins; 0 / Receptors, Cell Surface; 0 / SOX9 Transcription Factor; 0 / SOX9 protein, human; 0 / Shh protein, mouse; 0 / Sox9 protein, mouse; 0 / patched receptors; 68238-35-7 / Keratins
  • [Other-IDs] NLM/ NIHMS176618; NLM/ PMC3422577
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58. Theisen J, Stein HJ, Feith M, Kauer WK, Dittler HJ, Pirchi D, Siewert JR: Preferred location for the development of esophageal adenocarcinoma within a segment of intestinal metaplasia. Surg Endosc; 2006 Feb;20(2):235-8
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] Preferred location for the development of esophageal adenocarcinoma within a segment of intestinal metaplasia.
  • BACKGROUND: Barrett's metaplasia is the predominant precursor for the development of esophageal adenocarcinoma.
  • This study aimed to identify preferred locations within a segment of Barrett's mucosa for the development of esophageal adenocarcinoma.
  • METHODS: The study group consisted of 213 patients with histologically proven esophageal adenocarcinoma.
  • The frequency of intestinal metaplasia and the location of the tumor occurrence within the segment of intestinal metaplasia were assessed.
  • RESULTS: Intestinal metaplasia was found in 83% of the early lesions and in 98% of the advanced tumors after neoadjuvant chemotherapy.
  • In 82.2% of the cases, the tumor was located at the distal margin of the intestinal metaplasia in patients with early tumor manifestations.
  • The remaining tumor mass after neoadjuvant therapy also was located predominantly at the distal margin of the segment of intestinal metaplasia (85% of the cases).
  • CONCLUSIONS: The results demonstrate that almost all adenocarcinomas of the esophagus are based on the development of a segment of intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / etiology. Esophageal Neoplasms / etiology. Intestines / pathology. Precancerous Conditions / complications. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Endoscopy, Gastrointestinal. Female. Humans. Intestinal Mucosa / pathology. Male. Metaplasia. Middle Aged. Neoadjuvant Therapy. Neoplasm Invasiveness / pathology

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  • (PMID = 16391958.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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59. Goda K, Tajiri H, Ikegami M, Urashima M, Nakayoshi T, Kaise M: Usefulness of magnifying endoscopy with narrow band imaging for the detection of specialized intestinal metaplasia in columnar-lined esophagus and Barrett's adenocarcinoma. Gastrointest Endosc; 2007 Jan;65(1):36-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Usefulness of magnifying endoscopy with narrow band imaging for the detection of specialized intestinal metaplasia in columnar-lined esophagus and Barrett's adenocarcinoma.
  • BACKGROUND: Barrett's esophagus with specialized intestinal metaplasia (SIM) from columnar-lined esophagus is difficult to distinguish with routine endoscopy.
  • OBJECTIVE: To examine the values of fine mucosal patterns and the capillary patterns observed by magnifying endoscopy with narrow band imaging (MENBI) for the detection of SIM in columnar-lined esophagus and superficial Barrett's adenocarcinoma.
  • PATIENTS: Fifty-eight patients, including 4 with superficial Barrett's adenocarcinoma.
  • RESULTS: Upon observation, all 6 adenocarcinoma sites were classified as irregular patterns in both the fine mucosal patterns and capillary patterns.
  • The addition of capillary patterns to fine mucosal patterns appeared to improve the diagnostic value for detecting SIM and superficial Barrett's adenocarcinoma upon observation by MENBI.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal / methods. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Intestinal Mucosa / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Capillaries / pathology. Female. Humans. Image Processing, Computer-Assisted. Male. Metaplasia. Microscopy, Confocal. Middle Aged. Prospective Studies. Sensitivity and Specificity

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  • [CommentIn] Gastrointest Endosc. 2007 Jan;65(1):47-9 [17185079.001]
  • (PMID = 17185078.001).
  • [ISSN] 0016-5107
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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60. Nieuwenhuizen L, Khalil MK, Naik VR, Othman NH: Prevalence of goblet cell metaplasia in endocervical and endometrial adenocarcinoma : a histochemical study. Malays J Med Sci; 2007 Jan;14(1):56-61
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  • [Title] Prevalence of goblet cell metaplasia in endocervical and endometrial adenocarcinoma : a histochemical study.
  • To determine the prevalence of goblet cell metaplasia in endocervical and endometrial adenocarcinomas by histochemial staining and to investigate the most sensitive histochemical staining method to detect this metaplasia, a total of 90 tissue blocks representing 30 non-neoplastic cervix, 30 non-neoplastic endometrium, 30 endocervical and endometrial adenocarcinoma cases were obtained for histochemical staining with Toluidine Blue (TB), Methylene Blue (MB), Mucicarmine (MUC), Periodic Acid Schiff before and after Diastase digestion (PAS, PAS-D), Alcian Blue pH 2.5 (AB), and Periodic Acid Schiff after Alcian Blue pH 2.5 (PAB).
  • The cases were blinded and evaluated by a pathologist [NHO] for the presence of goblet cell metaplasia, the amount of goblet cells present and the histochemical differentiation of the goblet cells compared with its surrounding glandular epithelium.
  • Goblet cell metaplasia was present in 2 out of 30 cases in non-neoplastic cervix, 0 out of 30 cases in non-neoplastic endometrium, 7 out of 15 cases in endocervical adenocarcinoma and in 2 out of 15 cases in endometrial adenocarcinoma.
  • Relatively few goblet cells were seen in endometrial adenocarcinoma, few to moderate amounts were seen in endocervical adenocarcinoma and relatively more goblet cells were seen in non-neoplastic cervix.
  • The differentiation of the goblet cells with its surrounding glandular epithelium was moderate to strong in non-neoplastic cervix and endocervical adenocarcinoma, while the differentiation in endometrial adenocarcinoma was weak to moderate.
  • Goblet cell metaplasia of the reproductive organs is not as rare as previously reported.
  • The must optimum staining methods for staining goblet cells in non-neoplastic cervix, endocervical adenocarcinoma and endometrial adenocarcinoma were PAS, PASD and AB.

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  • (PMID = 22593653.001).
  • [ISSN] 1394-195X
  • [Journal-full-title] The Malaysian journal of medical sciences : MJMS
  • [ISO-abbreviation] Malays J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Malaysia
  • [Other-IDs] NLM/ PMC3351219
  • [Keywords] NOTNLM ; endocervical adenocarinoma / endometrial adenocarcinoma / goblet cell metaplasia / histochemical staining / intestinal metaplasia / prevalence
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61. 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.
  • 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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62. Tadiparthi R, Bansal A, Sharma P: What's new in columnar lined esophagus (Barrett's metaplasia)? Curr Opin Gastroenterol; 2008 Jul;24(4):516-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] What's new in columnar lined esophagus (Barrett's metaplasia)?
  • PURPOSE OF REVIEW: The rising incidence of esophageal adenocarcinoma in the Western world has led to continued interest in its precursor lesion, Barrett's esophagus.
  • Central obesity rather than BMI could be a more important determinant of Barrett's metaplasia and neoplasia.
  • Novel imaging techniques, in feasibility trials, have shown high accuracy for the detection of metaplasia and dysplasia.
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Adenocarcinoma / prevention & control. Esophageal Neoplasms / etiology. Esophageal Neoplasms / pathology. Esophageal Neoplasms / prevention & control. Humans. Metaplasia / pathology. Risk Factors

