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1. Pereira C, Sousa H, Ferreira P, Fragoso M, Moreira-Dias L, Lopes C, Medeiros R, Dinis-Ribeiro M: -765G > 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
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  • [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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2. 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.
  • Stomach sections were stained using antibodies for TFF2, intrinsic factor, H/K-ATPase, BrdU and MUC2.
  • 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-major] Helicobacter Infections / pathology. Helicobacter pylori. Peptides / metabolism. Stomach / pathology
  • [MeSH-minor] Animals. Gastric Mucosa / metabolism. Gastric Mucosa / pathology. Gerbillinae. Goblet Cells / metabolism. Goblet Cells / pathology. Male. Metaplasia


3. 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.
  • Two lesions (17%) were positive for only 45M1 (gastric phenotypic mucin).
  • 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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4. 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).
  • The transcription factor Pdx-1 is expressed in the adult pancreatic islet cells as well as the gastric antrum and duodenum.
  • 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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5. 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-major] Barrett Esophagus / pathology. Gastroesophageal Reflux / pathology. Helicobacter Infections / pathology. Intestines / pathology. Stomach / pathology
  • [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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6. 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.
  • In gastric cancer patients bcl-2 was expressed in early gastric cancer more frequently than in advanced stage.
  • 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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7. 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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8. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The stomach was used for culture, and for histology.
  • 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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9. 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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  • [Title] [Intestinal metaplasia, dysplasia, gastric cancer and Helicobacter pylori: epidemiological observations].
  • [Transliterated title] Metaplasia intestinale, displasia, cancro gastrico e Helicobacter pylori: considerazioni epidemiologiche.
  • Gastric cancer (GC) is the world's second leading cause of cancer-related mortality, and carries a bad prognosis.
  • There are increasing indications that this infection is associated with both the initiation and progress of gastric carcinoma and lymphoma.
  • [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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10. 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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11. 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.
  • 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.
  • All of the metaplastic gastric glands showed diffuse and strong immunopositivity for gastric foveolar mucin (MUC5AC).
  • 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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12. 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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13. 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.
  • The present study investigated the relationship of CDX2 and LI-cadherin expression in gastric cancer.
  • One hundred and nine pairs of tumour and non-cancerous gastric mucosa were collected from gastrectomy specimens.
  • 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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14. 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.
  • Furthermore, immunohistochemical analysis of the stomach using a H. pylori polyclonal antibody detected positive-staining bacteria within the pyloric region of three of nine hamsters including the neoplastic glands.
  • 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.
  • Syrian hamsters appear suitable as potential model for studying development of helicobacter-associated gastric adenocarcinomas.
  • [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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15. 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.
  • However, the expression and distribution of Ep-CAM in gastric premalignant and malignant lesions are not well known.
  • 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.
  • CONCLUSION: Our findings suggest that increased levels of Ep-CAM represent an early event in gastric carcinogenesis, and seem to have a specific relation with the development of IM as a morphoregulatory molecule.
  • [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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16. 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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  • [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.
  • As CDX2 is differentially expressed in normal stomach and intestine, we sought to relate the CDX2 expression to gastrointestinal differentiation along gastric carcinogenesis.
  • 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.
  • Moreover, CDX2 expression was progressively reduced in gastric dysplasia and cancer.
  • The CDX2 expression in gastric cancer was also inversely correlated with the expression of gastric mucins.
  • 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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17. Rieder G, Tessier AJ, Qiao XT, Madison B, Gumucio DL, Merchant JL: Helicobacter-induced intestinal metaplasia in the stomach correlates with Elk-1 and serum response factor induction of villin. J Biol Chem; 2005 Feb 11;280(6):4906-12
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  • [Title] Helicobacter-induced intestinal metaplasia in the stomach correlates with Elk-1 and serum response factor induction of villin.
  • Chronic Helicobacter pylori infection results in serious sequelae, including atrophy, intestinal metaplasia, and gastric cancer.
  • Intestinal metaplasia in the stomach is defined by the presence of intestine-like cells expressing enterocyte-specific markers, such as villin.
  • In this study, we demonstrate that villin is expressed in intestine-like cells that develop after chronic infection with H. pylori in both human stomach and in a mouse model.
  • We demonstrated that induction of the villin promoter by H. pylori in a human gastric adenocarcinoma cell line (AGS) required activation of the Erk pathway.
  • Thus, H. pylori induction of villin in the stomach correlates with activation and cooperative binding of Elk-1 and the SRF to the proximal promoter of villin.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. Helicobacter pylori / metabolism. Intestines / microbiology. Metaplasia / microbiology. Microfilament Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Serum Response Factor / metabolism. Stomach / microbiology. Transcription Factors / biosynthesis

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  • (PMID = 15576363.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA46952; United States / NIDDK NIH HHS / DK / P01DK62041; United States / NIDDK NIH HHS / DK / R01DK61410
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / ELK1 protein, human; 0 / Elk1 protein, mouse; 0 / Microfilament Proteins; 0 / Proto-Oncogene Proteins; 0 / Serum Response Factor; 0 / Transcription Factors; 0 / ets-Domain Protein Elk-1; 0 / villin; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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18. Baczewska-Mazurkiewicz D, Rydzewska G, Milewski J, Durlik M, Lao M, Rydzewski A: Magnification chromoendoscopy in comparison to standard chromoendoscopy for detection of intestinal metaplasia in renal transplant recipients. Adv Med Sci; 2006;51:115-8
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  • [Title] Magnification chromoendoscopy in comparison to standard chromoendoscopy for detection of intestinal metaplasia in renal transplant recipients.
  • Intestinal metaplasia is a feature of atrophic gastritis whereas the diagnosis of Barrett's esophagus is based on histological demonstration of specialized metaplasia.
  • Both conditions are associated with increased risk of adenocarcinoma.
  • The aim of the present study was to assess whether magnification endoscopy improves the diagnostic accuracy of intestinal metaplasia in stomach and in esophagus.
  • MATERIAL AND METHODS: In this non-randomized, feasibility study thirty one (12 women and 19 men) renal transplant recipients, with a mean age of 44.0 years were evaluated for the presence of intestinal metaplasia.
  • The presence of gastritis and intestinal metaplasia was classified according to modified updated Sydney classification.
  • RESULTS: Of 31 patients, 16 patients had endoscopic and histopathological evidence of gastric intestinal metaplasia, and standard endoscopy with methylene blue staining was sufficient for diagnosis (15 from 16).
  • Magnification endoscopy allowed identification of 6 patients with specialized intestinal metaplasia in Barrett's esophagus, which would be otherwise missed.
  • CONCLUSIONS: In this study diagnostic accuracy of standard endoscopy for identification of intestinal metaplasia in the stomach was not improved by the use of magnification endoscopy, but the latter was an accurate method of predicting specialized intestinal metaplasia in Barrett's esophagus.
  • [MeSH-major] Endoscopy, Gastrointestinal / methods. Intestinal Diseases / diagnosis. Intestines / pathology. Kidney Transplantation
  • [MeSH-minor] Adult. Barrett Esophagus / pathology. Feasibility Studies. Female. Humans. Intestinal Neoplasms / diagnosis. Male. Metaplasia / diagnosis. Middle Aged. Reproducibility of Results. Sensitivity and Specificity

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  • (PMID = 17357289.001).
  • [ISSN] 1896-1126
  • [Journal-full-title] Advances in medical sciences
  • [ISO-abbreviation] Adv Med Sci
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Poland
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19. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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20. Bao H, Boussioutas A, Reynolds J, Russell S, Gu M: Imaging of goblet cells as a marker for intestinal metaplasia of the stomach by one-photon and two-photon fluorescence endomicroscopy. J Biomed Opt; 2009 Nov-Dec;14(6):064031
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  • [Title] Imaging of goblet cells as a marker for intestinal metaplasia of the stomach by one-photon and two-photon fluorescence endomicroscopy.
  • Goblet cells are a requirement for the diagnosis of intestinal metaplasia of the stomach.
  • The gastric mucosa is lined by a monolayer of columnar epithelium with some specialization at the crypts, but there are no goblet cells in normal gastric epithelium.
  • The appearance of goblet cells in gastric epithelium is an indicator of potential malignant progression toward adenocarcinoma.
  • Therefore, in vivo three-dimensional imaging of goblet cells is essential for diagnoses of a premalignant stage of gastric cancers called intestinal metaplasia.
  • We used mouse intestine, which has goblet cells, as a model of intestinal metaplasia.
  • These results prove that two-photon fluorescence endomicroscopy is advantageous in diagnoses of a premalignant stage of gastric cancers.
  • [MeSH-minor] Animals. Fluorescein. Imaging, Three-Dimensional / methods. Metaplasia / pathology. Mice. Precancerous Conditions / pathology. Stomach Neoplasms / pathology

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  • (PMID = 20059269.001).
  • [ISSN] 1560-2281
  • [Journal-full-title] Journal of biomedical optics
  • [ISO-abbreviation] J Biomed Opt
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] TPY09G7XIR / Fluorescein
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21. 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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22. Li JH, Shi XZ, Lv S, Liu M, Xu GW: Effect of Helicobacter pylori infection on p53 expression of gastric mucosa and adenocarcinoma with microsatellite instability. World J Gastroenterol; 2005 Jul 28;11(28):4363-6
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  • [Title] Effect of Helicobacter pylori infection on p53 expression of gastric mucosa and adenocarcinoma with microsatellite instability.
  • AIM: To investigate the relationship between Helicobacter pylori (H pylori) infection, microsatellite instability and the expressions of the p53 in gastritis, intestinal metaplasia and gastric adenocarcinoma and to elucidate the mechanism of gastric carcinogenesis relating to H pylori infection.
  • METHODS: One hundred and eight endoscopic biopsies and gastric adenocarcinoma were available for the study including 33 cases of normal, 45 cases of gastritis, 30 cases of intestinal metaplasia, and 46 cases of gastric adenocarcinoma.
  • MSI was defined as the peak shift in the DNA of the gastric tissue compared with that of the peripheral blood samples.
  • RESULTS: H pylori infection was detected in the samples of gastritis, intestinal metaplasia, and gastric adenocarcinoma and the infection frequencies were 84.4%, 76.7%, and 65.2%, respectively, whereas no H pylori infection was detected in the samples of normal control.
  • No MSI was detected in gastritis samples, one MSI-H and two MSI-L were detected among the 30 intestinal metaplasia samples, and 12 MSI-H and 3 MSI-L were detected in the 46 gastric carcinomas.
  • In those gastric carcinomas, the MSI-H frequency in H pylori-positive group was significantly higher than that in H pylori-negative group.
  • P53-positive immunohistochemical staining was detected in 13.3% of intestinal metaplasia samples and in 43.5% of gastric carcinoma samples.
  • CONCLUSION: H pylori affect the p53 pattern in gastric mucosa when MMR system fails to work.
  • Mutations of the p53 gene seem to be an early event in gastric carcinogenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Helicobacter Infections / physiopathology. Helicobacter pylori. Stomach Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adult. Aged. Female. Gastric Mucosa / microbiology. Gastric Mucosa / physiology. Gene Expression Regulation, Neoplastic. Humans. Male. Microsatellite Repeats. Middle Aged

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  • (PMID = 16038035.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC4434663
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23. 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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  • [Title] Prevalence of Helicobacter pylori infection and intestinal metaplasia in subjects who had undergone surgery for gastric adenocarcinoma in Northwest Italy.
  • AIM: To investigate the seroprevalence of Helicobacter pylori (H pylori) infection and its more virulent strains as well as the correlation with the histologic features among patients who had undergone surgery for gastric cancer (GC).
  • 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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24. Sun JH, Das KK, Amenta PS, Yokota K, Watari J, Sato T, Kohgo Y, Das KM: Preferential expression of cyclooxygenase-2 in colonic-phenotype of gastric intestinal metaplasia: association with helicobacter pylori and gastric carcinoma. J Clin Gastroenterol; 2006 Feb;40(2):122-8
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  • [Title] Preferential expression of cyclooxygenase-2 in colonic-phenotype of gastric intestinal metaplasia: association with helicobacter pylori and gastric carcinoma.
  • OBJECTIVES: Gastric intestinal metaplasia (GIM) associated with H. pylori (HP) has been considered a premalignant lesion.
  • However, GIM phenotype associated with HP infection and gastric cancer is unclear.
  • METHODS: We evaluated cellular phenotype and COX-2 expression in the GIM from HP-positive and -negative patients from Japan in the absence of gastric cancer (n = 31) by using a colon epithelium specific monoclonal antibody (mAb Das-1) and anti-COX-2 antibody.
  • COX-2 expression was also examined in patients with gastric cancer (n = 34), both in the cancer and in the GIM areas away from the cancer field.
  • COX-2 expression was frequent in both gastric cancer and the GIM adjacent to the cancer.
  • The results suggest that the presence of mAb Das-1 and COX-2 reactivity in the GIM identify the subgroup of patients who may be at risk for gastric cancer and may need close surveillance.
  • [MeSH-major] Adenocarcinoma / metabolism. Cyclooxygenase 2 / metabolism. Gastric Mucosa / metabolism. Helicobacter Infections / metabolism. Helicobacter pylori / metabolism. Metaplasia / metabolism. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism

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  • (PMID = 16394872.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Grant] United States / PHS HHS / / R01 47673
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / DAS-1 protein, human; EC 1.14.99.1 / Cyclooxygenase 2
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25. Leung WK, Ng EK, Chan WY, Auyeung AC, Chan KF, Lam CC, Chan FK, Lau JY, Sung JJ: Risk factors associated with the development of intestinal metaplasia in first-degree relatives of gastric cancer patients. Cancer Epidemiol Biomarkers Prev; 2005 Dec;14(12):2982-6
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  • [Title] Risk factors associated with the development of intestinal metaplasia in first-degree relatives of gastric cancer patients.
  • Family relatives of gastric cancer patients have a higher risk of gastric cancer and premalignant gastric lesions.
  • We sought to determine the risk factors associated with the presence of intestinal metaplasia in a large cohort of gastric cancer relatives.
  • First-degree relatives of gastric cancer patients were invited for screening gastroscopy.
  • Endoscopic gastric biopsies were obtained from the antrum and corpus.
  • Gastric biopsies were analyzed for Helicobacter pylori infection, severity of inflammation, and presence of intestinal metaplasia.
  • Stepwise logistic regressions were used to identify for risk factors associated with presence of intestinal metaplasia in cancer relatives.
  • Among them, 161 (59.6%) were H. pylori positive and 81 (30%) had confirmed intestinal metaplasia.
  • The following factors were found to be associated with the presence of intestinal metaplasia: age, male sex, H. pylori infection, birth order, alcohol use, siblings with stomach cancer, childhood living conditions, and water supply.
  • Individuals with intestinal metaplasia had more severe acute and chronic inflammation in the antrum and corpus (P < 0.003).
  • With multiple logistic regression, H. pylori infection [odds ratio (OR), 3.23], male gender (OR, 2.09), age (OR, 1.07), and a history of gastric cancer in siblings (OR, 1.91) were independent factors associated with the development of intestinal metaplasia in cancer relatives.
  • In conclusion, we have identified risk factors associated with gastric intestinal metaplasia in stomach cancer relatives, which may be useful in the understanding of gastric carcinogenesis in these high-risk individuals.
  • [MeSH-major] Adenocarcinoma / genetics. Intestines / pathology. Stomach Neoplasms / genetics
  • [MeSH-minor] Adult. Chi-Square Distribution. Endoscopy, Gastrointestinal. Female. Helicobacter Infections / epidemiology. Helicobacter pylori. Humans. Logistic Models. Male. Metaplasia / genetics. Middle Aged. Risk Factors. Statistics, Nonparametric

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  • (PMID = 16365021.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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26. Chandrasoma P, Wickramasinghe K, Ma Y, DeMeester T: Is intestinal metaplasia a necessary precursor lesion for adenocarcinomas of the distal esophagus, gastroesophageal junction and gastric cardia? Dis Esophagus; 2007;20(1):36-41
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  • [Title] Is intestinal metaplasia a necessary precursor lesion for adenocarcinomas of the distal esophagus, gastroesophageal junction and gastric cardia?
  • Adenocarcinoma of the distal esophagus and gastroesophageal junction are believed to arise in Barrett's esophagus with intestinal metaplasia.
  • Whether adenocarcinoma can arise in columnar lined esophagus without intestinal metaplasia is in doubt.
  • Whether adenocarcinoma of the gastric cardia arises in intestinal metaplasia of the gastric cardia is also in doubt.
  • We aim to evaluate the relationship of size and stage of adenocarcinoma of the distal esophagus, gastroesophageal junction and gastric cardia to intestinal metaplasia and other types of columnar epithelium.
  • Seventy-four patients who had esophagogastrectomy for adenocarcinomas in this region were examined histologically to assess the frequency of residual intestinal metaplasia in the surrounding epithelium.
  • Tumors without residual intestinal metaplasia were evaluated for the presence of other columnar epithelia and correlated with tumor size and stage.
  • Residual intestinal metaplasia was present in 48 (65%) tumors, including 33/38 (87%) distal esophageal, 10/25 (45%) junctional and 5/11 (45%) gastric cardia tumors.
  • The prevalence of intestinal metaplasia was 100% in all tumors that were less than 1 cm in maximum diameter and all intramucosal tumors.
  • The prevalence of residual intestinal metaplasia decreased with increasing tumor size and stage.
  • These data strongly support the contention that adenocarcinomas of this region, including those in the gastric cardia, arise in intestinal metaplastic epithelium.
  • The absence of residual intestinal metaplasia in larger tumors is the result of tumor overgrowing the intestinal metaplasia from which it arose.