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  • (PMID = 18622169.001).
  • [ISSN] 1531-7056
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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63. Ueo T, Kashima K, Daa T, Kondo Y, Sasaki A, Yokoyama S: Immunohistochemical analysis of morules in colonic neoplasms: morules are morphologically and qualitatively different from squamous metaplasia. Pathobiology; 2005;72(5):269-78
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  • [Title] Immunohistochemical analysis of morules in colonic neoplasms: morules are morphologically and qualitatively different from squamous metaplasia.
  • Morules develop in several neoplasms and have been considered as a type of squamous metaplasia despite the absence of keratinization and intercellular bridges.
  • The objective of this study was to clarify the pathological significance of morules and to distinguish morules from squamous metaplasia in colonic neoplasms.
  • Ten cases of morule-associated colonic neoplasms (4 adenocarcinomas, 1 adenoma with carcinoma in situ, and 5 adenomas), and 3 cases of squamous metaplasia in colonic adenocarcinoma were examined morphologically and immunohistochemically.
  • Thus, morules were morphologically and qualitatively different from squamous metaplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Carcinoma in Situ / pathology. Colonic Neoplasms / pathology. Immunoenzyme Techniques / methods. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Female. Humans. Intranuclear Inclusion Bodies / chemistry. Intranuclear Inclusion Bodies / ultrastructure. Male. Metaplasia / metabolism. Metaplasia / pathology. Middle Aged. beta Catenin / metabolism

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  • (PMID = 16374071.001).
  • [ISSN] 1015-2008
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / beta Catenin
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64. Wada R, Yamaguchi T, Tanizaki T: Mucin phenotypic expression and p53 gene abnormality of gastric super-minute well-differentiated adenocarcinoma: re-evaluation with relationship between histogenesis of well-differentiated adenocarcinoma and intestinal metaplasia in distal stomach. J Carcinog; 2005 Sep 1;4:14
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  • [Title] Mucin phenotypic expression and p53 gene abnormality of gastric super-minute well-differentiated adenocarcinoma: re-evaluation with relationship between histogenesis of well-differentiated adenocarcinoma and intestinal metaplasia in distal stomach.
  • BACKGROUND: Although the gastric well-differentiated adenocarcinoma in the distal stomach has been thought to develop via a intestinal metaplasia-carcinoma sequence, there are some disproofs from new mucin examinations for minute-size lesions in same type carcinoma.
  • METHODS: 12 super-minute lesions (less than 1 mm in maximum diameter) of well-differentiated adenocarcinoma in distal stomach (SMCa), which were detected from the pathological examinations of 210 surgically resected stomach specimens, and the mucosa adjacent to these carcinoma lesions, were examined by immunohistochemical mucin stainings (MUC2 and CD-10: intestinal phenotype, 45M1 and MUC6: gastric phenotype) and p53-overexpression.
  • And the analyses of the replication error of the microsatellites in chromosome 17 related p53 gene (TP53 and D17S786) (RER-p53MS) were performed in SMCa lesions, adjacent mucosa to each lesion and other gastric mucosa with intestinal metaplasia, because all SMCa lesions showed p53-overexpression immunohistochemically, described below.
  • 2. All of the mucosa adjacent to SMCa showed intestinal metaplasia (complete type: 7 regions, incomplete type: 5 regions).
  • 3. RER-p53MS was confirmed in 42% (5/12 regions) of SMCa, in 42% (5/12 regions) of the mucosa adjacent to SMCa and 14% (6/42 regions) of the other intestinal metaplasia mucosa.
  • CONCLUSION: Most of the super-minute well-differentiated adenocarcinoma lesions in the distal stomach, which had both gastric and intestinal phenotypic mucin, are considered to develop from the tubular proliferative zone with the incomplete type of the intestinal metaplasia and p53 gene abnormality, while a part of them, which had only gastric phenotypic mucin, may derive from the gastric native tubules (non-metaplastic epithelium) with p53 gene abnormality.

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  • (PMID = 16135257.001).
  • [ISSN] 1477-3163
  • [Journal-full-title] Journal of carcinogenesis
  • [ISO-abbreviation] J Carcinog
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1232858
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65. Palestro G, Pellicano R, Fronda GR, Valente G, De Giuli M, Soldati T, Pugliese A, Taraglio S, Garino M, Campra D, Cutufia MA, Margaria E, Spinzi G, Ferrara A, Marenco G, Rizzetto M, Ponzetto A: Prevalence of Helicobacter pylori infection and intestinal metaplasia in subjects who had undergone surgery for gastric adenocarcinoma in Northwest Italy. World J Gastroenterol; 2005 Dec 7;11(45):7131-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of Helicobacter pylori infection and intestinal metaplasia in subjects who had undergone surgery for gastric adenocarcinoma in Northwest Italy.
  • METHODS: Samples from 317 (184 males, 133 females, mean age 69+/-3.4 years) consecutive patients who had undergone surgery for gastric non-cardia adenocarcinoma were included in the study.
  • Intestinal metaplasia (IM) was more frequent but not significant in the intestinal type cancer (83.4% vs 75.2% in diffuse type and 72.5% in mixed type).
  • CONCLUSION: This study confirms a high seroprevalence of H pylori infection in patients suffering from gastric adenocarcinoma and provides further evidence that searching for CagA status over H pylori infection might confer additional benefit in identifying populations at greater risk for this tumor.
  • [MeSH-major] Adenocarcinoma / complications. Helicobacter Infections / complications. Helicobacter Infections / epidemiology. Helicobacter pylori. Intestines / pathology. Stomach Neoplasms / complications
  • [MeSH-minor] Aged. Antibodies, Bacterial / blood. Antigens, Bacterial / immunology. Bacterial Proteins / immunology. Case-Control Studies. Female. Humans. Italy / epidemiology. Male. Metaplasia. Middle Aged. Seroepidemiologic Studies

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  • (PMID = 16437659.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / cagA protein, Helicobacter pylori
  • [Other-IDs] NLM/ PMC4725078
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66. Bresalier R: Barrett's Metaplasia: defining the problem. Semin Oncol; 2005 Dec;32(6 Suppl 8):21-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Barrett's Metaplasia: defining the problem.
  • Concern over how best to manage individuals with Barrett's esophagus (BE) has grown because of the consistent rise in the incidence of esophageal adenocarcinoma.
  • Since the 1970s, the rate of increase in incidence of esophageal adenocarcinoma has been greater than that for any other cancer in the US population.
  • Much remains to be learned about BE and its association with adenocarcinoma before effective surveillance or management strategies can be defined and implemented.
  • In this article, the relationship between BE and gastroesophageal reflux disease, risk for adenocarcinoma, and prospects for molecular diagnosis are discussed.
  • [MeSH-minor] Humans. Metaplasia

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  • (PMID = 16360008.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 24
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67. Nam KT, Varro A, Coffey RJ, Goldenring JR: Potentiation of oxyntic atrophy-induced gastric metaplasia in amphiregulin-deficient mice. Gastroenterology; 2007 May;132(5):1804-19
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potentiation of oxyntic atrophy-induced gastric metaplasia in amphiregulin-deficient mice.
  • BACKGROUND & AIMS: The loss of parietal cells from the gastric mucosa (oxyntic atrophy) is a critical step in the pathogenesis of chronic gastritis and gastric adenocarcinoma.
  • Previous investigations have suggested that a deficit in EGFR signaling in waved-2 mice accelerates the emergence of metaplasia after induction of acute oxyntic atrophy.
  • METHODS: To induce spasmolytic polypeptide-expressing metaplasia (SPEM), amphiregulin (AR) and transforming growth factor-alpha-deficient mice and their wild-type littermates were treated with DMP-777 for 0-14 days and for 14 days followed by 14 days of recovery off drug.
  • [MeSH-minor] Amphiregulin. Animals. Atrophy / chemically induced. Atrophy / pathology. Azetidines. EGF Family of Proteins. Gastric Mucosa / metabolism. Gastric Mucosa / pathology. Gastrins / genetics. Gastrins / metabolism. Gene Expression Regulation. Intrinsic Factor / genetics. Intrinsic Factor / metabolism. Male. Metaplasia / chemically induced. Metaplasia / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Piperazines. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / physiology. S Phase. Somatostatin / genetics. Somatostatin / metabolism. Transforming Growth Factor alpha / genetics. Transforming Growth Factor alpha / physiology

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  • [CommentIn] Gastroenterology. 2007 May;132(5):2053-6 [17484897.001]
  • (PMID = 17484876.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P 50 CA95103; United States / NCI NIH HHS / CA / R01 CA46413; United States / NCI NIH HHS / CA / U01 CA1084239
  • [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 / Amphiregulin; 0 / Areg protein, mouse; 0 / Azetidines; 0 / DMP 777; 0 / EGF Family of Proteins; 0 / Gastrins; 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Peptides; 0 / Piperazines; 0 / Transforming Growth Factor alpha; 0 / spasmolytic polypeptide; 146046-78-8 / trefoil factor; 51110-01-1 / Somatostatin; 9008-12-2 / Intrinsic Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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68. Ling FC, Khochfar J, Baldus SE, Brabender J, Drebber U, Bollschweiler E, Hoelscher AH, Schneider PM: HIF-1alpha protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasia. Dis Esophagus; 2009;22(8):694-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIF-1alpha protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasia.
  • Squamous epithelium (SE), metaplastic, low- and high-grade dysplastic lesions, and tumor tissue of 57 resection specimens from patients with Barrett's adenocarcinoma were immunohistochemically analyzed.
  • HIF-1alpha protein expression increased significantly from SE to Barrett's metaplasia (BM) (P < 0.0001).
  • From metaplasia through low- and high-grade dysplasia to cancer, no further increase could be detected.
  • All were significantly increased in metaplasia compared to SE without further change in tumor development.

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  • (PMID = 19302222.001).
  • [ISSN] 1442-2050
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit
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69. Pereira C, Sousa H, Ferreira P, Fragoso M, Moreira-Dias L, Lopes C, Medeiros R, Dinis-Ribeiro M: -765G &gt; C COX-2 polymorphism may be a susceptibility marker for gastric adenocarcinoma in patients with atrophy or intestinal metaplasia. World J Gastroenterol; 2006 Sep 14;12(34):5473-8
Hazardous Substances Data Bank. GUANINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] -765G > C COX-2 polymorphism may be a susceptibility marker for gastric adenocarcinoma in patients with atrophy or intestinal metaplasia.
  • AIM: To investigate the relationship between the -765G > C COX-2 polymorphism and the development of different gastric lesions: atrophy or intestinal metaplasia and gastric adenocarcinoma.
  • METHODS: A cross-sectional study was performed involving 320 Portuguese individuals (210 without evidence of neoplastic disease, 73 patients with gastric adenocarcinomas and 37 with atrophy or intestinal metaplasia) using a PCR-RFLP method.
  • RESULTS: -765C allele was overrepresented in the patients with gastric adenocarcinoma (51%) when compared either with the control group (38%) or patients with atrophy or intestinal metaplasia (27%).
  • Callele was found to be very common in our population (0.22), and a multivariate logistic regression analysis revealed nearly 3-fold increased risk for the progression to gastric adenocarcinoma in patients with atrophy or intestinal metaplasia carrying the -765C allele (OR = 2.67, 95% CI = 1.03-6.93; P = 0.04).
  • CONCLUSION: -765C carrier status should be considered as another susceptibility marker for gastric adenocarcinoma development in patients with atrophy or intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Cyclooxygenase 2 / genetics. Intestines / pathology. Membrane Proteins / genetics. Polymorphism, Genetic / genetics. Stomach Neoplasms / genetics. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Alleles. Atrophy / genetics. Atrophy / pathology. Cross-Sectional Studies. Cystine / analysis. DNA, Neoplasm / analysis. Female. Genetic Predisposition to Disease. Guanine / analysis. Humans. Male. Metaplasia / genetics. Metaplasia / pathology. Middle Aged. Portugal. Regression Analysis. Risk Factors

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  • (PMID = 17006983.001).
  • [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 / DNA, Neoplasm; 0 / Membrane Proteins; 48TCX9A1VT / Cystine; 5Z93L87A1R / Guanine; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  • [Other-IDs] NLM/ PMC4088228
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70. Gatenby PA, Ramus JR, Caygill CP, Shepherd NA, Watson A: Relevance of the detection of intestinal metaplasia in non-dysplastic columnar-lined oesophagus. Scand J Gastroenterol; 2008;43(5):524-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relevance of the detection of intestinal metaplasia in non-dysplastic columnar-lined oesophagus.
  • OBJECTIVE: In the USA, detection of intestinal metaplasia is a requirement for enrollment in surveillance programmes for dysplasia or adenocarcinoma in columnar-lined oesophagus.
  • In the UK, it is believed that failure to detect intestinal metaplasia at index endoscopy does not imply its absence within the columnarized segment or that the tissue is not at risk of neoplastic transformation.
  • The aim of this study was to investigate the factors predicting the probability of detection of intestinal metaplasia in the columnarized segment.
  • MATERIAL AND METHODS: Demonstration of intestinal metaplasia was analysed in 3568 biopsies of non-dysplastic columnar-lined oesophagus from 1751 patients from 7 centres in the UK.
  • Development of dysplasia and adenocarcinoma was analysed in 322 patients without intestinal metaplasia and compared with that in 612 patients with intestinal metaplasia.
  • RESULTS: Intestinal metaplasia was more commonly detected in males than in females (odds ratio 1.244), longer segment length (10.3% increase per centimetre) and increasing number of biopsies taken (24% increase per unit increase).
  • After 5 years of follow-up, 54.8% of patients without intestinal metaplasia at index endoscopy demonstrated intestinal metaplasia, and 90.8% after 10 years.
  • There was no significant difference in the rate of development of dysplasia or adenocarcinoma between patients with or without intestinal metaplasia detection at index endoscopy.
  • CONCLUSIONS: Detection of intestinal metaplasia is subject to significant sampling error.
  • In the majority of patients, if sufficient biopsies are taken over time, intestinal metaplasia will be demonstrated.
  • The decision to offer surveillance should not be based upon the presence or absence of intestinal metaplasia at index endoscopy as the risk of dysplasia and adenocarcinoma is similar in both groups.
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Biopsy, Needle. Esophageal Neoplasms / etiology. Esophageal Neoplasms / pathology. Female. Follow-Up Studies. Humans. Male. Metaplasia

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  • (PMID = 18415743.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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71. 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
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] 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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72. Fléjou JF: Barrett's oesophagus: from metaplasia to dysplasia and cancer. Gut; 2005 Mar;54 Suppl 1:i6-12
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  • [Title] Barrett's oesophagus: from metaplasia to dysplasia and cancer.
  • Barrett's oesophagus is a premalignant condition that predisposes to the development of oesophageal adenocarcinoma.
  • It is detected on endoscopy and confirmed histologically by the presence in the lower oesophagus of a metaplastic mucosa, the so-called specialised epithelium, which resembles incomplete intestinal metaplasia in the stomach.
  • These similarities with incomplete intestinal metaplasia are present on histology, mucin histochemistry, and immunohistochemistry with various differentiation markers (cytokeratins and MUC antigens).