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  • (PMID = 17227308.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Zaky AH, Watari J, Tanabe H, Sato R, Moriichi K, Tanaka A, Maemoto A, Fujiya M, Ashida T, Kohgo Y: Clinicopathologic implications of genetic instability in intestinal-type gastric cancer and intestinal metaplasia as a precancerous lesion: proof of field cancerization in the stomach. Am J Clin Pathol; 2008 Apr;129(4):613-21
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  • [Title] Clinicopathologic implications of genetic instability in intestinal-type gastric cancer and intestinal metaplasia as a precancerous lesion: proof of field cancerization in the stomach.
  • To clarify field cancerization in the stomach by genetic alterations, we studied 83 cases of intestinal-type gastric cancer (GC) and paired intestinal metaplasia (IM) distant from GC and 39 cases of chronic gastritis with IM (CG-IM) for genetic instability (GIN).
  • By tumor location, MSI showed the highest incidence in GC and GC-IM with the tumor located in the upper third of the stomach.
  • The condition is consistent with the hypothesis of field cancerization in the stomach.
  • [MeSH-major] Adenocarcinoma / genetics. Loss of Heterozygosity. Microsatellite Repeats. Precancerous Conditions / genetics. Stomach Neoplasms / genetics
  • [MeSH-minor] Aged. DNA, Neoplasm / analysis. Female. Humans. Lymph Nodes / pathology. Male. Metaplasia / genetics. Metaplasia / pathology

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  • (PMID = 18343789.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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28. Shiotani A, Uedo N, Iishi H, Tatsuta M, Ishiguro S, Nakae Y, Kamada T, Haruma K, Merchant JL: Re-expression of sonic hedgehog and reduction of CDX2 after Helicobacter pylori eradication prior to incomplete intestinal metaplasia. Int J Cancer; 2007 Sep 15;121(6):1182-9
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  • [Title] Re-expression of sonic hedgehog and reduction of CDX2 after Helicobacter pylori eradication prior to incomplete intestinal metaplasia.
  • Loss of Sonic Hedgehog (Shh) and aberrant CDX2 expression are early changes correlating with the presence of intestinal metaplasia that occur in the gastric mucosa prior to neoplastic transformation.
  • The aim of this study was to compare the improvement in corpus gastritis with Shh and CDX2 expression after H. pylori eradication between subjects at high risk for gastric cancer and controls.
  • Seventy patients with endoscopic resection for early gastric cancer and 30 controls were studied.
  • 1.6-13.5) and in the mucosa with incomplete intestinal metaplasia rather than in those without incomplete intestinal metaplasia (OR 7.6 95% C.I. 2.4-24.3).
  • Atrophy, expression of Shh and CDX2 at the corpus lesser curve significantly improved in mucosa without incomplete intestinal metaplasia (p < 0.01), but not in mucosa with incomplete intestinal metaplasia.
  • In conclusion, H. pylori eradication prior to development of incomplete intestinal metaplasia improves corpus gastritis and may prevent gastric cancer.
  • Pepsinogen I may be a useful marker in patients with a residual higher risk of gastric cancer after H. pylori eradication.

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17520681.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P01 DK062041; United States / NIDDK NIH HHS / DK / R01 DK61410; United States / NIDDK NIH HHS / DK / R01 DK061410-04; United States / NIDDK NIH HHS / DK / DK061410-04; United States / NIDDK NIH HHS / DK / R01 DK061410
  • [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 / Anti-Bacterial Agents; 0 / Anti-Ulcer Agents; 0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / Hedgehog Proteins; 0 / Homeodomain Proteins; 0 / SHH protein, human; 804826J2HU / Amoxicillin; 9001-10-9 / Pepsinogen A; H1250JIK0A / Clarithromycin
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29. Norimura D, Isomoto H, Nakayama T, Hayashi T, Suematsu T, Nakashima Y, Inoue N, Matsushima K, Yamaguchi N, Ohnita K, Mizuta Y, Inoue K, Shikuwa S, Nakao K, Kohno S: Magnifying endoscopic observation with narrow band imaging for specialized intestinal metaplasia in barrett's esophagus with special reference to light blue crests. Dig Endosc; 2010 Apr;22(2):101-6
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  • [Title] Magnifying endoscopic observation with narrow band imaging for specialized intestinal metaplasia in barrett's esophagus with special reference to light blue crests.
  • AIM: Barrett's esophagus (BE) with specialized intestinal metaplasia (SIM) is at high risk of esophageal adenocarcinoma.
  • In addition to pit patterns, light blue crests (LBC), blue-whitish patchy areas on the metaplastic epithelia of the stomach, can predict SIM in BE under ME-NBI observation.
  • RESULTS: IM pit pattern with ME-NBI for the diagnosis of IM yielded acceptable sensitivity, specificity and accuracy at 92%, 77% and 83%, respectively.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Endoscopy, Gastrointestinal / methods. Intestinal Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cohort Studies. Female. Humans. Male. Metaplasia. Middle Aged. Predictive Value of Tests. Reproducibility of Results. Retrospective Studies

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  • (PMID = 20447202.001).
  • [ISSN] 1443-1661
  • [Journal-full-title] Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
  • [ISO-abbreviation] Dig Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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30. Leung WK, Ng EK, Chan FK, Chan WY, Chan KF, Auyeung AC, Lam CC, Lau JY, Sung JJ: Effects of long-term rofecoxib on gastric intestinal metaplasia: results of a randomized controlled trial. Clin Cancer Res; 2006 Aug 1;12(15):4766-72
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  • [Title] Effects of long-term rofecoxib on gastric intestinal metaplasia: results of a randomized controlled trial.
  • PURPOSE: Gastric cancer and its premalignant gastric lesion, intestinal metaplasia (IM), frequently express cyclooxygenase-2 (COX-2) at high levels.
  • We tested whether long-term use of specific COX-2 inhibitors regress gastric IM.
  • Patients on rofecoxib (19.1%) and on placebo (16.1%) had no IM detected in the stomach (P = 0.59).
  • CONCLUSIONS: There was no trend to suggest that treatment with rofecoxib for 2 years resulted in the regression of gastric IM.
  • Although our findings cast doubt on the reversibility of gastric IM by COX-2 inhibitor, further studies are needed to establish the role of COX-2 inhibitors in different stages of gastric carcinogenesis.
  • [MeSH-major] Adenocarcinoma / drug therapy. Gastrointestinal Neoplasms / drug therapy. Lactones / administration & dosage. Metaplasia / drug therapy. Sulfones / administration & dosage

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  • (PMID = 16899628.001).
  • [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] Controlled Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lactones; 0 / Placebos; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib
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31. Leys CM, Nomura S, LaFleur BJ, Ferrone S, Kaminishi M, Montgomery E, Goldenring JR: Expression and prognostic significance of prothymosin-alpha and ERp57 in human gastric cancer. Surgery; 2007 Jan;141(1):41-50
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  • [Title] Expression and prognostic significance of prothymosin-alpha and ERp57 in human gastric cancer.
  • PURPOSE: Prothymosin-alpha and ERp57 were previously identified as markers for gastric metaplasia in a mouse model of Helicobacter-induced gastric metaplasia and neoplasia.
  • In this paper we assess whether the expression of these putative biomarkers in humans is correlated with gastric metaplasia and adenocarcinoma and clinical outcomes.
  • METHODS: Eight tissue microarrays, containing 749 paraffin-embedded tissue cores from 164 gastric cancer patients, were stained for prothymosin-alpha and ERp57 by horseradish peroxidase immunohistochemical techniques.
  • RESULTS: Prothymosin-alpha stained a significantly higher percentage of nuclei in cancer and metastases compared with normal gastric mucosa.
  • ERp57 staining was significantly decreased in cancer and metastases compared with both normal gastric mucosa and metaplasias.
  • CONCLUSIONS: These results suggest that although prothymosin-alpha is overexpressed in gastric adenocarcinoma, it is not associated with alterations in survival.
  • In contrast, loss of ERp57 expression correlated with more aggressive disease and could provide useful prognostic information for gastric cancer patients.
  • [MeSH-major] Protein Disulfide-Isomerases / metabolism. Protein Precursors / metabolism. Stomach Neoplasms / metabolism. Thymosin / analogs & derivatives
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / mortality. Adenocarcinoma / pathology. Biomarkers, Tumor / metabolism. Down-Regulation. Endoplasmic Reticulum / metabolism. Humans. Immunohistochemistry. Metaplasia / metabolism. Molecular Chaperones / metabolism. Prognosis. Protein Array Analysis. Retrospective Studies. Stomach / metabolism. Stomach / pathology. Survival Rate

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  • (PMID = 17188166.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P50 CA95103; United States / NCI NIH HHS / CA / CA67108; United States / NCI NIH HHS / CA / K12 CA090625; United States / NCI NIH HHS / CA / P50 CA62924
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Molecular Chaperones; 0 / Protein Precursors; 0 / prothymosin alpha; 61512-21-8 / Thymosin; EC 5.3.4.1 / Protein Disulfide-Isomerases; EC 5.3.4.1. / PDIA3 protein, human
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32. Choi SY, Lee JI, Noh TJ, Jang JY, Nam KD, Kim NH, Lee SK, Joo KR, Dong SH, Kim HJ, Kim BH, Chang YW, Chang R: [A case of stump MALT lymphoma after partial gastrectomy]. Korean J Gastroenterol; 2006 May;47(5):394-6
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  • Gastrectomy is known to be a risk factor for adenocarcinoma in remnant stomach.
  • It is suggested that reflux of bile juice or duodenal secretion to remnant stomach induces atrophic gastritis, intestinal metaplasia, and gastric adenocarcinoma.
  • Malignant lymphoma in remnant stomach after gastrectomy is very rare.
  • Gastric MALT (mucosa-associated lymphoid tissue) lymphoma is associated with Helicobacter pylori infection but the mechanism of lymphoma development in remnant stomach is still unknown.
  • We report a case of low grade gastric MALT lymphoma of gastric stump after 10 years from partial gastrectomy.
  • [MeSH-major] Gastrectomy. Gastric Stump. Lymphoma, B-Cell, Marginal Zone. Neoplasms, Second Primary. Stomach Neoplasms / surgery

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  • (PMID = 16714883.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
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33. Zhang X, Gupta R, Nicastri AD: Bladder adenocarcinoma following gastrocystoplasty. J Pediatr Urol; 2010 Oct;6(5):525-7
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  • [Title] Bladder adenocarcinoma following gastrocystoplasty.
  • Bladder augmentation with segments of small bowel (ileocystoplasty), large intestine (colocystoplasty) or stomach (gastrocystoplasty) has been used to treat patients with small or noncompliant bladders by increasing the capacity or compliance.
  • Carcinomas following gastrocystoplasty have been observed in the segments of stomach; however, to our knowledge, carcinoma arising in the residual native bladder has not been reported.
  • 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.
  • Patients with gastrocystoplasty are at an increased risk for carcinoma in stomach segments and require close long-term follow up; however, the risk of carcinoma in native bladder is still unclear.
  • [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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34. Yao T, Utsunomiya T, Oya M, Nishiyama K, Tsuneyoshi M: Extremely well-differentiated adenocarcinoma of the stomach: clinicopathological and immunohistochemical features. World J Gastroenterol; 2006 Apr 28;12(16):2510-6
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  • [Title] Extremely well-differentiated adenocarcinoma of the stomach: clinicopathological and immunohistochemical features.
  • AIM: Minimal deviation carcinoma of the uterine cervix, otherwise known as extremely well-differentiated adenocarcinoma (EWDA), is characterized by its benign microscopic appearance in contrast to its aggressive behavior.
  • In order to elucidate the clinicopathological features and biological behavior of the gastric counterpart of EWDA, we, using immunohistochemistry, analyzed nine lesions for the phenotypic expression, proliferative activity, and the expression of oncogene-associated products.
  • METHODS: Clinicopathological features, including pre-operative biopsy diagnosis, were reviewed.
  • Using immunohistochemistry, Ki-67 labeling index and expression of p53 and c-erbB-2 protein in the gastric lesions were detected.
  • RESULT: Locations in the middle or upper third of the stomach and polypoid macroscopic features are characteristic of EWDA of the stomach.
  • All 9 cases of EWDA could be classified into gastric phenotype (5 lesions) and intestinal phenotype (4 lesions).
  • The former resembled gastric foveolar epithelium, mucous neck cells or pyloric glands, but their papillary structures were frequently elongated and the tumor cells and their nuclei were slightly larger and more hyperchromatic compared to normal epithelium.
  • The latter resembled intestinal metaplasia with minimal nuclear atypia and irregular glands; two of these lesions demonstrated complete intestinal phenotype, while two demonstrated incomplete intestinal phenotype.
  • CONCLUSION: Unlike minimal deviation carcinoma of the cervix, these findings suggest that EWDA of the stomach is a lesion of low-grade malignancy.
  • Because of its resemblance to normal gastric mucosa or mucosa with intestinal metaplasia, EWDA is often misdiagnosed.
  • [MeSH-major] Adenocarcinoma / pathology. Stomach Neoplasms / pathology

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  • [Cites] Nihon Shokakibyo Gakkai Zasshi. 1994 Apr;91(4):839-48 [7513368.001]
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  • (PMID = 16688795.001).
  • [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 / Ki-67 Antigen; 0 / MUC6 protein, human; 0 / Mucin-6; 0 / Mucins; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.4.24.11 / Neprilysin
  • [Other-IDs] NLM/ PMC4087982
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35. Proença-Modena JL, Acrani GO, Brocchi M: Helicobacter pylori: phenotypes, genotypes and virulence genes. Future Microbiol; 2009 Mar;4(2):223-40
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  • Helicobacter pylori is a Gram-negative, microaerophilic bacterium that colonizes the gastric mucus overlying the epithelium of the stomach in more than 50% of the world's population.
  • This gastric colonization induces chronic gastric inflammation in all infected individuals, but only induces clinical diseases in 10-20% of infected individuals.
  • These include peptic ulcers, acute and atrophic gastritis, intestinal metaplasia, gastric adenocarcinoma and gastric B-cell lymphoma.
  • Various bacterial virulence factors are associated with the development of such gastric diseases, and the characterization of these markers could aid medical prognosis, which could be extremely important in predicting clinical outcomes.
  • The purpose of this review is to summarize the role of the phenotypes, virulence-related genes and genotypes of H. pylori in the establishment of gastric colonization and the development of associated diseases.