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  • (PMID = 15711008.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Mucins
  • [Number-of-references] 66
  • [Other-IDs] NLM/ PMC1867794
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73. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • [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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74. 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
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  • [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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75. Biancone L, Calabrese E, Palmieri G, Petruzziello C, Onali S, Sica GS, Cossignani M, Condino G, Das KM, Pallone F: Ileal lesions in patients with ulcerative colitis after ileo-rectal anastomosis: relationship with colonic metaplasia. World J Gastroenterol; 2008 Sep 14;14(34):5290-300
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  • [Title] Ileal lesions in patients with ulcerative colitis after ileo-rectal anastomosis: relationship with colonic metaplasia.
  • Possible relation between development of colonic metaplasia and ileal lesions was investigated.
  • RESULTS: Stenosing adenocarcinoma of the rectal stump was detected in 1 UC patient.
  • Ileal ulcers were detected in 7/10 UC, associated with colonic metaplasia in 4/7 (57.1%) and Das-1 and CG3 reactivity in 3/4 UC.
  • In controls, recurrence occurred in 4/6 CD, associated with colonic metaplasia in 3/4 and reactivity with Das-1 and CG3 in 2/3.
  • Changes of the ileal content after colectomy may contribute to the development of colonic metaplasia, leading to ileal lesions both in the pouch and in the neo-terminal ileum after IRA.
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Anastomosis, Surgical / adverse effects. Capsule Endoscopy. Case-Control Studies. Colectomy / adverse effects. Colon / pathology. Colon / surgery. Female. Humans. Male. Metaplasia. Middle Aged. Rectal Neoplasms / pathology. Rectum / surgery. Young Adult

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  • (PMID = 18785281.001).
  • [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/ PMC2744059
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76. Dietz J, Chaves-E-Silva S, Meurer L, Sekine S, de Souza AR, Meine GC: Short segment Barrett's esophagus and distal gastric intestinal metaplasia. Arq Gastroenterol; 2006 Apr-Jun;43(2):117-20
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  • [Title] Short segment Barrett's esophagus and distal gastric intestinal metaplasia.
  • BACKGROUND: Short segment Barrett's esophagus is defined by the presence of <3 cm of columnar-appearing mucosa in the distal esophagus with intestinal metaplasia on histophatological examination.
  • Barrett's esophagus is a risk factor to develop adenocarcinoma of the esophagus.
  • While Barrett's esophagus develops as a result of chronic gastroesophageal reflux disease, intestinal metaplasia in the gastric cardia is a consequence of chronic Helicobacter pylori infection and is associated with distal gastric intestinal metaplasia.
  • It can be difficult to determine whether short-segment columnar epithelium with intestinal metaplasia are lining the esophagus (a condition called short segment Barrett's esophagus) or the proximal stomach (a condition called intestinal metaplasia of the gastric cardia).
  • AIMS: To study the association of short segment Barrett's esophagus (length <3 cm) with gastric intestinal metaplasia (antrum or body) and infection by H. pylori.
  • Biopsies were obtained immediately below the squamous-columnar lining, from gastric antrum and gastric corpus for investigation of intestinal metaplasia and H. pylori.
  • RESULTS: Forty-two from 89 (47.2%) patients were diagnosed with esophageal intestinal metaplasia by histopathology.
  • The mean-age was significantly higher in the group with esophageal intestinal metaplasia.
  • Gastric intestinal metaplasia (antrum or body) was diagnosed in 21 from 42 (50.0%) patients in the group with esophageal intestinal metaplasia and 7 from 47 (14.9%) patients in the group with esophageal columnar appearing mucosa but without intestinal metaplasia.
  • CONCLUSION: Intestinal metaplasia is a frequent finding in patients with <3 cm of columnar-appearing mucosa in the distal esophagus.
  • In the present study, short segment intestinal metaplasia in the esophagus is associated with distal gastric intestinal metaplasia.
  • [MeSH-minor] Biopsy. Cardia / pathology. Esophagoscopy. Female. Gastritis / microbiology. Gastritis / pathology. Humans. Male. Metaplasia / pathology. Middle Aged

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  • (PMID = 17119666.001).
  • [ISSN] 0004-2803
  • [Journal-full-title] Arquivos de gastroenterologia
  • [ISO-abbreviation] Arq Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
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77. Ormeci N, Savas B, Coban S, Palabiyikoğlu M, Ensari A, Kuzu I, Kursun N: The usefulness of chromoendoscopy with methylene blue in Barrett's metaplasia and early esophageal carcinoma. Surg Endosc; 2008 Mar;22(3):693-700
Hazardous Substances Data Bank. METHYLENE BLUE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The usefulness of chromoendoscopy with methylene blue in Barrett's metaplasia and early esophageal carcinoma.
  • BACKGROUND: Barrett's esophagus is a condition that is premalignant for adenocarcinoma of the esophagus and the esophagogastric junction.
  • Early detection of Barrett's metaplasia and dysplasia is very important to decrease the mortality and morbidity from esophageal adenocarcinoma cancer.
  • This study aimed to evaluate the effectiveness of methylene blue-targeted biopsies in the differential diagnosis of intestinal metaplasia, dysplasia, and superficial esophageal carcinoma.
  • However, there was no statistical difference between the two methods in the diagnosis of esophagitis or esophageal carcinoma (p > 0.05).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Needle. Cohort Studies. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Risk Assessment. Sensitivity and Specificity. Staining and Labeling / methods

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  • (PMID = 17704887.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] T42P99266K / Methylene Blue
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78. Morton MJ, Zhang S, Lopez-Beltran A, MacLennan GT, Eble JN, Montironi R, Sung MT, Tan PH, Zheng S, Zhou H, Cheng L: Telomere shortening and chromosomal abnormalities in intestinal metaplasia of the urinary bladder. Clin Cancer Res; 2007 Oct 15;13(20):6232-6
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  • [Title] Telomere shortening and chromosomal abnormalities in intestinal metaplasia of the urinary bladder.
  • PURPOSE: Although intestinal metaplasia is often found in association with adenocarcinoma of the urinary bladder, it is unclear whether intestinal metaplasia of the bladder is a premalignant lesion.
  • We used quantitative fluorescent in situ hybridization (FISH) to measure telomere length and UroVysion FISH to detect cytogenetic abnormalities in urinary bladder specimens with intestinal metaplasia.
  • EXPERIMENTAL DESIGN: Paraffin-embedded tissue blocks from 34 patients with intestinal metaplasia of the urinary bladder were evaluated.
  • Multicolor FISH was used to analyze for cytogenic abnormalities in the interphase nuclei of intestinal metaplasia.
  • RESULTS: In all 34 cases, reduced average telomere signal intensity was observed in the nuclei of intestinal metaplasia cells compared with adjacent control nuclei to produce a mean relative intensity of 48.5% (P < 0.0001).
  • When cystitis glandularis was present, significant differences in the telomere-specific signal intensity existed between cystitis glandularis and normal cells (P = 0.0005) and between cystitis glandularis and intestinal metaplasia cells (P = 0.0015).
  • CONCLUSIONS: Our findings indicate that intestinal metaplasia in the urinary bladder is associated with significant telomere shortening relative to telomere length in adjacent normal urothelial cells.
  • Our findings support the hypothesis that intestinal metaplasia of the urinary bladder is a precursor lesion to and could be a marker in the development of adenocarcinoma of the urinary bladder.
  • [MeSH-major] Chromosome Aberrations. Intestines / pathology. Metaplasia / pathology. Telomere / ultrastructure. Urinary Bladder Neoplasms / genetics. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / genetics. Chromosomes / ultrastructure. Cystitis / complications. Cytogenetics. Humans. Immunohistochemistry / methods. In Situ Hybridization, Fluorescence. Precancerous Conditions / genetics

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  • (PMID = 17947491.001).
  • [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
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79. Forones NM, Carvalho AP, Giannotti-Filho O, Lourenço LG, Oshima CT: Cell proliferation and apoptosis in gastric cancer and intestinal metaplasia. Arq Gastroenterol; 2005 Jan-Mar;42(1):30-4
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  • [Title] Cell proliferation and apoptosis in gastric cancer and intestinal metaplasia.
  • AIM: To study proliferation and apoptosis on gastric cancer and in intestinal metaplasia.
  • METHODOLOGY: Twenty-two samples from gastric adenocarcinomas and 22 biopsies from intestinal metaplasia were studied.
  • Ki 67LI increased from intestinal metaplasia to gastric cancer. p53 was positive in 68% of the patients with cancer, more frequently in advanced stage and negative in samples of intestinal metaplasia.
  • Although there was no significant difference between the groups, bcl-2 was positive in 45% of gastric cancer tissue and in 68% of metaplasia.
  • CONCLUSION: The positivity of bcl-2 was higher in metaplasia and probably is involved in the progression of carcinogenesis. p53 was negative in metaplasia and positive in more than half of the gastric cancer, mostly in stage IV, suggesting a late event in gastric cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Apoptosis. Cell Proliferation. Intestines / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Female. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Male. Metaplasia / metabolism. Metaplasia / pathology. Neoplasm Staging. Proto-Oncogene Proteins c-bcl-2 / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 15976908.001).
  • [ISSN] 0004-2803
  • [Journal-full-title] Arquivos de gastroenterologia
  • [ISO-abbreviation] Arq Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53
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80. Dickman R, Levi Z, Vilkin A, Zvidi I, Niv Y: Predictors of specialized intestinal metaplasia in patients with an incidental irregular Z line. Eur J Gastroenterol Hepatol; 2010 Feb;22(2):135-8
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  • [Title] Predictors of specialized intestinal metaplasia in patients with an incidental irregular Z line.
  • INTRODUCTION: Barrett's esophagus is a well-known complication of gastroesophageal reflux disease (GERD) and is associated with dysplasia and esophageal adenocarcinoma.
  • Data on the prevalence of specialized intestinal metaplasia (SIM) in biopsy taken from an incidental irregular Z line are scarce.
  • Specialized intestinal metaplasia was found in 43.5% of all cases.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Female. Hernia, Hiatal / complications. Humans. Israel / epidemiology. Logistic Models. Male. Metaplasia. Middle Aged. Prevalence. Retrospective Studies. Risk Assessment. Risk Factors. Sex Factors. Young Adult

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  • [CommentIn] Eur J Gastroenterol Hepatol. 2010 Aug;22(8):1022 [20631542.001]
  • (PMID = 19907339.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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81. Villanacci V, Bellone G, Battaglia E, Rossi E, Carbone A, Prati A, Verna C, Niola P, Morelli A, Grassini M, Bassotti G: Ski/SnoN expression in the sequence metaplasia-dysplasia-adenocarcinoma of Barrett's esophagus. Hum Pathol; 2008 Mar;39(3):403-9
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  • [Title] Ski/SnoN expression in the sequence metaplasia-dysplasia-adenocarcinoma of Barrett's esophagus.
  • Biopsy samples from 37 patients (26 men, aged 60 +/- 8 years) with histologically proven BE were evaluated; 10 patients had concomitant low-grade dysplasia, 7 high-grade dysplasia (HGD), and 6 HGD associated with adenocarcinoma.
  • Expression of these proteins decreased markedly in dysplastic areas in patients with low-grade dysplasia and was absent in those with HGD or HGD/adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / metabolism. DNA-Binding Proteins / biosynthesis. Esophageal Neoplasms / metabolism. Precancerous Conditions / metabolism. Proto-Oncogene Proteins / biosynthesis
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Humans. Immunohistochemistry. Intracellular Signaling Peptides and Proteins. Male. Metaplasia. Middle Aged. Transforming Growth Factor beta / metabolism

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  • (PMID = 18261624.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins; 0 / SKIL protein, human; 0 / Transforming Growth Factor beta; 126648-96-2 / SKI protein, human
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82. Liu Q, Teh M, Ito K, Shah N, Ito Y, Yeoh KG: CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer. Mod Pathol; 2007 Dec;20(12):1286-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CDX2 expression is progressively decreased in human gastric intestinal metaplasia, dysplasia and cancer.
  • Intestinal metaplasia is a key event in multistep gastric carcinogenesis.
  • However, it was reported to be expressed in nearly all gastric intestinal metaplasia and many gastric cancers.
  • The expression of CDX2 protein in gastric intestinal metaplasia, dysplasia and cancer was examined and related to their gastrointestinal differentiation.
  • CDX2 expression was significantly decreased in incomplete intestinal metaplasia, which expresses both gastric mucins (MUC5AC and MUC6) and intestinal mucin (MUC2), compared with complete intestinal metaplasia, which expresses intestinal mucin (MUC2) only.
  • Although incomplete intestinal metaplasia morphologically resembles colon, its CDX2 expression was apparently lower than that in the normal colon.
  • As incomplete intestinal metaplasia is associated with higher risk of gastric cancer, its lower CDX2 expression compared with that in complete intestinal metaplasia and normal colon epithelium resolved the current contradiction between the tumor-suppressive role of CDX2 in the colon and the high prevalence of CDX2 in intestinal metaplasia.
  • Further decrease of CDX2 expression in gastric dysplasia and cancer suggests that CDX2 plays a similar anticarcinogenic role in intestinal metaplasia as it does in colon.
  • Intestinal metaplasia or dysplasia with low expression of CDX2 may serve as predictive markers for gastric cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / analysis. Gastrointestinal Neoplasms / metabolism. Gastrointestinal Neoplasms / pathology. Homeodomain Proteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Male. Metaplasia / pathology. Middle Aged. Mucin 5AC. Mucin-2. Mucin-6. Mucins / biosynthesis. Precancerous Conditions / pathology

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  • (PMID = 17906616.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / MUC6 protein, human; 0 / Mucin 5AC; 0 / Mucin-2; 0 / Mucin-6; 0 / Mucins
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83. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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84. Grassi A, Giannarelli D, Iacopini F, Paoluzi P, Iannetti A, Giovannelli L, Efrati C, Barberani F, Giovannone M, Tosoni M: Prevalence of intestinal metaplasia in the distal esophagus in patients endoscopically suspected for short Barrett's esophagus. J Exp Clin Cancer Res; 2006 Sep;25(3):297-302
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of intestinal metaplasia in the distal esophagus in patients endoscopically suspected for short Barrett's esophagus.
  • The clinical importance of Barrett's esophagus is related to its correlation to adenocarcinoma.
  • The diagnosis is based on histologic demonstration of specialized intestinal metaplasia in the distal esophagus.
  • The aim of this study was to assess the prevalence of intestinal metaplasia of the distal esophagus in a population submitted to gastroscopy not selected for reflux disease, and with columnar lined distal esophagus between 0.5 and 2 cm.
  • In four Centers 224 patients received endoscopy with biopsies demonstrating specialized intestinal metaplasia in 21% of cases.
  • A significant association was present in over 70 (females), as well as with the presence of antral intestinal metaplasia demonstrated in 45 patients by gastric biopsies.
  • Biopsy samplings can diagnose the presence of intestinal metaplasia during endoscopy in patients endoscopically suspected for Barrett's esophagus: at present there is not clear evidence to promote this screening to achieve mortality reduction of esophageal adenocarcinoma.
  • [MeSH-major] Barrett Esophagus / diagnosis. Endoscopy, Gastrointestinal. Esophagus / pathology. Intestinal Mucosa / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Male. Metaplasia / epidemiology. Middle Aged. Prevalence