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  • (PMID = 19257848.001).
  • [ISSN] 1746-0921
  • [Journal-full-title] Future microbiology
  • [ISO-abbreviation] Future Microbiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Virulence Factors
  • [Number-of-references] 176
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36. 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.
  • 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.
  • CONCLUSION: The classification of adenocarcinomas of the esophago-gastric junction in three types, AEG type I, type II and type III shows marked differences between the tumor entities and is recommended for selection of a proper surgical approach.
  • [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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37. He XX, Yang J, Ding YW, Liu W, Shen QY, Xia HH: Increased epithelial and serum expression of macrophage migration inhibitory factor (MIF) in gastric cancer: potential role of MIF in gastric carcinogenesis. Gut; 2006 Jun;55(6):797-802
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  • [Title] Increased epithelial and serum expression of macrophage migration inhibitory factor (MIF) in gastric cancer: potential role of MIF in gastric carcinogenesis.
  • This study was conducted to determine whether MIF expression is associated with gastric pathology and whether MIF expression is increased in malignant gastric cells in vitro.
  • MATERIALS AND METHODS: Patients with a normal gastric mucosa, Helicobacter pylori infected gastritis, intestinal metaplasia, and gastric adenocarcinoma were included.
  • Immunohistochemistry and enzyme linked immunosorbent assay (ELISA) were used to determine MIF expression in gastric epithelial cells and MIF levels in serum, respectively.
  • Five gastric cancer cell lines (AGS, MKN-45, MKN-28, MGC-803, and SGC-7901) and one non-malignant gastric cell line (GES-1) were cultured for 24 hours.
  • RESULTS: The percentage of MIF expressing epithelial cells was low in normal mucosa (12%) but substantially higher in gastritis (52%), intestinal metaplasia (66%), and gastric cancer (96%) (p<0.001, ANOVA).
  • Serum MIF levels were low in patients with a normal mucosa (576 (82) pg/ml) but higher in patients with gastritis (2100 (349) pg/ml), intestinal metaplasia (4498 (253) pg/ml), and gastric cancer (9737 (1249) pg/ml) (p<0.001, ANOVA).
  • CONCLUSIONS: Epithelial and serum MIF expression was progressively increased in H pylori induced gastritis, intestinal metaplasia, and gastric cancer, suggesting that MIF is involved in gastric carcinogenesis and may be a valuable biomarker for the early detection of gastric cancer.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Macrophage Migration-Inhibitory Factors / metabolism. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Cell Transformation, Neoplastic / metabolism. Chronic Disease. Disease Progression. Enzyme-Linked Immunosorbent Assay / methods. Female. Gastric Mucosa / pathology. Gastritis / metabolism. Gastritis / microbiology. Helicobacter Infections / complications. Helicobacter Infections / metabolism. Helicobacter pylori. Humans. Male. Metaplasia. Middle Aged. Neoplasm Proteins / blood. Neoplasm Proteins / metabolism. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Tumor Cells, Cultured

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  • (PMID = 16488898.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Macrophage Migration-Inhibitory Factors; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  • [Other-IDs] NLM/ PMC1856238
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38. Huang W, Zhao J, Li L, Huang Y, Yang X, Wang J, Zhang T: a-Methylacyl coenzyme A racemase is highly expressed in the intestinal-type adenocarcinoma and high-grade dysplasia lesions of the stomach. Histol Histopathol; 2008 11;23(11):1315-20
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  • [Title] a-Methylacyl coenzyme A racemase is highly expressed in the intestinal-type adenocarcinoma and high-grade dysplasia lesions of the stomach.
  • To study a-Methylacyl coenzyme A racemase (AMACR) expression in gastric intestinal-type adenocarcinoma and its precursors, we performed an immunohistochemical assay (using an avidin-biotin-peroxidase complex method) on 106 paraffin-embedded gastric mucosal biopsy samples and 25 gastrectomy samples (37 negative for dysplasia; 30 indefinite for dysplasia; 22 low-grade dysplasia; 25 high-grade dysplasia; and 34 invasive intestinal adenocarcinoma).
  • In the groups of high-grade dysplasia and invasive intestinal-type adenocarcinoma, however, 19 of 25 (76%) and 18 of 34 (52.9%) were positive for AMACR respectively.
  • Pylori infection or intestinal metaplasia.
  • These results suggested that AMACR may play a role in the intermediate stage of gastric carcinogenesis.
  • [MeSH-major] Adenocarcinoma / enzymology. Biomarkers, Tumor / analysis. Gastric Mucosa / enzymology. Precancerous Conditions / enzymology. Racemases and Epimerases / analysis. Stomach Neoplasms / enzymology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Cell Transformation, Neoplastic / metabolism. Female. Helicobacter pylori / isolation & purification. Humans. Immunohistochemistry. Male. Metaplasia. Middle Aged. Neoplasm Staging

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  • (PMID = 18785113.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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39. Bai JG, Lv Y, Dang CX: Adenocarcinoma of the Esophagogastric Junction in China according to Siewert's classification. Jpn J Clin Oncol; 2006 Jun;36(6):364-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenocarcinoma of the Esophagogastric Junction in China according to Siewert's classification.
  • BACKGROUND: There had never been a clear definition of the cancer of cardia before Siewert's classification, which was proposed in 1996 and approved in 1997 at the second International Gastric Cancer Congress in Munich.
  • On the basis of the classification, this study aims to research into the clinicopathological characteristics and surgical modes of adenocarcinoma of the esophagogastric junction in China.
  • METHODS: The study reviewed the data of the distal esophageal cancer, the cancer of cardia and the proximal gastric cancer at the First Hospital of Xi'an Jiaotong University from January 1995 to December 1999.
  • RESULTS: Among the 203 patients, there were 29 patients with adenocarcinoma of the distal esophagus (Type I); 80 patients with true carcinoma of cardia (Type II); and 94 patients with subcardial carcinoma (Type III).
  • [MeSH-major] Adenocarcinoma / classification. Esophageal Neoplasms / classification. Esophagectomy. Esophagogastric Junction. Lymph Node Excision. Stomach Neoplasms / classification
  • [MeSH-minor] Barrett Esophagus / pathology. Cardia. China / epidemiology. Female. Gastrectomy. Gastric Mucosa / pathology. Humans. Lymph Nodes / pathology. Male. Metaplasia. Middle Aged. Morbidity. Postoperative Complications / etiology. Survival Rate

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  • (PMID = 16766566.001).
  • [ISSN] 0368-2811
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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40. Tsukamoto T, Mizoshita T, Mihara M, Tanaka H, Takenaka Y, Yamamura Y, Nakamura S, Ushijima T, Tatematsu M: Sox2 expression in human stomach adenocarcinomas with gastric and gastric-and-intestinal-mixed phenotypes. Histopathology; 2005 Jun;46(6):649-58
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  • [Title] Sox2 expression in human stomach adenocarcinomas with gastric and gastric-and-intestinal-mixed phenotypes.
  • AIMS: Other than ectopic expression of intestinal transcription factors, Cdx1 and Cdx2, the molecular mechanisms underlying gastric and intestinal phenotypes of human stomach adenocarcinomas have yet to be clarified in detail.
  • We have reported that Sox2, an HMG-box gastric transcription factor, is expressed in normal gastric mucosa and down-regulated in intestinal metaplasia.
  • METHODS AND RESULTS: We analysed mRNA levels of Sox2 and other differentiation markers in 50 surgically resected stomach adenocarcinomas, immunohistochemically classified into gastric (G), gastric-and-intestinal (GI)-mixed, solely intestinal (I), and null (N) types.
  • In the N type, both gastric and intestinal transcription factors were suppressed.
  • A stomach adenocarcinoma cell line, KATOIII, demonstrated both MUC5AC and Sox2, although MUC5AC mRNA was not detected in the Sox2+ AGS cell line.
  • CONCLUSIONS: Sox2 may play an important role in maintaining a gastric phenotype in stomach cancers as well as in normal tissue, in cooperation with other cofactor(s).
  • [MeSH-major] Adenocarcinoma / pathology. HMGB Proteins / genetics. Intestinal Neoplasms / pathology. Stomach Neoplasms / pathology. Transcription Factors / genetics

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  • (PMID = 15910596.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / HMGB Proteins; 0 / Homeodomain Proteins; 0 / MUC5AC protein, human; 0 / MUC6 protein, human; 0 / Microfilament Proteins; 0 / Mucin 5AC; 0 / Mucin-6; 0 / Mucins; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors; 0 / Transcription Factors; 0 / villin
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41. Brundler MA, Harrison JA, de Saussure B, de Perrot M, Pepper MS: Lymphatic vessel density in the neoplastic progression of Barrett's oesophagus to adenocarcinoma. J Clin Pathol; 2006 Feb;59(2):191-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lymphatic vessel density in the neoplastic progression of Barrett's oesophagus to adenocarcinoma.
  • BACKGROUND: Oesophageal adenocarcinoma is an aggressive neoplasm with poor prognosis as a result of early lymph node metastasis.
  • AIMS: To measure lymphatic vessel density (LVD) in the neoplastic progression from Barrett's metaplasia to adenocarcinoma and determine whether LVD can predict the risk of cancer.
  • METHODS: LVD and microvascular density (MVD) were assessed after immunohistochemical staining of vessels in Barrett's metaplasia, dysplasia, and adenocarcinoma tissues and were correlated with clinicopathological features.
  • RESULTS: LVD was significantly reduced in adenocarcinoma, being half that seen in normal stomach/oesophagus or metaplasia/dysplasia.
  • MVD was also assessed as a prognostic marker; its increase appeared to be linked more with the development of Barrett's metaplasia than adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Lymphatic Vessels / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Esophagus / pathology. Female. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Metaplasia / pathology. Middle Aged. Neoplasm Staging. Prognosis. Survival Analysis

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  • (PMID = 16443737.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860317
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42. Mattioli S, Ruffato A, Di Simone MP, Corti B, D'Errico A, Lugaresi ML, Mattioli B, D'Ovidio F: Immunopathological patterns of the stomach in adenocarcinoma of the esophagus, cardia, and gastric antrum: gastric profiles in Siewert type I and II tumors. Ann Thorac Surg; 2007 May;83(5):1814-9
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  • [Title] Immunopathological patterns of the stomach in adenocarcinoma of the esophagus, cardia, and gastric antrum: gastric profiles in Siewert type I and II tumors.
  • BACKGROUND: The morphologic and immunohistochemical profiles of gastric mucosa and of the tumor were assessed in Siewert type I, type II, and gastric antrum adenocarcinomas.
  • METHODS: Sixty-two patients, prospectively operated upon, were included in the study: 37 type II, 15 type I, and 10 antrum adenocarcinoma.
  • Samples of the tumor, the surrounding area, and the gastric corpus and antrum were analyzed histologically, and immunostained for cytokeratins (CK)7/20 (staining positive for cells labeled > or = 50%).
  • (1) 13 of 37 (35%) had intestinal metaplasia (IM) in the stomach;.
  • (5) 100% showed the same CK immunoprofile, both in IM and adenocarcinoma (measure of agreement k = 1, p = 0.000).
  • (2) 100% gastric samples devoid of both IM and HP infection.
  • One hundred percent of antrum adenocarcinomas showed a no Barrett's type CK profile, both in the tumor and in the IM of the entire stomach.
  • CONCLUSIONS: Data suggest that type II adenocarcinoma cannot be always considered a gastroesophageal reflux disease-related tumor; other pathogenetic pathways should be taken into consideration.
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Stomach / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Barrett Esophagus / pathology. Cardia / pathology. Esophagogastric Junction / pathology. Female. Gastric Mucosa / pathology. Humans. Immunohistochemistry. Keratin-20 / analysis. Keratin-7 / analysis. Male. Middle Aged. Pyloric Antrum / pathology


43. Ye BD, Kim SG, Park JH, Kim JS, Jung HC, Song IS: The interleukin-8-251 A allele is associated with increased risk of noncardia gastric adenocarcinoma in Helicobacter pylori-infected Koreans. J Clin Gastroenterol; 2009 Mar;43(3):233-9
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  • [Title] The interleukin-8-251 A allele is associated with increased risk of noncardia gastric adenocarcinoma in Helicobacter pylori-infected Koreans.
  • BACKGROUND AND GOALS: Chronic inflammation associated with Helicobacter pylori infection is a risk factor of gastric adenocarcinoma.
  • Interleukin-8 (IL-8) plays an important role in gastric mucosal inflammation induced by H. pylori infection.
  • Recently, studies on the association of genetic polymorphisms of various proinflammatory cytokines with gastric carcinogenesis showed varying results on the basis of the ethnicity.
  • We conducted this study to investigate the association of IL-8-251 A/T polymorphism with gastric carcinogenesis in H. pylori-infected Koreans.
  • STUDY: The IL-8-251 A/T polymorphism was identified by polymerase chain reaction-restriction fragment length polymorphism using DNA from a total of 605 H. pylori-infected subjects; 206 controls, 149 chronic atrophic gastritis and/or intestinal metaplasia, 97 gastric dysplasia, and 153 gastric adenocarcinoma.
  • Degrees of gastric mucosal inflammation and mucosal IL-8 level were also assessed.
  • RESULTS: The IL-8-251 A carriers showed a higher risk of gastric adenocarcinoma (adjusted odds ratio 2.06, 95% confidence interval 1.16-3.68) than IL-8-251 T/T genotypes.
  • The IL-8-251 A allele was also significantly associated with the degree of neutrophil infiltration, atrophy, and intestinal metaplasia in a younger age group.
  • Among the chronic atrophic gastritis and/or intestinal metaplasia group, mucosal IL-8 level was significantly higher in subjects with IL-8-251 A allele than those with IL-8-251 T/T genotypes (P=0.011).
  • CONCLUSIONS: The IL-8-251 A allele is associated with higher IL-8 production, more severe inflammation, mucosal atrophy, and intestinal metaplasia than IL-8-251 T/T genotype in H. pylori-infected hosts.
  • The IL-8-251 A allele may also increase the risk of gastric adenocarcinoma through an enhanced inflammatory process in H. pylori-infected Koreans.
  • [MeSH-major] Adenocarcinoma / genetics. Asian Continental Ancestry Group / genetics. Gastric Mucosa / immunology. Gastric Mucosa / microbiology. Helicobacter Infections / complications. Helicobacter pylori. Interleukin-8 / genetics. Polymorphism, Restriction Fragment Length. Stomach Neoplasms / genetics
  • [MeSH-minor] Age Factors. Analysis of Variance. Female. Gastritis, Atrophic / microbiology. Gastritis, Atrophic / pathology. Gene Frequency. Genetic Predisposition to Disease. Genotype. Humans. Korea. Male. Metaplasia / microbiology. Metaplasia / pathology. Middle Aged. Odds Ratio. Polymerase Chain Reaction. Sex Factors

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  • (PMID = 18542040.001).
  • [ISSN] 1539-2031
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-8
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44. Zou XP, Zhang B, Zhang XQ, Chen M, Cao J, Liu WJ: Promoter hypermethylation of multiple genes in early gastric adenocarcinoma and precancerous lesions. Hum Pathol; 2009 Nov;40(11):1534-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter hypermethylation of multiple genes in early gastric adenocarcinoma and precancerous lesions.
  • Promoter hypermethylation is an alternative mechanism of gene silencing in human cancers including gastric cancer.
  • To date, several reports on methylation of various genes in gastric cancer have been published.
  • In this study, we determined the methylation frequency of 5 genes, including p16, Runx3, MGMT, DAPK, and RASSF1A, by methylation-specific polymerase chain reaction, in a series of formalin-fixed paraffin-embedded tissues including normal gastric mucosa (n = 20), intestinal metaplasia (n = 14), gastric epithelial dysplasia (n = 27), and early gastric adenocarcinoma (n = 16).
  • All 20 histologically normal gastric biopsy specimens were methylation-free for all 5 genes.
  • Aberrant hypermethylation of RASSF1A was not detected in any case from intestinal metaplasia to early gastric adenocarcinoma.
  • The methylation rate of the other 4 genes increased with the histological progression from intestinal metaplasia to gastric epithelial dysplasia, to early gastric adenocarcinoma.
  • Methylation was detected in 28.6% of intestinal metaplasia (4/14), in 77.8% of gastric epithelial dysplasia (21/27), and in 87.5% of early gastric adenocarcinoma (14/16).
  • The average number of methylated genes in intestinal metaplasia, gastric epithelial dysplasia, and early gastric adenocarcinoma was 0.43, 1.3, and 1.8, respectively.
  • Concurrent methylation in 3 or more genes was found in 7.1% of intestinal metaplasia, 11.1% of gastric epithelial dysplasia, and 31.3% of early gastric adenocarcinoma.
  • Our results suggest that promoter hypermethylation of the p16, Runx3, MGMT, and DAPK genes may play an important role in the pathogenesis of gastric precancerous lesions and early gastric adenocarcinoma.
  • Further studies are warranted to determine whether the presence of promoter hypermethylation in gastric precancerous lesions is associated with higher risk of subsequent cancer development and how to interrupt the malignant transition from intestinal metaplasia and gastric epithelial dysplasia to early gastric adenocarcinoma by developing some gene-targeting therapies that may reverse aberrant methylation.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / genetics. DNA Methylation / genetics. Precancerous Conditions / genetics. Promoter Regions, Genetic / genetics. Stomach Neoplasms / genetics

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  • (PMID = 19695681.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Biomarkers, Tumor; 0 / Core Binding Factor Alpha 3 Subunit; 0 / RASSF1 protein, human; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 6.5.1.- / DNA Repair Enzymes
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45. Siewert JR, Feith M, Stein HJ: Biologic and clinical variations of adenocarcinoma at the esophago-gastric junction: relevance of a topographic-anatomic subclassification. J Surg Oncol; 2005 Jun 1;90(3):139-46; discussion 146
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  • [Title] Biologic and clinical variations of adenocarcinoma at the esophago-gastric junction: relevance of a topographic-anatomic subclassification.
  • A topographic-anatomic subclassification of adenocarcinomas of the esophago-gastric junction (AEG) in distal esophageal adenocarcinoma (AEG Type I), true carcinoma of the cardia (AEG Type II), and subcardial gastric cancer (AEG Type III) was introduced in 1987 and is now increasingly accepted and used worldwide.
  • While underlying specialized intestinal metaplasia can be found in basically all patients with AEG Type I tumors, this is uncommon in Type II tumors and virtually absent in Type III tumors.
  • [MeSH-major] Adenocarcinoma / classification. Cardia. Esophageal Neoplasms / classification. Esophagogastric Junction. Stomach Neoplasms / classification
  • [MeSH-minor] Esophagectomy / methods. Esophagectomy / mortality. Female. Gastrectomy / methods. Gastrectomy / mortality. Humans. Intestinal Mucosa / pathology. Male. Metaplasia. Middle Aged. Survival Rate

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 15895452.001).
  • [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
  • [Number-of-references] 35
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46. Cunningham SC, Kamangar F, Kim MP, Hammoud S, Haque R, Iacobuzio-Donahue CA, Maitra A, Ashfaq R, Hustinx S, Heitmiller RE, Choti MA, Lillemoe KD, Cameron JL, Yeo CJ, Schulick RD, Montgomery E: Claudin-4, mitogen-activated protein kinase kinase 4, and stratifin are markers of gastric adenocarcinoma precursor lesions. Cancer Epidemiol Biomarkers Prev; 2006 Feb;15(2):281-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Claudin-4, mitogen-activated protein kinase kinase 4, and stratifin are markers of gastric adenocarcinoma precursor lesions.
  • Approximately 23,000 new gastric cancer cases and 12,000 associated deaths occur annually in the United States.
  • Intestinal metaplasia and gastric epithelial dysplasia are precursor lesions to gastric adenocarcinoma, but are not readily detectable clinically, radiographically, or endoscopically.
  • In search of such markers, tissue microarrays were prepared for 133 patients of resected gastric adenocarcinoma.
  • Tissue microarrays contained primary cancer, normal stomach, intestinal metaplasia, and gastric epithelial dysplasia and were probed with antibodies against nine potential markers that were either identified in a database of genes overexpressed in gastric adenocarcinoma or were already of interest to our laboratory: claudin-4, mitogen-activated protein kinase kinase 4 (MKK4), 14-3-3sigma (stratifin), S100A4, mesothelin, fascin, topoisomerase IIalpha, HER-2/neu, and epithelial growth factor receptor.
  • Three markers discriminated gastric adenocarcinoma precursor lesions from normal gastric mucosa.
  • Claudin-4 expression was present in 36 intestinal metaplasia lesions (100%) and 14 gastric epithelial dysplasia lesions (100%), but in only 16 normal stomach samples (15%).
  • MKK4 expression was present in 24 intestinal metaplasia lesions (89%) and 12 gastric epithelial dysplasia lesions (100%), but in only 6 normal stomach samples (8%).
  • Stratifin expression was present in 29 intestinal metaplasia lesions (97%) and 8 gastric epithelial dysplasia lesions (100%), but in only 2 normal stomach samples (3%).
  • Sensitivity and specificity for detection of the precursor lesion intestinal metaplasia were 100% and 85%, respectively, for claudin-4; 89% and 92%, respectively, for MKK4; and 97% and 97%, respectively, for stratifin.
  • In conclusion, claudin-4, MKK4, and stratifin immunolabeling detects precursor lesions of gastric adenocarcinoma that are otherwise clinically, radiographically, and endoscopically inapparent.
  • These findings may prove useful in the diagnosis and therapeutic targeting of gastric adenocarcinoma precursor lesions.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / biosynthesis. Exonucleases / biosynthesis. MAP Kinase Kinase 4 / biosynthesis. Membrane Proteins / biosynthesis. Neoplasm Proteins / biosynthesis. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism
  • [MeSH-minor] 14-3-3 Proteins. Aged. Claudin-4. Exoribonucleases. Female. Gene Expression. Humans. Immunohistochemistry. Male. Metaplasia / pathology. Microarray Analysis. Tissue Array Analysis


47. 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.
  • However, they were associated with a wide variety of complications, including intractable dysphagia, prosthesis migration and erosion into the stomach, and a significant proportion had to be removed.
  • 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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48. Sampliner RE, Camargo E, Prasad AR: Association of ablation of Barrett's esophagus with high grade dysplasia and adenocarcinoma of the gastric cardia. Dis Esophagus; 2006;19(4):277-9
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  • [Title] Association of ablation of Barrett's esophagus with high grade dysplasia and adenocarcinoma of the gastric cardia.
  • Three cases are reported in which the patient developed adenocarcinoma of the gastric cardia after thermal ablation of HGD.
  • A definition of BE including endoscopic abnormality and intestinal metaplasia by biopsy was used.
  • Biopsies documented adenocarcinoma of the gastric cardia.
  • The development of adenocarcinoma of the cardia is unexpected.

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  • (PMID = 16866860.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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49. Randjelovic T, Filipovic B, Babic D, Cemerikic V, Filipovic B: Carcinosarcoma of the stomach: a case report and review of the literature. World J Gastroenterol; 2007 Nov 7;13(41):5533-6
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  • [Title] Carcinosarcoma of the stomach: a case report and review of the literature.
  • We report the case of a 62-year-old man with gastric carcinosarcoma, along with its clinical, macroscopic and histopathological features.
  • Macroscopically, a specimen of deformed stomach was obtained that measured 200 mm x 150 mm x 100 mm.
  • Histopathologically, a mixed type of malignancy was revealed: an adenocarcinoma with intestinal metaplasia, with interposed fascicles of fusiform atypical cells and numerous large, rounded and oval cells.
  • [MeSH-major] Adenocarcinoma / secondary. Carcinosarcoma / secondary. Liver Neoplasms / secondary. Stomach Neoplasms / pathology
  • [MeSH-minor] Anastomosis, Roux-en-Y. Carcinoembryonic Antigen / analysis. Cell Differentiation. Chromogranin A / analysis. Esophagostomy. Fatal Outcome. Gastrectomy. Humans. Jejunostomy. Keratin-18 / analysis. Male. Metaplasia. Middle Aged. Mucin-1 / analysis. Vimentin / analysis

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  • (PMID = 17907304.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen; 0 / Chromogranin A; 0 / KRT18 protein, human; 0 / Keratin-18; 0 / Mucin-1; 0 / Vimentin
  • [Number-of-references] 15
  • [Other-IDs] NLM/ PMC4171295
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50. Popnikolov NK, Gatalica Z, Adegboyega PA, Norris BA, Pasricha PJ: Downregulation of TNF-related apoptosis-inducing ligand (TRAIL)/Apo2L in Barrett's esophagus with dysplasia and adenocarcinoma. Appl Immunohistochem Mol Morphol; 2006 Jun;14(2):161-5
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  • [Title] Downregulation of TNF-related apoptosis-inducing ligand (TRAIL)/Apo2L in Barrett's esophagus with dysplasia and adenocarcinoma.
  • The aim of this study was to compare TRAIL/Apo2L expression in normal gastroesophageal (GE) junction, Barrett's esophagus with and without dysplasia, and associated adenocarcinoma.
  • Immunohistochemical evaluation of TRAIL expression was performed on formalin-fixed paraffin-embedded sections from 29 GE junction/esophageal biopsies, 20 gastric biopsies, 6 esophagectomies, 2 small bowel resection specimens, and 5 colon biopsies.
  • TRAIL was expressed in the foveolar epithelium of the histologically normal GE junctional mucosa and stomach as well as in the normal intestinal epithelium, with maximal expression in the surface epithelium.
  • TRAIL was always detected in Barrett's metaplasia (21/21, 100%), and the overall expression was similar to that of the columnar portion of the normal GE junction (8/8, 100%).
  • TRAIL was rarely and weakly (1+) expressed in Barrett's esophagus with dysplasia (3/18, 16.7%) and adenocarcinoma (1/10, 10.0%) (P<0.001).
  • Similarities in the topographic pattern of TRAIL expression in the normal GE junction, stomach, small intestine, and colon suggest a common function of TRAIL throughout the gastrointestinal tract.

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  • (PMID = 16785783.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TNF-Related Apoptosis-Inducing Ligand
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51. Yap YL, So JB: Gastric adenocarcinoma occurring in a young patient with common variable immunodeficiency syndrome. Singapore Med J; 2009 Jun;50(6):e201-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gastric adenocarcinoma occurring in a young patient with common variable immunodeficiency syndrome.
  • Patients with common variable immunodeficiency syndrome (CVID) have an increased risk of gastric adenocarcinoma.
  • We describe a case of gastric adenocarcinoma in a 29-year-old man with CVID.
  • CVID is a predisposing factor for gastric adenocarcinoma.
  • Gastric complaints are common among these patients and should be viewed seriously.
  • Premalignant conditions like chronic atrophic gastritis, intestinal metaplasia and dysplasia require regular endoscopic surveillance in these high-risk patients.
  • [MeSH-major] Adenocarcinoma / complications. Adenocarcinoma / diagnosis. Common Variable Immunodeficiency / complications. Common Variable Immunodeficiency / diagnosis. Stomach Neoplasms / complications. Stomach Neoplasms / diagnosis
  • [MeSH-minor] Adult. Disease-Free Survival. Endoscopy. Humans. Male. Pyloric Stenosis / diagnosis. Tomography, X-Ray Computed / methods. Treatment Outcome

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  • (PMID = 19551296.001).
  • [ISSN] 0037-5675
  • [Journal-full-title] Singapore medical journal
  • [ISO-abbreviation] Singapore Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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52. Wijnhoven BP, Pignatelli M, Dinjens WN, Tilanus HW: Reduced p120ctn expression correlates with poor survival in patients with adenocarcinoma of the gastroesophageal junction. J Surg Oncol; 2005 Nov 1;92(2):116-23
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  • [Title] Reduced p120ctn expression correlates with poor survival in patients with adenocarcinoma of the gastroesophageal junction.
  • METHODS: Immunohistochemical staining for p120ctn was performed on 96 tumor samples, 20 cases of Barretts metaplasia and 13 lymph node metastases.
  • RESULTS: Loss of normal surface p120ctn expression was found in 4/20 (20%) Barretts metaplasia, in 65/96 (68%) tumors, and 11/13 (85%) lymph node metastases.
  • [MeSH-major] Adenocarcinoma / metabolism. Cell Adhesion Molecules / metabolism. Esophageal Neoplasms / metabolism. Esophagogastric Junction. Lymph Nodes / pathology. Phosphoproteins / metabolism. Stomach Neoplasms / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16231374.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Catenins; 0 / Cell Adhesion Molecules; 0 / Phosphoproteins; 0 / delta catenin
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53. Bîrla R, Iosif C, Gîndea C, Hoară P, Constantinoiu S: [Clinical diagnosis of adenocarcinoma of the esophago-gastric junction]. Chirurgia (Bucur); 2007 Sep-Oct;102(5):511-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical diagnosis of adenocarcinoma of the esophago-gastric junction].
  • The aim of the work paper is to present the diagnosis methods of the esophago-gastric junction adenocarcinoma, based on our experience and literature data.
  • The later reveal many novelties about diagnosis means in Barrett's esophagus (BE), the definition and classification of BE, as well as the progress of the endoscopical, immunohistochemical and molecular methods in surveillance of the dysplasia arising in BE and in detection of intraepithelial neoplasia.
  • Early esophago-gastric junction (EGJ) adenocarcinoma (AC) is asymptomatic and its detection may be possible only through endoscopical surveillance.
  • For this reason is necessary to use some more precise methods for identifying intestinal metaplasia on distal esophagus, in patients with gastro-esophageal reflux disease, as well as for risk stratification in patients with dysplasia and for detection of intraepithelial neoplasia.
  • Applying modern methods of immunohistochemical and molecular diagnosis on endoscopical biopsy or esophageal brushing samples, the diagnosis rate for BE, dysplasia and early AC is improved and using the imaging means permits to obtain preoperative TNM staging and tumoral type (Siewert), with implications in therapeutical management.
  • [MeSH-major] Adenocarcinoma / diagnosis. Esophageal Neoplasms / diagnosis. Esophagogastric Junction. Stomach Neoplasms / diagnosis
  • [MeSH-minor] Barrett Esophagus / complications. Barrett Esophagus / pathology. Diagnosis, Differential. Humans. Neoplasm Staging. Risk Factors

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  • (PMID = 18018349.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Romania
  • [Number-of-references] 47
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54. Bîrlă R, Losif C, Gîndea C, Hoară P, Constantinoiu S: [Treatment of the esophago-gastric junction adenocarcinoma]. Chirurgia (Bucur); 2008 Mar-Apr;103(2):143-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of the esophago-gastric junction adenocarcinoma].
  • The aim of the work paper is to present the treatment methods of the esophago-gastric junction adenocarcinoma, (AC) based on our experience and literature data.
  • The later reveal many novelties about AC prophylaxis through Barrett's esophagus (BE) treatment, using proton pomp inhibitors or antireflux surgical procedures, the progress of the endoluminal ablative methods for intestinal metaplasia, as well as a new surgical approach for advances tumors based on Siewert classification.
  • Surgical procedure selection at patients with resectable tumours should be based on the tendency of esophago-gastric junction adenocarcinomas to extend on longitudinal axis, at the submucosa level and the possibility of abdomino-mediastinal lymph nodes metastasis.
  • [MeSH-major] Adenocarcinoma / surgery. Esophageal Neoplasms / surgery. Esophagogastric Junction. Stomach Neoplasms / surgery

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  • (PMID = 18457092.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Romania
  • [Number-of-references] 43
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55. Zissis D, Zizi-Serbetzoglou A, Grammatoglou X, Glava C, Katsamagkou E, Nikolaidou ME, Vasilakaki T: Combined carcinoid and mixed (composite) glandular - endocrine cell carcinoma of the stomach in atrophic gastritis. J BUON; 2009 Jan-Mar;14(1):127-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined carcinoid and mixed (composite) glandular - endocrine cell carcinoma of the stomach in atrophic gastritis.
  • We describe a case of gastric carcinoid and inflammatory fibroid polyp concomitant with a composite tumor of the gastric antrum composed of poorly differentiated adenocarcinoma - endocrine carcinoma with immunohistochemical documentation of endocrine and non endocrine differentiation in a 67-year-old man with atrophic gastritis and intestinal metaplasia.
  • The same occurrence is reported in several cases in the literature, which suggests that the association of gastric carcinoid to adenocarcinoma could point to the malignant nature of carcinoid.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoid Tumor / pathology. Endocrine Gland Neoplasms / pathology. Gastritis, Atrophic / pathology. Polyps / pathology. Precancerous Conditions / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Aged. Cell Differentiation. Gastrectomy. Humans. Immunohistochemistry. Lymphatic Metastasis. Male. Metaplasia. Treatment Outcome