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  • (PMID = 17167967.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Italy
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85. 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
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  • [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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86. Sung MT, Lopez-Beltran A, Eble JN, MacLennan GT, Tan PH, Montironi R, Jones TD, Ulbright TM, Blair JE, Cheng L: Divergent pathway of intestinal metaplasia and cystitis glandularis of the urinary bladder. Mod Pathol; 2006 Nov;19(11):1395-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Divergent pathway of intestinal metaplasia and cystitis glandularis of the urinary bladder.
  • Intestinal metaplasia has been proposed to be a precursor lesion of adenocarcinoma in the urinary bladder.
  • Hepatocyte-specific antigen (Hep) has also been shown to be a useful marker of intestinal metaplasia.
  • Tissues from 46 patients, including 22 cases of intestinal metaplasia of the urinary bladder, 11 cases of typical cystitis glandularis, and 13 cases containing both lesions, were selected and immunohistochemical stains for CDX2, Hep, cytokeratin 20 (CK20), and cytokeratin 7 (CK7) were performed.
  • Nuclear staining for CDX2 was observed in 29 of 35 (83%) cases of intestinal metaplasia of the urinary bladder.
  • CK20 was expressed in 28 of 35 (80%) cases of intestinal metaplasia, but was observed in only one of 24 (4%) cases of cystitis glandularis in 15% of cells.
  • CK7 was expressed in only six of 35 (17%) cases of intestinal metaplasia, whereas expression of CK7 was observed in all cases (100%) of typical cystitis glandularis with a mean percentage of positively staining cells of 63%.
  • The mean percentages of positively staining cells in intestinal metaplasia with CDX2, CK20, and CK7 were 55, 49, and 53%, respectively.
  • All examples of both intestinal metaplasia and typical cystitis glandularis were uniformly negative for Hep.
  • In the urinary bladder, intestinal metaplasia and typical cystitis glandularis have sharply contrasting immunoprofiles.
  • Additionally, the absence of Hep staining in intestinal metaplasia of the urinary bladder, despite its morphologic resemblance to normal colonic mucosa and intestinal metaplasia in other organs, may signify the presence of unique metaplastic pathways in the urinary bladder.
  • [MeSH-minor] Autoantigens / analysis. Cell Transformation, Neoplastic / pathology. Hepatocytes / immunology. Homeodomain Proteins / analysis. Humans. Immunohistochemistry. Keratin-20 / analysis. Keratin-7 / analysis. Metaplasia. Retrospective Studies

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  • (PMID = 16951671.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / KRT20 protein, human; 0 / KRT7 protein, human; 0 / Keratin-20; 0 / Keratin-7
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87. Yang L, Lu X, Nossa CW, Francois F, Peek RM, Pei Z: Inflammation and intestinal metaplasia of the distal esophagus are associated with alterations in the microbiome. Gastroenterology; 2009 Aug;137(2):588-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inflammation and intestinal metaplasia of the distal esophagus are associated with alterations in the microbiome.
  • BACKGROUND & AIMS: Gastroesophageal reflux causes inflammation and intestinal metaplasia and its downstream sequelum adenocarcinoma in the distal esophagus.
  • The incidence of esophageal adenocarcinoma has increased approximately 6-fold in the United States since the 1970s, accompanied with a significant increase in the prevalence of gastroesophageal reflux disease (GERD).
  • Host phenotypes were histologically defined as normal, esophagitis, or Barrett's esophagus (intestinal metaplasia).
  • CONCLUSIONS: In the human distal esophagus, inflammation and intestinal metaplasia are associated with global alteration of the microbiome.

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  • (PMID = 19394334.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI063477-05; United States / NCI NIH HHS / CA / R01 CA097946; United States / NCI NIH HHS / CA / UH2CA140233; United States / NCI NIH HHS / CA / CA140233-01; United States / NCI NIH HHS / CA / R01 CA097946-04; United States / NCI NIH HHS / CA / R01CA97946; United States / NIAID NIH HHS / AI / R01AI063477; United States / NIAID NIH HHS / AI / AI063477-05; United States / NCI NIH HHS / CA / UH2 CA140233-01; United States / NCI NIH HHS / CA / UH2 CA140233; United States / NCI NIH HHS / CA / CA097946-04; United States / NIAID NIH HHS / AI / R01 AI063477
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS135974; NLM/ PMC2963147
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88. Kelty CJ, Gough MD, Van Wyk Q, Stephenson TJ, Ackroyd R: Barrett's oesophagus: intestinal metaplasia is not essential for cancer risk. Scand J Gastroenterol; 2007 Nov;42(11):1271-4
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] Barrett's oesophagus: intestinal metaplasia is not essential for cancer risk.
  • OBJECTIVE: Barrett's oesophagus is the main identifiable risk factor for oesophageal adenocarcinoma.
  • It has been suggested that only patients with intestinal metaplasia are at risk of cancer, but the British Society of Gastroenterology (BSG) guidelines suggest that glandular mucosa is all that is needed.
  • The aim of this study was to quantify the risk of adenocarcinoma in columnar-lined lower oesophagus, with or without specialized intestinal metaplasia.
  • All histological specimens were re-examined and reported according to whether they contained columnar epithelial-lined lower oesophagus, glandular mucosa, with or without intestinal metaplasia.
  • The primary outcome measure was the development of adenocarcinoma.
  • Of these, 379 (55.1%) were found to have specialized intestinal metaplasia (SIM), and the remaining 309 (44.9%, p = NS) were reported as having glandular mucosa (GM).
  • Twenty-eight patients went on to develop adenocarcinoma (4.1%) during the follow-up period - 17 in the SIM group (4.5%) and 11 in the GM group (3.6%, p =NS).
  • CONCLUSIONS: Patients who have glandular mucosa on biopsy without intestinal metaplasia have a similar cancer risk to those with specialized intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Barrett Esophagus / complications. Barrett Esophagus / pathology. Esophageal Neoplasms / etiology. Esophageal Neoplasms / pathology. Esophagus / pathology
  • [MeSH-minor] Biopsy. Female. Humans. Incidence. Male. Metaplasia. Mucous Membrane / pathology. Risk Factors


89. Nunobe S, Nakanishi Y, Taniguchi H, Sasako M, Sano T, Kato H, Yamagishi H, Sekine S, Shimoda T: Two distinct pathways of tumorigenesis of adenocarcinomas of the esophagogastric junction, related or unrelated to intestinal metaplasia. Pathol Int; 2007 Jun;57(6):315-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two distinct pathways of tumorigenesis of adenocarcinomas of the esophagogastric junction, related or unrelated to intestinal metaplasia.
  • It is still uncertain whether intestinal metaplasia (IM) of the esophagogastric junction (EGJ) plays a role in the development of adenocarcinoma of the esophagogastric junction (AEGJ).
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Esophagogastric Junction / pathology. Gastric Mucosa / pathology. Intestinal Mucosa / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / metabolism. Barrett Esophagus / pathology. Biomarkers, Tumor / metabolism. Female. Humans. Lymphatic Metastasis. Male. Metaplasia / metabolism. Metaplasia / pathology. Middle Aged. Phenotype