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  • (PMID = 19365883.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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56. Asthana N, Mandich D, Ligato S: Esophageal polypoid dysplasia of gastric foveolar phenotype with focal intramucosal carcinoma associated with Barrett's esophagus. Am J Surg Pathol; 2008 Oct;32(10):1581-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Esophageal polypoid dysplasia of gastric foveolar phenotype with focal intramucosal carcinoma associated with Barrett's esophagus.
  • We describe a rare case of esophageal polypoid dysplasia with gastric phenotype and focal intramucosal carcinoma associated with Barrett's esophagus.
  • Surgery was performed with resection of the distal esophagus and proximal stomach.
  • The histopathologic examination of this lesion revealed an exuberant polypoid gastric epithelium with areas of low-grade dysplasia, high-grade dysplasia, and focal intramucosal carcinoma.
  • A few residual foci of specialized intestinal metaplasia consistent with Barrett's esophagus without dysplasia were identified at the proximal and distal ends of the lesion.
  • Immunohistochemically, this lesion revealed a pattern of expression of apomucins (MUC5AC diffusely positive, MUC1 and MUC6 focally positive, and MUC2 negative) consistent with a gastric foveolar phenotype.
  • In our opinion, this case represents a precursor lesion of an extremely well-differentiated adenocarcinoma of gastric foveolar phenotype that has been previously documented in the stomach and in the duodenum and that now for the first time we report in the esophagus in association with Barrett's intestinal metaplasia.
  • [MeSH-major] Adenocarcinoma / pathology. Barrett Esophagus / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Cell Differentiation. Esophagoscopy. Humans. Immunohistochemistry. Male. Metaplasia. Mucous Membrane / pathology. Phenotype


57. Wang DC, Wang LD, Zheng S, Fan ZM, Li JL, Feng CW, Zhang YR, Liu B, Gao SS, He X: [The application of surface-enhanced laser desorption/ionization-time of flight-mass spectrometry in diagnosing dysplasia and chronic atrophic gastric-carditis in population with high risk of gastric-cardia adenocarcinoma]. Zhonghua Nei Ke Za Zhi; 2005 Aug;44(8):573-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The application of surface-enhanced laser desorption/ionization-time of flight-mass spectrometry in diagnosing dysplasia and chronic atrophic gastric-carditis in population with high risk of gastric-cardia adenocarcinoma].
  • OBJECTIVES: To evaluate the serum biomarkers for diagnosis of gastric cardia dysplasia (DYS) and chronic atrophic gastric-carditis (CAG) and to provide a novel screening method for high risk population of gastric-cardia adenocarcinoma (GCA).
  • A set of spectra derived from analysis of serum from 143 symptom-free subjects at high-risk area for GCA, including 63 cases with histologically normal gastric cardia epithelia, 57 of CAG and 23 of DYS, were analyzed by bioinformatics like decision tree classification algorithm.
  • CONCLUSIONS: The gastric cardia lesions of DYS and CAG could be identified by SELDI-TOF-MS technique specifically in symptom-free subjects at high incidence area for GCA.
  • [MeSH-major] Biomarkers, Tumor / blood. Cardia. Gastritis, Atrophic / diagnosis. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization / methods. Stomach Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Chronic Disease. Female. Humans. Male. Mass Screening / methods. Metaplasia / diagnosis. Middle Aged. Sensitivity and Specificity

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  • (PMID = 16194406.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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58. Cao X, Tsukamoto T, Nozaki K, Tanaka H, Cao L, Toyoda T, Takasu S, Ban H, Kumagai T, Tatematsu M: Severity of gastritis determines glandular stomach carcinogenesis in Helicobacter pylori-infected Mongolian gerbils. Cancer Sci; 2007 Apr;98(4):478-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Severity of gastritis determines glandular stomach carcinogenesis in Helicobacter pylori-infected Mongolian gerbils.
  • Helicobacter pylori (H. pylori) infection causes chronic gastritis and is also related to gastric carcinoma.
  • The respective incidences of glandular stomach adenocarcinomas were 65.0% (13/20), 20.0% (2/10), and 23.0% (3/13) (P<0.05).
  • Higher scores of infiltration of inflammatory cells, hyperplasia, intestinal metaplasia and mucosal bromodeoxyuridine (BrdU) labeling index in antrum and corpus mucosa, were seen in group A than B or C (P<0.05) and serum anti-H. pylori IgG titer and gastrin levels were also significantly higher, along with mRNA levels for mucosal interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS).
  • The results demonstrated the term and severity of H. pylori infection to play important roles in gastric carcinogenesis, with essential involvement of chronic inflammation, especially increased rates of cell proliferation, in H. pylori-associated carcinogenesis.
  • [MeSH-major] Adenocarcinoma / microbiology. Gastric Mucosa / microbiology. Gastritis / complications. Helicobacter Infections / complications. Helicobacter pylori. Stomach Neoplasms / microbiology

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  • (PMID = 17284248.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha
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59. Callacondo D, Ganoza-Salas A, Anicama-Lima W, Quispe-Mauricio A, Longacre TA: Primary squamous cell carcinoma of the stomach with paraneoplastic leukocytosis: a case report and review of literature. Hum Pathol; 2009 Oct;40(10):1494-8
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  • [Title] Primary squamous cell carcinoma of the stomach with paraneoplastic leukocytosis: a case report and review of literature.
  • Apparently pure, primary squamous cell carcinoma of the stomach is exceedingly rare.
  • Here, we describe a case of primary squamous cell carcinoma arising in the gastric antrum of an 83-year-old man with persistent leukocytosis, which resolved on resection of the tumor.
  • No foci of squamous metaplasia or gland-forming elements were identified in the resection specimen, although there was marked chronic gastritis with intestinal metaplasia.
  • This case suggests that gastric squamous cell carcinoma likely arises in the setting of long-standing, chronic inflammation, and like squamous cell carcinoma in other organ systems, may be associated with paraneoplastic leukocytosis.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Leukocytosis / pathology. Paraneoplastic Syndromes / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Aged, 80 and over. Diabetes Mellitus, Type 2 / complications. Humans. Hypertension / complications. Immunohistochemistry. In Situ Hybridization. Male. Neoplasms, Multiple Primary / pathology. Prostatic Neoplasms / pathology

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  • [ErratumIn] Hum Pathol. 2010 Feb;41(2):307. Callacondo-Riva, David [corrected to Callacondo, David]
  • (PMID = 19467693.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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60. Takubo K, Vieth M, Aida J, Sawabe M, Kumagai Y, Hoshihara Y, Arai T: Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia. Digestion; 2009;80(4):248-57
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  • [Title] Differences in the definitions used for esophageal and gastric diseases in different countries: endoscopic definition of the esophagogastric junction, the precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus, and histologic criteria for mucosal adenocarcinoma or high-grade dysplasia.
  • METHODS: Here we discuss four such important differences: the definition of the esophagogastric junction (EGJ), the possible precursor of Barrett's adenocarcinoma, the definition of Barrett's esophagus (BE), and the histologic criteria for mucosal adenocarcinoma.
  • If an area of columnar-lined esophagus (CLE) is only partially involved by intestinal metaplasia, then the latter cannot always be demonstrated in biopsy specimens.
  • Therefore, we do not think that a definition of BE as CLE with histologic intestinal metaplasia is practical.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Esophageal Neoplasms / diagnosis. Gastroenterology / standards. Precancerous Conditions / diagnosis. Terminology as Topic
  • [MeSH-minor] Esophagogastric Junction / pathology. Esophagoscopy. Gastroscopy. Humans. Stomach Neoplasms / diagnosis

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  • [Copyright] 2009 S. Karger AG, Basel.
  • (PMID = 19828957.001).
  • [ISSN] 1421-9867
  • [Journal-full-title] Digestion
  • [ISO-abbreviation] Digestion
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 59
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61. Gomes LI, Esteves GH, Carvalho AF, Cristo EB, Hirata R Jr, Martins WK, Marques SM, Camargo LP, Brentani H, Pelosof A, Zitron C, Sallum RA, Montagnini A, Soares FA, Neves EJ, Reis LF: Expression profile of malignant and nonmalignant lesions of esophagus and stomach: differential activity of functional modules related to inflammation and lipid metabolism. Cancer Res; 2005 Aug 15;65(16):7127-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profile of malignant and nonmalignant lesions of esophagus and stomach: differential activity of functional modules related to inflammation and lipid metabolism.
  • Adenocarcinomas of stomach and esophagus are frequently associated with preceding inflammatory alterations of the normal mucosa.
  • Whereas intestinal metaplasia of the gastric mucosa is associated with higher risk of malignization, Barrett's disease is a risk factor for adenocarcinoma of the esophagus.
  • Barrett's disease is characterized by the substitution of the squamous mucosa of the esophagus by a columnar tissue classified histopathologically as intestinal metaplasia.
  • Using cDNA microarrays, we determined the expression profile of normal gastric and esophageal mucosa as well as intestinal metaplasia and adenocarcinomas from both organs.
  • Data were explored to define functional alterations related to the transformation from squamous to columnar epithelium and the malignant transformation from intestinal metaplasia to adenocarcinomas.
  • Based on their expression profile, adenocarcinomas of the esophagus showed stronger correlation with intestinal metaplasia of the stomach than with Barrett's mucosa.
  • Whereas the lipid metabolism module is active in samples representing intestinal metaplasia and inactive in adenocarcinomas, the cytokine module is inactive in samples representing normal esophagus and esophagitis.
  • Exploitation of the data presented herein will help in the precise molecular characterization of adenocarcinoma from the distal esophagus, avoiding the topographical and descriptive classification that is currently adopted, and help with the proper management of patients with Barrett's disease.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Esophageal Neoplasms / genetics. Esophageal Neoplasms / metabolism. Lipid Metabolism. Stomach Neoplasms / genetics. Stomach Neoplasms / metabolism

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  • (PMID = 16103062.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
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62. Otabor IA, Abdessalam SF, Erdman SH, Hammond S, Besner GE: Gastric outlet obstruction due to adenocarcinoma in a patient with Ataxia-Telangiectasia syndrome: a case report and review of the literature. World J Surg Oncol; 2009;7:29
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  • [Title] Gastric outlet obstruction due to adenocarcinoma in a patient with Ataxia-Telangiectasia syndrome: a case report and review of the literature.
  • Clinical and radiographic evaluation for malignancy in ataxia-telangiectasia patients is usually atypical, leading to delays in diagnosis.
  • CASE PRESENTATION: We report the case of a 20 year old ataxia-telangiectasia patient with gastric adenocarcinoma that presented as complete gastric outlet obstruction.
  • CONCLUSION: A literature search of adenocarcinoma associated with ataxia-telangiectasia revealed 6 cases.
  • Although there was no correlation between immunoglobulin levels and development of gastric adenocarcinoma, the presence of chronic gastritis and intestinal metaplasia seem to lead to the development of gastric adenocarcinoma.
  • One should consider adenocarcinoma in any patient with ataxia-telangiectasia who presents with non-specific gastrointestinal complaints, since this can lead to earlier diagnosis.
  • [MeSH-major] Adenocarcinoma / complications. Ataxia Telangiectasia / complications. Gastric Outlet Obstruction / etiology. Stomach Neoplasms / complications

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  • (PMID = 19284625.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 18
  • [Other-IDs] NLM/ PMC2662841
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63. Lisovsky M, Dresser K, Baker S, Fisher A, Woda B, Banner B, Lauwers GY: Cell polarity protein Lgl2 is lost or aberrantly localized in gastric dysplasia and adenocarcinoma: an immunohistochemical study. Mod Pathol; 2009 Jul;22(7):977-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell polarity protein Lgl2 is lost or aberrantly localized in gastric dysplasia and adenocarcinoma: an immunohistochemical study.
  • The diagnosis of gastric epithelial dysplasia, a precursor lesion of gastric adenocarcinoma, is hindered by interobserver variability and by its resemblance to regenerative changes.
  • Loss of cell polarity, a histological feature of gastric epithelial dysplasia, may be difficult to ascertain, especially in the setting of inflammation or injury.
  • A biomarker of cell polarity could be useful in diagnosis of dysplasia, but has not been reported.
  • Two homologs, lgl1 and lgl2, are present in mammals and lgl2 mRNA is highly expressed in the stomach.
  • The goal of our study was to test the hypothesis that Lgl2 protein expression and/or localization are disrupted in gastric epithelial dysplasia and adenocarcinoma.
  • Routinely processed pathology specimens including 94 benign mucosae of digestive organs, in addition to 36 reactive gastropathy, 57 gastric epithelial dysplasia, and 77 gastric adenocarcinomas, were immunostained for Lgl2 protein.
  • All normal, reactive, and chronically inflamed gastric epithelia showed basolateral Lgl2 staining.
  • Normal esophageal, duodenal, colonic, biliary, and pancreatic duct mucosae, as well as gastric intestinal metaplasia, did not express Lgl2.
  • All but one case each of gastric epithelial dysplasia and adenocarcinoma showed either complete loss of anti-Lgl2 immunoreactivity or diffuse, mostly weak, cytoplasmic staining.
  • Our data suggest that Lgl2 expression is either aberrantly localized or lost in gastric epithelial dysplasia and adenocarcinoma, whereas it is maintained in reactive gastric mucosa.
  • We propose that Lgl2 may be a potential marker to rule out gastric epithelial dysplasia and adenocarcinoma in diagnostic specimens.
  • However, the consistently negative anti-Lgl2 immunoreactivity seen in intestinal metaplasia does not allow differentiation of dysplasia from intestinal metaplasia with reactive change.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Cytoskeletal Proteins / metabolism. Gastric Mucosa / metabolism. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism

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  • (PMID = 19407852.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytoskeletal Proteins; 0 / Hugl-2 protein, human
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64. Lord RV, Brabender J, Wickramasinghe K, DeMeester SR, Holscher A, Schneider PM, Danenberg PV, DeMeester TR: Increased CDX2 and decreased PITX1 homeobox gene expression in Barrett's esophagus and Barrett's-associated adenocarcinoma. Surgery; 2005 Nov;138(5):924-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased CDX2 and decreased PITX1 homeobox gene expression in Barrett's esophagus and Barrett's-associated adenocarcinoma.
  • Forced expression of Cdx2 alone in the murine stomach results in gastric intestinal metaplasia (IM).
  • METHODS: CDX2 and PITX1 messenger RNA (mRNA) expression levels, relative to the control gene beta-actin, were measured by reverse transcription-polymerase chain reaction in specimens of Barrett's IM (n = 21), dysplasia (n = 18), adenocarcinoma (n = 20), and matching normal squamous esophagus tissues (n = 39) collected from 19 patients with Barrett's esophagus and 20 patients with esophageal adenocarcinoma.
  • CDX2 protein expression was assessed by immunohistochemistry in specimens of normal squamous esophagus (n = 13), IM (n = 10), dysplasia (n = 8,) and adenocarcinoma (n = 5).
  • There was no significant difference between the mRNA expression levels in Barrett's esophagus and adenocarcinoma.
  • There was no CDX2 protein expression in normal squamous esophagus, but moderate to strong protein expression was seen in all Barrett's tissues and in a majority of the dysplasia and adenocarcinoma cells.
  • CONCLUSIONS: CDX2 mRNA and CDX2 protein expression are upregulated in Barrett's IM tissues, compared with normal squamous esophagus, and remain elevated in dysplasia and adenocarcinoma tissues.
  • These descriptive findings suggest a possible role for these genes in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
  • [MeSH-major] Adenocarcinoma / genetics. Barrett Esophagus / genetics. Esophageal Neoplasms / genetics. Homeodomain Proteins / genetics. Paired Box Transcription Factors / genetics

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  • (PMID = 16291394.001).
  • [ISSN] 0039-6060
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Paired Box Transcription Factors; 0 / RNA, Messenger; 0 / homeobox protein PITX1
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65. Kacar F, Meteoğlu I, Yasa H, Levi E: Helicobacter pylori-induced changes in the gastric mucosa are associated with mitogen-activated protein kinase (MAPK) activation. Appl Immunohistochem Mol Morphol; 2007 Jun;15(2):224-8
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  • [Title] Helicobacter pylori-induced changes in the gastric mucosa are associated with mitogen-activated protein kinase (MAPK) activation.
  • BACKGROUND: Gastric cancers are usually associated with and preceded by Helicobacter pylori (HP) infection, gastric atrophy, intestinal metaplasia, and dysplasia.
  • HP infection alters cell kinetics of the gastric mucosa.
  • In this study, we investigated the effects of HP infection on gastric mucosal proliferation, apoptotic mechanisms, and the activation status of the MAPK signaling pathway at various stages of gastric carcinogenesis, especially intestinal metaplasia and dysplasia caused by HP infection.
  • DESIGN: Stomach biopsies representing normal (n=20), HP+ (n=25), HP+ with intestinal metaplasia (n=25), HP+ with dysplasia (n=15) and gastric adenocarcinoma (n=30; 20 HP+ and 10 HP-) cases were selected.
  • RESULTS: Proliferation index (proliferating cell nuclear antigen) and cleaved caspase-3 expression were higher in the HP+, HP+ with intestinal metaplasia, and HP+ with dysplasia groups than in normal controls (P<0.05).
  • Phospho-MAPK(ERK) expression was increased in the HP+, HP+ with intestinal metaplasia, HP+ with dysplasia and adenocarcinomas compared with the normal control group.
  • Whereas HP- gastric carcinomas had a lower expression of phospho-MAPK.
  • CONCLUSIONS: HP infection increases the proliferative rate of gastric foveolar cells in conjunction with an increased apoptotic rate and activation of MAPK(ERK).

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  • (PMID = 17525639.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3
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66. Oue N, Mitani Y, Aung PP, Sakakura C, Takeshima Y, Kaneko M, Noguchi T, Nakayama H, Yasui W: Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma. J Pathol; 2005 Oct;207(2):185-98
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  • [Title] Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma.
  • In the stomach, foveolar epithelium was negative for Reg IV, whereas goblet cells of intestinal metaplasia and neuroendocrine cells at the base of intestinal metaplasia expressed Reg IV.
  • Among 143 gastric adenocarcinomas, Reg IV expression was detected in 42 (29.4%) and was associated with both the intestinal mucin phenotype and neuroendocrine differentiation.
  • These data suggest that Reg IV is expressed by gastrointestinal and pancreatic tumours, including adenocarcinomas and carcinoid tumours, and that Reg IV is associated with intestinal and neuroendocrine differentiation of the stomach and gastric carcinoma.
  • [MeSH-major] Adenocarcinoma / chemistry. Lectins, C-Type / analysis. Neoplasm Proteins / analysis. Stomach Neoplasms / chemistry
  • [MeSH-minor] Adenoma / chemistry. Biomarkers, Tumor / analysis. Blotting, Western / methods. Breast Neoplasms / chemistry. Carcinoid Tumor / chemistry. Cell Differentiation / physiology. Cell Line, Tumor. Colon / metabolism. Colorectal Neoplasms / chemistry. Female. Humans. Immunohistochemistry / methods. Intestine, Small / metabolism. Lung Neoplasms / chemistry. Pancreas / metabolism. Pancreatic Neoplasms / chemistry. Phenotype. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Stomach / metabolism

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  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16086444.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Neoplasm Proteins; 0 / REG4 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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67. Kim CG, Choi IJ, Lee JY, Cho SJ, Nam BH, Kook MC, Hong EK, Kim YW: Biopsy site for detecting Helicobacter pylori infection in patients with gastric cancer. J Gastroenterol Hepatol; 2009 Mar;24(3):469-74
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  • [Title] Biopsy site for detecting Helicobacter pylori infection in patients with gastric cancer.
  • BACKGROUND: Helicobacter pylori eradication is recommended in post-gastric cancer resection, but premalignant changes may prevent the detection of H. pylori.
  • The aim of this study was to determine appropriate biopsy site for detecting H. pylori in gastric cancer patients.
  • MATERIALS AND METHODS: Consecutive patients (194) with gastric adenocarcinoma were prospectively enrolled.
  • Sensitivities of histology decreased in correlation with increasing severity of atrophy and intestinal metaplasia (both P < 0.001 using the chi-square test for trend).
  • The proportions of moderate to marked atrophy/intestinal metaplasia at UBGC (12.8%/14.7%) were significantly lower than those at antrum (50.0%/57.8%, P < 0.001 respectively) or UBLC (40.0%/48.9%, P < 0.001 respectively).
  • CONCLUSIONS: The UBGC side is the most sensitive and specific biopsy site to detect H. pylori in gastric cancer patients due to less frequent atrophy and intestinal metaplasia than at the antrum or UBLC side.
  • [MeSH-major] Adenocarcinoma / microbiology. Biopsy / methods. Gastroscopy. Helicobacter Infections / diagnosis. Helicobacter pylori / isolation & purification. Stomach / microbiology. Stomach Neoplasms / microbiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Bacterial / blood. Atrophy. Breath Tests. Female. Humans. Male. Metaplasia. Middle Aged. Predictive Value of Tests. Prospective Studies. Sensitivity and Specificity. Urease / analysis

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  • (PMID = 19067779.001).
  • [ISSN] 1440-1746
  • [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 / Antibodies, Bacterial; EC 3.5.1.5 / Urease
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68. Genta RM, Pusztaszeri M: The gastric mucosa in gastric cancer patients in a low-incidence area. Eur J Gastroenterol Hepatol; 2006 Oct;18(10):1085-93
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  • [Title] The gastric mucosa in gastric cancer patients in a low-incidence area.
  • BACKGROUND AND AIMS: Atrophic gastritis, intestinal metaplasia, and pyloric metaplasia are frequent precursors of noncardial intestinal-type gastric adenocarcinoma in populations in which both gastric cancer and Helicobacter pylori infection are common.
  • We hypothesized that such lesions would be less prevalent in European gastric cancer patients.
  • METHODS: Slides from patients who underwent gastrectomy for adenocarcinoma between 1997 and 2004 were reviewed.
  • Tumors were categorized as intestinal or diffuse; non-neoplastic mucosa was evaluated for gastritis, atrophy, intestinal metaplasia and pyloric metaplasia.
  • Nineteen patients (23.4%) had a normal stomach; 30% of T1 tumors and 90% of T4s arose in a normal stomach (P<0.02). H. pylori gastritis was found in 47 patients (58%); they did not differ in age, sex, national origin, cancer location or type from those without gastritis.
  • Intestinal metaplasia correlated with H. pylori gastritis (P=0.002).
  • Pyloric metaplasia was infrequent and limited to rare microfoci.
  • CONCLUSIONS: A quarter of the patients had a normal stomach, and pyloric metaplasia was distinctly uncommon.
  • Approaches to prevention and early detection of gastric cancer based on bioptic or serological demonstration of atrophy and metaplasia could overlook at least 25% of the people at risk in certain populations and may need to be adapted to local conditions.
  • [MeSH-major] Gastric Mucosa / pathology. Precancerous Conditions / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Aged. Aged, 80 and over. Female. Gastrectomy. Gastritis, Atrophic / pathology. Humans. Male. Metaplasia / pathology. Middle Aged. Neoplasm Staging. Pyloric Antrum / pathology. Specimen Handling / methods

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  • (PMID = 16957515.001).
  • [ISSN] 0954-691X
  • [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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69. Chebib I, Beck PL, Church NG, Medlicott SA: Gastric pouch adenocarcinoma and tubular adenoma of the pylorus: a field effect of dysplasia following bariatric surgery. Obes Surg; 2007 Jun;17(6):843-6
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  • [Title] Gastric pouch adenocarcinoma and tubular adenoma of the pylorus: a field effect of dysplasia following bariatric surgery.
  • There are reports of gastric carcinoma following bariatric surgery, but it is unclear if these procedures predispose to malignancy.
  • Endoscopy revealed a large tumor of the gastric pouch.
  • Histology confirmed an intestinal type of gastric adenocarcinoma arising in a background of H. pylori-negative gastritis with atrophy, foveolar hyperplasia and intestinal metaplasia.
  • The pathogenesis of gastric pouch carcinoma is discussed.
  • [MeSH-major] Adenocarcinoma / etiology. Adenoma / etiology. Gastroplasty. Postoperative Complications. Stomach Neoplasms / etiology

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  • [ErratumIn] Obes Surg. 2007 Jul;17(7):996
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  • (PMID = 17879590.001).
  • [ISSN] 0960-8923
  • [Journal-full-title] Obesity surgery
  • [ISO-abbreviation] Obes Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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70. Yu M, Zheng H, Tsuneyama K, Takahashi H, Nomoto K, Xu H, Takano Y: Paradoxical expression of maspin in gastric carcinomas: correlation with carcinogenesis and progression. Hum Pathol; 2007 Aug;38(8):1248-55
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  • [Title] Paradoxical expression of maspin in gastric carcinomas: correlation with carcinogenesis and progression.
  • To clarify the role of maspin in the genesis and progression of gastric carcinomas, its expression pattern and level were studied by immunohistochemistry on tissue microarrays containing gastric carcinoma (n = 237), normal gastric mucosa (n = 23), intestinal metaplasia (n = 38), and adenoma (n = 42); and the findings were compared with clinicopathological parameters.
  • Furthermore, maspin expression in the gastric carcinoma cell lines (HCG-27, MKN28, and MKN45) was examined by immunohistochemistry and Western blotting.
  • We found that cytoplasmic and nuclear maspin expression paralleled each other (P < .05) and decreased from intestinal metaplasia, adenoma, and carcinoma to normal gastric mucosa (P < .05).
  • Univariate and multivariate analyses indicated that expression of maspin correlated negatively with cumulative patient survival in gastric carcinoma (P < .05) but was not an independent factor in the prognosis.
  • Our study indicated that maspin expression experiences upregulation in gastric precancerous lesions and then slight downregulation with malignant transformation.
  • High expression may paradoxically promote invasion and metastasis of gastric carcinomas and could be considered a good marker for the pathobiological behaviors of gastric carcinomas.
  • [MeSH-major] Adenocarcinoma / secondary. Adenoma / pathology. Biomarkers, Tumor / metabolism. Precancerous Conditions / pathology. Serpins / metabolism. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cytoplasm / metabolism. Cytoplasm / pathology. Disease Progression. Female. Fluorescent Antibody Technique, Direct. Humans. Lymph Nodes / pathology. Male. Metaplasia. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. Stomach / metabolism. Stomach / pathology. Survival Rate. Tissue Array Analysis

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  • (PMID = 17490717.001).
  • [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 / Biomarkers, Tumor; 0 / SERPIN-B5; 0 / Serpins
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71. Ringhofer C, Lenglinger J, Izay B, Kolarik K, Zacherl J, Eisler M, Wrba F, Chandrasoma PT, Cosentini EP, Prager G, Riegler M: Histopathology of the endoscopic esophagogastric junction in patients with gastroesophageal reflux disease. Wien Klin Wochenschr; 2008;120(11-12):350-9
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  • BACKGROUND: Discrepancy exists between the endoscopic (rugal folds) and the histopathologic (oxyntic mucosa) definition of proximal stomach.
  • All 19 patients with intestinal metaplasia (18.6%) were identified from 4-quadrant biopsies obtained at the squamocolumnar junction and at 0.5 cm distal from it.
  • Persons with intestinal metaplasia were significantly older, had increased frequency of endoscopic hiatal hernia, higher Hill grade and presence of endoscopic CLE (P < 0.05); no significant difference was observed regarding sex, endoscopic esophagitis or length of endoscopic and histopathologic CLE (P > 0.05).
  • The squamocolumnar junction harbors the highest yield of intestinal metaplasia.
  • [MeSH-major] Endoscopy, Digestive System. Esophagogastric Junction / pathology. Gastroesophageal Reflux / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Adolescent. Adult. Aged. Aged, 80 and over. Barrett Esophagus / diagnosis. Barrett Esophagus / pathology. Biopsy. Esophageal Neoplasms / diagnosis. Esophageal Neoplasms / pathology. Female. Gastric Mucosa / pathology. Hernia, Hiatal / diagnosis. Hernia, Hiatal / pathology. Humans. Male. Metaplasia. Middle Aged. Precancerous Conditions / diagnosis. Precancerous Conditions / pathology. Prospective Studies. Risk Factors

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  • (PMID = 18709523.001).
  • [ISSN] 0043-5325
  • [Journal-full-title] Wiener klinische Wochenschrift
  • [ISO-abbreviation] Wien. Klin. Wochenschr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
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72. Zavros Y, Eaton KA, Kang W, Rathinavelu S, Katukuri V, Kao JY, Samuelson LC, Merchant JL: Chronic gastritis in the hypochlorhydric gastrin-deficient mouse progresses to adenocarcinoma. Oncogene; 2005 Mar 31;24(14):2354-66
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  • [Title] Chronic gastritis in the hypochlorhydric gastrin-deficient mouse progresses to adenocarcinoma.
  • The current study tests the hypothesis that chronic atrophic gastritis from hypochlorhydria in the gastrin-deficient mouse predisposes the stomach to gastric cancer.
  • Compared to the WT and SOM-/- mice, hypochlorhydric G-/- mice developed parietal cell atrophy, significant antral inflammation and intestinal metaplasia.
  • Areas of metaplasia within the G-/- mouse stomach showed decreased RUNX3 expression with elevated MUC2 and villin expression.
  • However, the cells isolated from WT, nontransformed G-/- and SOM-/- gastric tissue did not form colonies in soft agar.
  • Therefore, we show here that in the hypochlorhydric mouse stomach, the chronic gastritis, atrophy, metaplasia, dysplasia paradigm can be recapitulated in mice.
  • Moreover, neoplastic transformation of the antral gastric mucosa does not require gastrin.