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  • [CommentIn] Z Gastroenterol. 2008 Nov;46(11):1333-4 [19012205.001]
  • (PMID = 17539961.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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90. Zhang X, Gupta R, Nicastri AD: Bladder adenocarcinoma following gastrocystoplasty. J Pediatr Urol; 2010 Oct;6(5):525-7
MedlinePlus Health Information. consumer health - Bladder Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bladder adenocarcinoma following gastrocystoplasty.
  • We report the first case of adenocarcinoma arising in the residual native bladder in association with intestinal metaplasia and dysplasia of bladder mucosa 17 years following gastrocystoplasty.
  • Intestinal metaplasia secondary to recurrent urinary infection, chronic inflammation, and some form of irritation may potentiate the development of native bladder adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / etiology. Urinary Bladder / surgery. Urinary Bladder Neoplasms / etiology. Urologic Surgical Procedures / adverse effects
  • [MeSH-minor] Gastric Mucosa / surgery. Humans. Intestines / pathology. Male. Metaplasia. Young Adult

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  • [Copyright] Copyright © 2010 Journal of Pediatric Urology Company. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 20392671.001).
  • [ISSN] 1873-4898
  • [Journal-full-title] Journal of pediatric urology
  • [ISO-abbreviation] J Pediatr Urol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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91. Albayrak F, Uyanik MH, Dursun H, Albayrak Y, Altas S, Uyanik A, Cerrah S, Bayir Y: Should increased levels of urinary 8-hydroxydeoxyguanosine in chronic gastritis imply intestinal metaplasia or gastric atrophy? South Med J; 2010 Aug;103(8):753-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Should increased levels of urinary 8-hydroxydeoxyguanosine in chronic gastritis imply intestinal metaplasia or gastric atrophy?
  • OBJECTIVES: Helicobacter pylori (H pylori) infection induces chronic inflammation that can progress to gastric atrophy, intestinal metaplasia, and gastric adenocarcinoma.
  • We have examined oxidative damage caused by Helicobacter pylori, metaplasia, and atrophy of gastric mucosal cells in patients with chronic gastritis by measuring their urinary 8-hydroxydeoxyguanosine (8-OHdG) levels.
  • The level of urinary 8-OHdG was markedly higher in patients with gastric atrophy and intestinal metaplasia than in those without (P=0.000, P=0.002, respectively).
  • There were significant correlations between levels of urinary 8-OHdG and both the atrophy score (r=0.441, P=0.000) and the intestinal metaplasia score (r=0.436, P=0.000).
  • In patients with high levels of urinary 8-OHdG, endoscopic procedures or even pathological investigation may then be carried out, with the consideration that there is a high risk of intestinal metaplasia or atrophy.
  • [MeSH-minor] Atrophy / etiology. Atrophy / urine. Chronic Disease. Female. Helicobacter Infections / complications. Helicobacter Infections / urine. Helicobacter pylori. Humans. Male. Metaplasia / etiology. Metaplasia / urine. Middle Aged. Prospective Studies

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  • (PMID = 20622725.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
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92. Kim GY, Kim J, Kim TS, Han J: Pulmonary adenocarcinoma with heterotopic ossification. J Korean Med Sci; 2009 Jun;24(3):504-10
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  • [Title] Pulmonary adenocarcinoma with heterotopic ossification.
  • Pulmonary adenocarcinoma is a common malignancy that often involves calcification; however, bone formation in primary lung adenocarcinoma is extremely rare.
  • In ten cases of primary pulmonary adenocarcinoma with heterotopic ossification, we detected immunoreactivity against TGF-beta1, osteopontin, osteocalcin and Runx2 in the fibroblastic stroma and tumor cells within the area of ossification.
  • Our results suggest that in primary pulmonary adenocarcinoma, heterotopic ossification occurs via intramembranous bone formation.
  • To our knowledge, only 11 other cases of pulmonary adenocarcinoma with heterotopic ossification have been reported.
  • Here, we present ten cases of pulmonary adenocarcinoma showing heterotopic ossification with a description of previously published results and the histogenesis of heterotopic bone formation.
  • [MeSH-major] Adenocarcinoma / diagnosis. Lung Neoplasms / diagnosis. Ossification, Heterotopic / diagnosis

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  • (PMID = 19543517.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 1 Subunit; 0 / RUNX2 protein, human; 0 / Transforming Growth Factor beta1; 104982-03-8 / Osteocalcin; 106441-73-0 / Osteopontin
  • [Other-IDs] NLM/ PMC2698200
  • [Keywords] NOTNLM ; Adenocarcinoma / Choristoma / Immunohistochemistry / Lung Neoplasms / Metaplasia / Ossification
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93. Lamarque D, Levy M, Chaumette MT, Roudot-Thoraval F, Cavicchi M, Auroux J, Courillon-Mallet A, Haioun C, Delchier JC: Frequent and rapid progression of atrophy and intestinal metaplasia in gastric mucosa of patients with MALT lymphoma. Am J Gastroenterol; 2006 Aug;101(8):1886-93
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  • [Title] Frequent and rapid progression of atrophy and intestinal metaplasia in gastric mucosa of patients with MALT lymphoma.
  • OBJECTIVES: Association of gastric mucosa-associated lymphoid tissue (MALT) low-grade lymphoma and adenocarcinoma has repeatedly been reported.
  • The aim of this study was to evaluate the frequency and the spreading of atrophy and intestinal metaplasia in gastric mucosa of patients with gastric MALT lymphoma followed after conservative treatment.
  • Univariate and multivariate analysis evaluated the association between the appearance of atrophy and intestinal metaplasia in antrum or corpus and different factors related to patients, H. pylori status, lymphoma features, and treatment.
  • In addition, histological aspects of gastric biopsies at the diagnosis period and at the end of follow-up were compared with those of two control groups of age-matched patients with H. pylori gastritis.
  • RESULTS: At the diagnosis time, only intestinal metaplasia in corpus was more frequent in patients with gastric MALT lymphoma than in patients with nonulcer dyspepsia.
  • Within median follow-up of 54.4 months (range 9-196), the percentage of patients with gastric atrophy and intestinal metaplasia increased significantly and became significantly higher than in age-matched nonulcer dyspepsia patients.
  • Multivariate analysis showed significant association between corpus intestinal metaplasia and corpus atrophy, intestinal metaplasia in antrum, and duration of the follow-up.
  • CONCLUSIONS: Conservative management of gastric MALT lymphoma including H. pylori eradication is associated with progression of gastric atrophy and intestinal metaplasia with frequent involvement of the corpus which is known to be a precancerous condition.
  • [MeSH-minor] Atrophy. Chi-Square Distribution. Disease Progression. Female. Gastroscopy. Helicobacter Infections / drug therapy. Helicobacter Infections / pathology. Helicobacter pylori. Humans. Male. Metaplasia. Middle Aged. Risk Factors