73. Forones NM, Kawamura KY, Segreto HR, Artigiani Neto R, Focchi GR, Oshima CT: Expression of COX-2 in stomach carcinogenesis. J Gastrointest Cancer; 2008;39(1-4):4-10
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  • [Title] Expression of COX-2 in stomach carcinogenesis.
  • BACKGROUND: Gastric cancer is a frequent cause of cancer in Brazil.
  • The understanding of gastric carcinogenesis is not completely known but the progress of the molecular biology has provided that the initiation and progression of gastric cancer process is a consequence of a cumulative series of multiple gene alterations.
  • AIM: The aim of the study is to investigate the relationship among cytoplasmatic COX-1 and COX-2, Bcl-2 and nuclear P53 in chronic gastritis, metaplasia, and intestinal and gastric cancer.
  • PATIENTS AND METHODS: COX-1, COX-2, P53, and Bcl-2 were evaluated by immunohistochemistry in 34 gastric adenocarcinoma (GA) tissues obtained from gastric resection, 21 tissues of patients with chronic gastritis (CG), and 34 with intestinal metaplasia (IM) obtained from endoscopic biopsies.
  • P53 staining was expressed more frequently in gastric cancer when compared to CG (p = 0.05) or IM (p = 0.003).
  • The expression of Bcl-2 was also higher in gastric cancer (p = 0.002) and in intestinal metaplasia (p = 0.04) when compared to CG.
  • There were no difference between metaplasia and chronic gastritis for P53 or Bcl-2.
  • The immunoreactivity of COX-2 in gastric cancer was higher in the intestinal type (58%) than in diffuse type.
  • A higher expression of COX-2 was found in advanced gastric cancer (p = 0.019).
  • CONCLUSION: COX-2 is probably involved in gastric carcinogenesis, being an early alteration in cancer.
  • P53 and Bcl-2 was expressed mainly in gastric cancer, being probably a latest alteration in gastric development.
  • [MeSH-major] Cyclooxygenase 2 / analysis. Stomach Neoplasms / enzymology

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  • (PMID = 19107602.001).
  • [ISSN] 1941-6628
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS1 protein, human; EC 1.14.99.1 / PTGS2 protein, human
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74. de Vries AC, van Grieken NC, Looman CW, Casparie MK, de Vries E, Meijer GA, Kuipers EJ: Gastric cancer risk in patients with premalignant gastric lesions: a nationwide cohort study in the Netherlands. Gastroenterology; 2008 Apr;134(4):945-52
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  • [Title] Gastric cancer risk in patients with premalignant gastric lesions: a nationwide cohort study in the Netherlands.
  • BACKGROUND & AIMS: A cascade of precursor lesions (eg, atrophic gastritis, intestinal metaplasia, and dysplasia) precedes most gastric adenocarcinomas.
  • Quantification of gastric cancer risk in patients with premalignant gastric lesions is unclear, however.
  • METHODS: To analyze current surveillance practice and gastric cancer risk in patients with premalignant gastric lesions, all patients with a first diagnosis between 1991 and 2004 were identified in the Dutch nationwide histopathology registry (PALGA); follow-up data were evaluated until December 2005.
  • RESULTS: In total, 22,365 (24%) patients were diagnosed with atrophic gastritis, 61,707 (67%) with intestinal metaplasia, 7616 (8%) with mild-to-moderate dysplasia, and 562 (0.6%) with severe dysplasia.
  • Patients with a diagnosis of atrophic gastritis, intestinal metaplasia, or mild-to-moderate dysplasia received re-evaluation in 26%, 28%, and 38% of cases, respectively, compared with 61% after a diagnosis of severe dysplasia (P < .001).
  • The annual incidence of gastric cancer was 0.1% for patients with atrophic gastritis, 0.25% for intestinal metaplasia, 0.6% for mild-to-moderate dysplasia, and 6% for severe dysplasia within 5 years after diagnosis.
  • Risk factors for gastric cancer development were increasing severity of premalignant gastric lesions at initial diagnosis (eg, severe dysplasia, hazard ratio 40.14, 95% confidence interval 32.2-50.1), increased age (eg, 75-84 years, hazard ratio 3.75, 95% confidence interval 2.8-5.1), and male gender (hazard ratio 1.50, 95% CI 1.3-1.7).
  • CONCLUSIONS: Patients with premalignant gastric lesions are at considerable risk of gastric cancer.
  • [MeSH-major] Adenocarcinoma / epidemiology. Gastric Mucosa / pathology. Gastritis, Atrophic / pathology. Population Surveillance. Precancerous Conditions / epidemiology. Stomach Neoplasms / epidemiology
  • [MeSH-minor] Adult. Age Factors. Aged. Aged, 80 and over. Confidence Intervals. Disease Progression. Endoscopy, Gastrointestinal / methods. Female. Follow-Up Studies. Humans. Incidence. Male. Metaplasia / pathology. Middle Aged. Netherlands / epidemiology. Odds Ratio. Retrospective Studies. Risk Factors. Time Factors

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  • [CommentIn] Gastroenterology. 2009 Apr;136(4):1461-2; author reply 1462 [19245871.001]
  • (PMID = 18395075.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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75. Osaki M, Inoue T, Yamaguchi S, Inaba A, Tokuyasu N, Jeang KT, Oshimura M, Ito H: MAD1 (mitotic arrest deficiency 1) is a candidate for a tumor suppressor gene in human stomach. Virchows Arch; 2007 Oct;451(4):771-9
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  • [Title] MAD1 (mitotic arrest deficiency 1) is a candidate for a tumor suppressor gene in human stomach.
  • We previously confirmed that the level of MAD1 protein was decreased in gastric carcinoma compared with non-tumoral mucosa by conducting proteome-based analyses (Nishigaki R, Osaki M, Hiratsuka M, Toda T, Murakami K, Jeang KT, Ito H, Inoue T, Oshimura M, Proteomics 5:3205-3213, 29).
  • In this study, an immunohistochemical analysis was performed to examine MAD1 expression histologically in gastric mucosa and tumor.
  • MAD1 was detected in the supranuclear portion of normal epithelial, intestinal metaplasia, and adenoma cells, but its expression was not restricted to any specific area in carcinoma cells.
  • Exogenous expression of wild-type MAD1, but not the mutant MAD1, inhibited cell proliferation and resulted in G2/M accumulation in MKN-1, a gastric carcinoma cell line.
  • Taken together, our findings suggest that the MAD1 gene could be a candidate tumor suppressor gene and that down-regulation of MAD1 expression contribute to tumorigenesis in human stomach.
  • [MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. Cell Cycle Proteins / genetics. Genes, Tumor Suppressor. Nuclear Proteins / genetics. Stomach Neoplasms / genetics
  • [MeSH-minor] Cell Cycle. Cell Line, Tumor. Cell Proliferation. Down-Regulation / genetics. Epithelium / metabolism. Epithelium / pathology. Gastric Mucosa / metabolism. Gastric Mucosa / pathology. Gene Expression Regulation, Neoplastic. Humans

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  • (PMID = 17674037.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / MAD1L1 protein, human; 0 / Nuclear Proteins
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76. Younes M: What is the role of cytokeratins in Barrett/cardia differentiation? Arch Pathol Lab Med; 2005 Feb;129(2):181-2
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  • The importance of distinguishing between Barrett metaplasia and intestinal metaplasia of the gastric cardia is now accepted, and the management of each entity is quite different.
  • Patients with Barrett metaplasia are enrolled in surveillance programs, consisting of periodic endoscopy and biopsy, because of the known risk of developing adenocarcinoma of the esophagus.
  • Patients with intestinal metaplasia of the gastric cardia, however, are not currently enrolled in such programs, because this condition carries a low risk of developing adenocarcinoma of the gastric cardia.
  • They concluded that the Barrett CK7/CK20 pattern was a highly sensitive and specific marker for Barrett metaplasia.
  • However, because it may be associated with premalignant lesions elsewhere in the gastric mucosa, we propose that intestinal metaplasia of the gastric cardia may have the same clinical implication as Barrett metaplasia.
  • [MeSH-major] Barrett Esophagus / etiology. Cardia / pathology. Keratins / physiology. Metaplasia / etiology. Stomach Diseases / etiology

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  • (PMID = 15679416.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 68238-35-7 / Keratins
  • [Number-of-references] 16
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77. Tsuji T, Iwahashi M, Nakamori M, Ueda K, Ishida K, Naka T, Ojima T, Akamatsu H, Yamaue H: Multiple early gastric cancer with gastritis cystica profunda showing various histological types. Hepatogastroenterology; 2008 May-Jun;55(84):1150-2
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  • [Title] Multiple early gastric cancer with gastritis cystica profunda showing various histological types.
  • We report a case of multiple early gastric cancer showing varied histological types associated with gastritis cystica profunda (GCP).
  • A 61-year-old man who had early gastric cancer associated with GCP underwent a distal gastrectomy with lymphadenectomy.
  • Histological examination showed various histological types of cancer -well differentiated, moderately differentiated, poorly differentiated adenocarcinoma, mucinous adenocarcinoma and signet ring cell carcinoma- that had developed independently in the mucosal and submucosal layers of the resected specimen.
  • Helicobacter pylori was detected in the residual stomach 3 months after surgery.
  • Although the mechanism of the relationship between gastric carcinoma and GCPs is obscure, we speculate that repeated erosion and regeneration induced by chronic inflammation causes multicentric carcinogenesis as well as an aberration of the gastric glands.
  • GCPs may be a risk factor for multiple gastric cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Mucinous / pathology. Carcinoma, Signet Ring Cell / pathology. Cysts / pathology. Gastritis, Atrophic / pathology. Helicobacter Infections / pathology. Helicobacter pylori. Neoplasms, Multiple Primary / pathology. Precancerous Conditions / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Endosonography. Gastrectomy. Gastric Mucosa / pathology. Gastroscopy. Humans. Lymph Node Excision. Male. Metaplasia. Middle Aged. Stomach / pathology

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  • (PMID = 18705349.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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78. Song JH, Kim SG, Jung SA, Lee MK, Jung HC, Song IS: The interleukin-8-251 AA genotype is associated with angiogenesis in gastric carcinogenesis in Helicobacter pylori-infected Koreans. Cytokine; 2010 Aug;51(2):158-65
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  • [Title] The interleukin-8-251 AA genotype is associated with angiogenesis in gastric carcinogenesis in Helicobacter pylori-infected Koreans.
  • Helicobacter pylori (H. pylori) is an important risk factor of gastric adenocarcinoma.
  • Interleukin (IL)-8 is a potent angiogenic factor and plays an important role in inflammation of gastric mucosa by H. pylori.
  • Host susceptibility may help to predict H. pylori-infected individuals with a higher risk of gastric adenocarcinoma.
  • The aim of this study was to clarify the effect of IL-8 polymorphism on angiogenesis in the process of gastric carcinogenesis in H. pylori-infected Koreans.
  • The IL-8-251A/T polymorphism was genotyped by PCR-RFLP from a total of 395 subjects; 92 normal controls, 87 H. pylori-infected controls, 108 chronic atrophic gastritis and/or intestinal metaplasia and 108 adenocarcinoma.
  • The gastric mucosal concentrations of IL-8, membrane metalloproteinase (MMP)-9, angiopoietin (Ang)-1, and vascular endothelial growth factor (VEGF) were measured by ELISA.
  • In conclusion, IL-8-251 AA genotype may be associated with angiogenesis in gastric carcinogenesis in H. pylori-infected Koreans.
  • [MeSH-major] Adenocarcinoma / pathology. Helicobacter Infections / pathology. Helicobacter pylori. Interleukin-8 / genetics. Neovascularization, Pathologic / genetics. Polymorphism, Genetic. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Angiopoietin-1 / metabolism. Asian Continental Ancestry Group / genetics. Disease Progression. Female. Gastric Mucosa / metabolism. Gastritis, Atrophic / genetics. Genetic Predisposition to Disease. Humans. Korea. Male. Matrix Metalloproteinase 9 / metabolism. Metaplasia / pathology. Middle Aged. Vascular Endothelial Growth Factor A / metabolism

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20621718.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANGPT1 protein, human; 0 / Angiopoietin-1; 0 / Interleukin-8; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.35 / Matrix Metalloproteinase 9
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79. Jung JT, Lee CH, You SS, Ha HK, Bae JS, Kwon JG, Kim EY, Kim HG, Cho CH, Shin IH: [Grading of histology, expression of apoptosis and cell proliferation in gastric mucosa adjacent to gastric adenoma or adenocarcinoma]. Korean J Gastroenterol; 2005 Oct;46(4):269-75
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  • [Title] [Grading of histology, expression of apoptosis and cell proliferation in gastric mucosa adjacent to gastric adenoma or adenocarcinoma].
  • BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection can lead to gastric adenoma and carcinoma through atrophic gastritis and intestinal metaplasia.
  • Imbalance between apoptosis and proliferation may play a role in gastric carcinogenesis.
  • We tried to investigate H. pylori infection rate, grade of gastritis, environmental risk factors, expression rate of apoptosis and cell proliferation in mucosa adjacent to tumor, and we also tried to find significant factors associated with gastric carcinogenesis.
  • METHODS: Endoscopically diagnosed twenty cases of intestinal type gastric carcinoma, 20 cases of gastric adenoma, and 40 cases of control (normal or gastritis) were enrolled. H. pylori infection rate, histologic grading, apoptosis and immunohistochemical stain (Ki-67 and p53) to check mucosal proliferation were done in endoscopically biopsied tissues at antrum and body at least 2 cm apart from adenoma or carcinoma.
  • Intestinal metaplasia in antrum and alcohol drinking were significant risk factors for carcinoma compared to control group (OR 4.4 and 4.9 respectively).
  • CONCLUSIONS: Intestinal metaplasia in antrum and alcohol drinking are significant risk factors for gastric carcinoma.
  • Degree of mucosal proliferation and apoptosis in gastric mucosa adjacent to tumor are not significantly different in three groups.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Apoptosis. Cell Proliferation. Gastric Mucosa / pathology. Stomach Neoplasms / pathology

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  • (PMID = 16247270.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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80. Gologan A, Acquafondata M, Dhir R, Sepulveda AR: Polymeric immunoglobulin receptor-negative tumors represent a more aggressive type of adenocarcinomas of distal esophagus and gastroesophageal junction. Arch Pathol Lab Med; 2008 Aug;132(8):1295-301
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  • CONTEXT: Polymeric immunoglobulin receptor (PIgR) expression has been found in gastric mucosa and gastric cancers, but it is not known whether PIgR expression is related to background intestinal metaplasia nor the patterns of PIgR expression in tumors arising in the distal esophagus and gastroesophageal (GE) junction.
  • OBJECTIVES: To identify clinicopathologic features of tumors associated with PIgR expression and to determine whether PIgR expression is associated with intestinal differentiation of tumors and intestinal metaplasia in background mucosa in 3 groups of upper gastrointestinal adenocarcinomas.
  • These groups are (1) gastric adenocarcinomas, (2) adenocarcinomas of the distal esophagus and GE junction with background intestinal metaplasia, and (3) adenocarcinomas of the distal esophagus and GE junction without background intestinal metaplasia.
  • DESIGN: Expression of PIgR and CDX2 in nonneoplastic mucosa, intestinal metaplasia, and adenocarcinomas was examined by immunohistochemistry in 42 cases: 14 gastric and 28 from the distal esophagus and GE junction, including 13 with esophageal or GE junction intestinal metaplasia.
  • RESULTS: PIgR and CDX2 were expressed in all cases of intestinal metaplasia.
  • PIgR expression was positive in 40% of group 3 versus 77% of group 2 and 71% of gastric adenocarcinomas (P = .06), and the expression of CDX2 was similar in all tumor groups (80%-83%).
  • CONCLUSIONS: PIgR is uniformly expressed in intestinal metaplasia and in a subgroup of adenocarcinomas of the distal esophagus, GE junction, and stomach.
  • [MeSH-major] Adenocarcinoma / pathology. Esophageal Neoplasms / pathology. Esophagogastric Junction. Intestines / pathology. Receptors, Polymeric Immunoglobulin / analysis. Stomach Neoplasms / pathology
  • [MeSH-minor] Aged. Female. Homeodomain Proteins / analysis. Humans. Immunohistochemistry / methods. Lymphatic Metastasis. Male. Metaplasia. Middle Aged. Neoplasm Staging. Staining and Labeling