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  • (PMID = 16780555.001).
  • [ISSN] 0002-9270
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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94. Mikami Y, Kiyokawa T, Sasajima Y, Teramoto N, Wakasa T, Wakasa K, Hata S: Reappraisal of synchronous and multifocal mucinous lesions of the female genital tract: a close association with gastric metaplasia. Histopathology; 2009 Jan;54(2):184-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reappraisal of synchronous and multifocal mucinous lesions of the female genital tract: a close association with gastric metaplasia.
  • AIMS: To describe the gastric phenotype of synchronous mucinous metaplasia and neoplasms of the female genital tract (SMMN-FGT).
  • All six patients had mucinous metaplasia of endometrium, which showed features of lobular endocervical glandular hyperplasia (LEGH)/pyloric gland metaplasia (PGM) in five and was associated with mucinous adenocarcinoma in three.
  • Five patients had mucinous metaplasia of the fallopian tubes, of which three showed borderline features.
  • Five patients had cervical lesions including LEGH/PGM associated with either adenocarcinoma in situ or minimal deviation adenocarcinoma of the cervix.
  • One patient with minimal deviation adenocarcinoma involving the vagina died of her disease, whereas five patients, including three with microinvasion and three with positive peritoneal cytology or mucinous ascites, were alive without recurrence after a mean follow-up of 46 months (range 13-102 months).
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Cervix Uteri / pathology. Gastric Mucosa / pathology. Genital Neoplasms, Female / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Hyperplasia. Metaplasia. Middle Aged

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  • (PMID = 19207943.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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95. 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
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  • 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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96. Murray L, Sedo A, Scott M, McManus D, Sloan JM, Hardie LJ, Forman D, Wild CP: TP53 and progression from Barrett's metaplasia to oesophageal adenocarcinoma in a UK population cohort. Gut; 2006 Oct;55(10):1390-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TP53 and progression from Barrett's metaplasia to oesophageal adenocarcinoma in a UK population cohort.
  • BACKGROUND AND AIMS: Oesophageal adenocarcinoma frequently develops on a background of metaplastic Barrett's epithelium.
  • For each case up to five controls were matched on age, sex, and year of diagnosis.
  • Biopsies from the time of diagnosis of Barrett's epithelium were stained immunohistochemically for TP53, cyclin D1, cyclooxygenase 2 (COX-2), and beta-catenin proteins.
  • The odds of diffuse or intense TP53 staining were substantially elevated in biopsies from patients who developed oesophageal adenocarcinoma compared with controls (odds ratio (OR) 11.7 (95% confidence interval (CI) 1.93, 71.4)).
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / pathology. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Aged. Biopsy. Case-Control Studies. Cohort Studies. Cyclin D1 / metabolism. Cyclooxygenase 2 / metabolism. Disease Progression. Female. Humans. Immunohistochemistry. Male. Metaplasia / pathology. beta Catenin / metabolism


97. Siewert JR, Stein HJ, Feith M: Adenocarcinoma of the esophago-gastric junction. Scand J Surg; 2006;95(4):260-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenocarcinoma of the esophago-gastric junction.
  • BACKGROUND: The border between the esophagus and stomach gives rise to many discrepancies in the current literature regarding the etiology, classification and surgical treatment of adenocarcinoma arising at the esophago-gastric junction.
  • We have consequently used the AEG-criteria (adenocarcinoma of the esophago-gastric junction) for classification and have based the selection of the surgical approach on the anatomic topographic subclassification.
  • METHODS: In the following we report an analysis of a large and homogeneously classified population of 1602 consecutive patients with adenocarcinoma of the esophago-gastric junction, with an emphasis on the surgical approach, the pattern of lymphatic spread, the outcome after surgical treatment and the prognostic factors.
  • Demographic data, morphologic and histopathologic tumor characteristics, and long-term survival rates were compared among the three tumor subclassifiations.
  • RESULTS: The study confirms the marked differences in sex distribution, associated specialized intestinal metaplasia in the esophagus, tumor grading, tumor growth pattern, lymphatic spread, and stage between the three tumor entities.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / surgery. Esophageal Neoplasms / classification. Esophageal Neoplasms / surgery. Esophagogastric Junction. Stomach Neoplasms / classification. Stomach Neoplasms / surgery

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  • (PMID = 17249275.001).
  • [ISSN] 1457-4969
  • [Journal-full-title] Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society
  • [ISO-abbreviation] Scand J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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98. Chennat J, Waxman I: Endoscopic treatment of Barrett's esophagus: From metaplasia to intramucosal carcinoma. World J Gastroenterol; 2010 Aug 14;16(30):3780-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic treatment of Barrett's esophagus: From metaplasia to intramucosal carcinoma.
  • The annual incidence of adenocarcinoma arising from Barrett's esophagus (BE) is approximately 0.5%.
  • Through a process of gradual transformation from low-grade dysplasia to high-grade dysplasia (HGD), adenocarcinoma can develop in the setting of BE.
  • The clinical importance of appropriate identification and treatment of BE in its various stages, from intestinal metaplasia to intramucosal carcinoma (IMC) hinges on the dramatically different prognostic status between early neoplasia and more advanced stages.
  • Once a patient has symptoms of adenocarcinoma, there is usually locally advanced disease with an approximate 5-year survival rate of about 20%.
  • [MeSH-major] Adenocarcinoma / surgery. Barrett Esophagus / surgery. Esophageal Neoplasms / surgery. Esophagoscopy. Esophagus / surgery. Precancerous Conditions / surgery
  • [MeSH-minor] Catheter Ablation. Cryosurgery. Disease Progression. Humans. Metaplasia. Mucous Membrane / pathology. Mucous Membrane / surgery. Photochemotherapy. Treatment Outcome

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  • (PMID = 20698040.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2921089
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99. Hansel DE, Meeker AK, Hicks J, De Marzo AM, Lillemoe KD, Schulick R, Hruban RH, Maitra A, Argani P: Telomere length variation in biliary tract metaplasia, dysplasia, and carcinoma. Mod Pathol; 2006 Jun;19(6):772-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomere length variation in biliary tract metaplasia, dysplasia, and carcinoma.
  • Using a novel, recently validated telomere fluorescence in situ hybridization method, we examined telomere length in normal and inflamed gallbladder epithelium, metaplasia and dysplasia of the gallbladder, and biliary tract carcinoma to determine whether telomere shortening is associated with neoplastic progression in the biliary tract.
  • In addition, invasive adenocarcinoma of the biliary tract frequently demonstrated intratumoral heterogeneity of telomere lengths.
  • [MeSH-minor] DNA, Neoplasm / analysis. Epithelium / pathology. Gallbladder / pathology. Humans. In Situ Hybridization, Fluorescence. Metaplasia / genetics. Metaplasia / pathology

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  • (PMID = 16557277.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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100. Koppert LB, Wijnhoven BP, van Dekken H, Tilanus HW, Dinjens WN: The molecular biology of esophageal adenocarcinoma. J Surg Oncol; 2005 Dec 1;92(3):169-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The molecular biology of esophageal adenocarcinoma.
  • This premalignant condition forms the most important risk factor for developing esophageal adenocarcinoma, which is an extremely aggressive tumor with a 5-year survival rate of less than 25%.
  • Carcinomas that arise in the setting of Barrett's esophagus are thought to develop as part of the metaplasia-dysplasia-carcinoma sequence.
  • RESULTS: Several changes in gene structure, gene expression, and protein structure are associated with the progression of Barrett's esophagus to adenocarcinoma.
  • Alterations in tumor suppressor genes, amongst which p53 and p16, are early events in the metaplasia-dysplasia-adenocarcinoma sequence, followed by loss of cell cycle checkpoints.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / pathology. Chromosome Aberrations. DNA, Neoplasm / genetics. Esophageal Neoplasms / genetics
  • [MeSH-minor] Apoptosis / genetics. Cyclin D1 / genetics. Epidermal Growth Factor / genetics. Gastroesophageal Reflux / complications. Gene Expression Regulation, Neoplastic. Humans. Metaplasia / pathology. Microsatellite Repeats. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics. Tumor Suppressor Protein p53 / genetics

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16299787.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  • [Number-of-references] 252
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