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  • (PMID = 18684029.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Receptors, Polymeric Immunoglobulin
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81. Wijetunge S, Ma Y, DeMeester S, Hagen J, DeMeester T, Chandrasoma P: Association of adenocarcinomas of the distal esophagus, "gastroesophageal junction," and "gastric cardia" with gastric pathology. Am J Surg Pathol; 2010 Oct;34(10):1521-7
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  • [Title] Association of adenocarcinomas of the distal esophagus, "gastroesophageal junction," and "gastric cardia" with gastric pathology.
  • Controversy exists as to whether adenocarcinomas occurring in the gastroesophageal junctional region and gastric cardia originate in the esophagus or the stomach.
  • Esophageal adenocarcinoma is known to be strongly associated with gastroesophageal reflux disease; gastric adenocarcinoma with Helicobacter pylori gastritis, and gastric intestinal metaplasia.
  • This study evaluates the association of these tumors with pathologic findings in the biopsies of the gastric body and the antrum.
  • It is hypothesized that if these malignancies are esophageal, they should have little or no significant association with gastric pathology; if they are gastric, these patients should have a high prevalence of gastric pathology.
  • Between 2004 and 2008, 234 patients were diagnosed with high-grade dysplasia (HGD) and/or adenocarcinoma; 107 were distal esophageal, 79 straddled the distal end of the tubular esophagus, and 48 were in the "gastric cardia."
  • Gastric biopsies were assessed for inflammation, H. pylori infection, and intestinal metaplasia.
  • During this period, 2146 patients had nonmalignant columnar epithelia in the esophagus with similar assessment of the stomach; these acted as a control group.
  • The gastric biopsy was normal in 201/234 (85.9%) patients and showed significant inflammation, H. pylori infection, and/or gastric intestinal metaplasia in 33/234 (14.1%) patients.
  • There was no gastritis, H. pylori infection, or intestinal metaplasia in 88/107 (82.2%) of the patients with distal esophageal HGD and/or adenocarcinoma, 70/79 (88.6%) with junctional HGD and/or adenocarcinoma, and 43/48 (85.9%) with "gastric cardiac" HGD and/or adenocarcinoma.
  • The incidence of gastritis was significantly higher in the patients with HGD and/or adenocarcinoma (33/234 or 14.1%) than in the control population (146/2146 or 9.0%; P=0.01).
  • This difference was largely the result of a higher incidence of gastritis in patients with HGD and/or adenocarcinoma in the distal third of the esophagus (19/107 or 17.8%) versus the control population (146/2146 or 9.0%; P=0.01).
  • The incidence of H. pylori positivity was also significantly higher in the patients with HGD and/or adenocarcinoma in the distal third of the esophagus (13/107 or 12.2%) than in the control population (117/2146 or 5.5%; P=0.01).
  • There was no significant difference between the control group and the patients with junctional and gastric cardiac HGD and/or adenocarcinoma for gastritis, H. pylori infection, or the gastric intestinal metaplasia.
  • The absence of gastritis, H. pylori, and the gastric intestinal metaplasia in 85.9% of the patients with HGD and/or adenocarcinoma of the gastroesophageal junctional region strongly suggest that most of these originate in the esophagus.
  • In the small minority of patients whose HGD and/or adenocarcinoma were associated with gastric pathology, the incidence of gastritis and H. pylori infection was significantly higher in patients with HGD and/or adenocarcinoma in the distal third of the esophagus and not in the junctional and "gastric cardiac" tumors.
  • This suggests that the reflux of the gastric juice whose composition has been altered by gastritis and H. pylori infection may be associated with an increased tendency to HGD and/or adenocarcinoma in the distal third of the esophagus.
  • [MeSH-major] Adenocarcinoma / pathology. Cardia / pathology. Esophagogastric Junction / pathology. Stomach / pathology. Stomach Neoplasms / pathology

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  • (PMID = 20871225.001).
  • [ISSN] 1532-0979
  • [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
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82. Gulmann C, Lantuejoul S, Grace A, Leader M, Patchett S, Kay E: Telomerase activity in proximal and distal gastric neoplastic and preneoplastic lesions using immunohistochemical detection of hTERT. Dig Liver Dis; 2005 Jun;37(6):439-45
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  • [Title] Telomerase activity in proximal and distal gastric neoplastic and preneoplastic lesions using immunohistochemical detection of hTERT.
  • BACKGROUND: The incidence of distal (corpus and antrum) gastric adenocarcinoma is decreasing with a simultaneous increase in incidence of proximal (cardia) adenocarcinoma.
  • Intestinal metaplasia may have a lower malignant potential in the proximal stomach but regardless of the locations, its specificity as a predictor of carcinoma is low.
  • AIMS: The aim of this study was to establish whether human telomerase reverse transcriptase expression differs at various points in proximal versus distal gastric carcinogenesis and to test the utility of human telomerase reverse transcriptase expression as a marker of cancer risk in intestinal metaplasia.
  • MATERIAL AND METHODS: Wax-embedded tissue from proximal and distal stomach including normal mucosa (n=86), intestinal metaplasia (n=83) and carcinoma (n=101) were used and slides were immunostained for human telomerase reverse transcriptase and pRb and scored semi-quantitatively.
  • RESULTS: The results showed that in both proximal and distal stomach, human telomerase reverse transcriptase expression rates increased from normal mucosa to cancer.
  • High rates of human telomerase reverse transcriptase expression were seen in the proliferative zones of glands in intestinal metaplasia.
  • CONCLUSIONS: In conclusion, telomerase activity appears to be an early event in both proximal and distal gastric carcinogenesis and human telomerase reverse transcriptase is expressed in intestinal metaplasia.
  • [MeSH-major] Carcinoma / metabolism. DNA-Binding Proteins / metabolism. Precancerous Conditions / metabolism. Stomach Neoplasms / metabolism. Telomerase / metabolism
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Female. Humans. Immunohistochemistry. Intestinal Mucosa / metabolism. Intestines / metabolism. Intestines / pathology. Male. Metaplasia / metabolism. Middle Aged. Retinoblastoma Protein / metabolism

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  • (PMID = 15893283.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Retinoblastoma Protein; EC 2.7.7.49 / Telomerase
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83. Vieth M, Stolte M: Elevated risk for gastric adenocarcinoma can be predicted from histomorphology. World J Gastroenterol; 2006 Oct 14;12(38):6109-14
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  • [Title] Elevated risk for gastric adenocarcinoma can be predicted from histomorphology.
  • The number of patients with gastric cancer has more than doubled since 1985 in developing countries.
  • Thus, the questions of whether it can be predicted from gastritis morphology, who is at risk and who has a lower risk of developing gastric carcinoma are raised.
  • The frequency of ulcerations among H pylori-infected individuals is estimated to be 13%, gastric cancer about 1% and MALT lymphoma around 0.1%.
  • In the literature a multistep model from chronic active H pylori-infection through multifocal atrophy, intestinal metaplasia, dysplasia (intraepithelial neoplasia) and carcinoma has been described.
  • Since risk factors such as metaplasia and atrophy are paracancerous rather than precancerous conditions, this raises the question whether there is a better morphological marker.
  • Differences in topography, grade and activity of Helicobacter gastritis in the antrum and corpus might be good markers for identifying those who are at risk of developing gastric cancer.
  • It is known that the so-called corpus dominant H pylori gastritis is found more frequently among individuals with early and advanced gastric cancer and within high risk populations.
  • This is valid both for first-degree relatives of gastric cancer patients and for patients with gastric adenoma and hyperplastic polyps.
  • In conclusion, corpus-dominant H pylori gastritis is significantly more common in patients with advanced and early gastric cancer, first-degree relatives of patients with gastric cancer, patients with gastric adenoma and gastric hyperplastic polyps.
  • Therefore, all these patients are at risk of developing gastric cancer.
  • It appears that patients with a low acid output more frequently develop gastric cancer.
  • Large prospective long term studies are necessary to prove this and identify new reliable markers for gastric cancer development.
  • [MeSH-major] Adenocarcinoma / etiology. Gastritis / pathology. Stomach / pathology. Stomach Neoplasms / etiology

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  • (PMID = 17036380.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 47
  • [Other-IDs] NLM/ PMC4088102
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84. Nomura S, Nakajima A, Ishimine S, Matsuhashi N, Kadowaki T, Kaminishi M: Differential expression of peroxisome proliferator-activated receptor in histologically different human gastric cancer tissues. J Exp Clin Cancer Res; 2006 Sep;25(3):443-8
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  • [Title] Differential expression of peroxisome proliferator-activated receptor in histologically different human gastric cancer tissues.
  • Gastric cancer cell lines express peroxisome proliferator-activated receptor gamma (PPARgamma), and treatment with PPARgamma ligands suppresses growth of subgroup of these cell lines.
  • However, expression and subcellular distribution of PPARgamma in human gastric cancer tissues is still unknown.
  • Therefore, expression and subcellular localization of PPARgamma were examined among different histological types of gastric cancer tissues.
  • Immunohistochemical staining for PPARgamma was performed using biopsy specimens of human gastric cancer of various histological types, gastric adenomas, and intestinal metaplasia.
  • All samples of intestinal metaplasia and most samples of gastric tumors, except for signet ring cell carcinoma, expressed PPARgamma in the epithelial cells.
  • All samples of intestinal metaplasia expressed PPARgamma only in the cytosol.
  • For adenoma, 90% was positive for PPARgamma in cytosol, and 40% was positive in nuclei, for well-differentiated adenocarcinoma, 80% was positive in cytosol, and 20% was positive in nuclei.
  • For moderately differentiated adenocarcinomas, 70% was positive for cytosol, and 80% was positive for nuclei; for poorly differentiated adenocarcinoma, 30% was positive in cytosol, and 70% was positive in nuclei.
  • The frequency of samples with positive cytosolic staining decreased as the differentiation stage turned from intestinal metaplasia to adenoma, well-, moderately-, and poorly-differentiated cancers.
  • Simultaneously, there was a tendency toward an increased frequency of samples with positive nuclear PPARgamma staining as the differentiation stage transformed from intestinal metaplasia to poorly-differentiated cancer.
  • There was a striking difference in subcellular localization according to the differentiation levels of gastric dysplastic cells.
  • The findings also supported an intestinal metaplasia-adenoma-well-differentiated gastric cancer sequence, and signet ring cell cancer was suggested to be of a different lineage from other types of gastric cancers.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma / metabolism. Carcinoma, Signet Ring Cell / metabolism. Intestinal Neoplasms / metabolism. Metaplasia / metabolism. PPAR gamma / metabolism. Stomach Neoplasms / metabolism
  • [MeSH-minor] Cell Differentiation. Cell Nucleus / metabolism. Cytoplasm / metabolism. Gastric Mucosa / metabolism. Gene Expression Regulation, Neoplastic. Humans. Subcellular Fractions

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  • (PMID = 17167986.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / PPAR gamma
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85. Park SY, Jeon SW, Jung MK, Cho CM, Tak WY, Kweon YO, Kim SK, Choi YH: Long-term follow-up study of gastric intraepithelial neoplasias: progression from low-grade dysplasia to invasive carcinoma. Eur J Gastroenterol Hepatol; 2008 Oct;20(10):966-70
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  • [Title] Long-term follow-up study of gastric intraepithelial neoplasias: progression from low-grade dysplasia to invasive carcinoma.
  • BACKGROUND AND STUDY AIMS: A gastric intraepithelial neoplasia (IEN) is usually regarded as a precancerous lesion; however, the natural history of the gastric IEN has not been clarified.
  • We aimed to evaluate the progression of dysplasia in gastric IENs.
  • PATIENTS AND METHODS: As a retrospective study, we reviewed 26 gastric adenomas with low-grade dysplasia (LGD) and one with high-grade dysplasia (HGD) from 18 patients.
  • The histological diagnosis was classified according to the Vienna classification.
  • We reviewed clinical (age and sex), morphological (size, color, shape, location in stomach, surface nodularity, and presence of the erosion), and histological (histological diagnosis, infection with Helicobacter pylori, infiltration of inflammatory cells, atrophy, intestinal metaplasia, microscopic erosions, and glandular appearance) characteristics with regard to progression of dysplasia.
  • One IEN with HGD and three IENs with LGD progressed to invasive adenocarcinoma (category 5).
  • Four gastric IENs with LGD progressed to HGD (category 4).
  • CONCLUSION: For the potential risk of progressive dysplasia, gastric IENs should be treated actively using the recently advanced therapeutic endoscopic techniques, regardless of the degrees of dysplasia.
  • [MeSH-major] Gastric Mucosa / pathology. Precancerous Conditions / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Chi-Square Distribution. Disease Progression. Female. Follow-Up Studies. Gastroscopy. Helicobacter Infections / pathology. Helicobacter pylori. Humans. Male. Metaplasia / pathology. Middle Aged. Neoplasm Staging. Risk

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  • (PMID = 18787462.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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86. Chandrasoma P: Controversies of the cardiac mucosa and Barrett's oesophagus. Histopathology; 2005 Apr;46(4):361-73
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  • Confusion regarding the diagnosis of Barrett's oesophagus exists because of a false dogma that cardiac mucosa is normally present in the gastro-oesophageal junctional region.
  • Recent data indicate that the only normal epithelia in the oesophagus and proximal stomach are squamous epithelium and gastric oxyntic mucosa.
  • When this fact is recognized, it becomes easy to develop precise histological definitions for the normal state (presence of only squamous and oxyntic mucosa), metaplastic oesophageal columnar epithelium (cardiac mucosa with and without intestinal metaplasia, and oxynto-cardiac mucosa), the gastro-oesophageal junction (the proximal limit of gastric oxyntic mucosa), the oesophagus (that part of the foregut lined by squamous and metaplastic columnar epithelium), reflux disease (the presence of metaplastic columnar epithelium), and Barrett's oesophagus (cardiac mucosa with intestinal metaplasia).
  • It is also possible to assess accurately the severity of reflux which is directly proportional to the amount of metaplastic columnar epithelium, and the risk of adenocarcinoma which is related to the amount of dysplasia in intestinal metaplastic epithelium present within the columnar lined segment of the oesophagus.
  • Histopathological precision cannot be matched by any other modality and can convert the confusion that exists regarding diagnosis of Barrett's oesophagus to complete lucidity in a manner that is simple, accurate, and reproducible.
  • [MeSH-major] Barrett Esophagus / pathology. Cardia / pathology. Gastric Mucosa / pathology
  • [MeSH-minor] Esophagogastric Junction / pathology. Humans. Metaplasia

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  • [CommentIn] Histopathology. 2006 Jul;49(1):97-8; author reply 98 [16842257.001]
  • (PMID = 15810947.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 48
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87. Farnedi A, Eusebi LH, Poli F, Foschini MP: Immunohistochemical expression of the human sodium/iodide symporter distinguishes malignant from benign gastric lesions. Int J Surg Pathol; 2009 Aug;17(4):327-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical expression of the human sodium/iodide symporter distinguishes malignant from benign gastric lesions.
  • The aim was to evaluate the immunohistochemical expression of the human homolog of NIS (hNIS) in a wide spectrum of gastric lesions.
  • MATERIALS AND METHODS: Seventy-seven samples were stained immunohistochemically with a monoclonal antibody for hNIS, including 14 with normal gastric mucosa, 14 with chronic atrophic gastritis with foveolar hyperplasia, 15 with chronic atrophic gastritis with intestinal metaplasia, 6 with chronic atrophic gastritis with atypical regenerative hyperplasia, 8 with chronic atrophic gastritis with dysplasia, 15 with invasive adenocarcinoma, 3 with well-differentiated neuroendocrine tumor, and 2 with gastrointestinal stromal tumors (GISTs).
  • RESULTS: hNIS stained the basolateral cytoplasmic portion of foveolae in normal mucosa, in 13 cases of chronic atrophic gastritis with foveolar hyperplasia, and in only 1 case of regenerative atypical hyperplasia. hNIS was consistently absent in intestinal metaplasia, in dysplastic glands, and in the cells constituting invasive carcinoma, well-differentiated neuroendocrine tumors, and GIST.
  • [MeSH-major] Gastritis, Atrophic / diagnosis. Gastrointestinal Stromal Tumors / diagnosis. Neuroendocrine Tumors / diagnosis. Precancerous Conditions / pathology. Stomach Neoplasms / diagnosis. Symporters / metabolism
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / metabolism. Adult. Aged. Aged, 80 and over. Chronic Disease. Diagnosis, Differential. Female. Gastric Mucosa / metabolism. Humans. Hyperplasia / diagnosis. Hyperplasia / metabolism. Male. Metaplasia / diagnosis. Metaplasia / metabolism. Middle Aged

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  • (PMID = 19124451.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Symporters; 0 / sodium-iodide symporter
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88. Hirahashi M, Yao T, Matsumoto T, Nishiyama K, Oya M, Iida M, Tsuneyoshi M: Intramucosal gastric adenocarcinoma of poorly differentiated type in the young is characterized by Helicobacter pylori infection and antral lymphoid hyperplasia. Mod Pathol; 2007 Jan;20(1):29-34
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  • [Title] Intramucosal gastric adenocarcinoma of poorly differentiated type in the young is characterized by Helicobacter pylori infection and antral lymphoid hyperplasia.
  • The aim of this investigation was to clarify the histological characteristics of gastric cancer in the young.
  • Within the background mucosa, antral chronic inflammatory infiltrates with lymphoid-follicle hyperplasia were more severe, and intestinal metaplasia was less frequent in the young group than in the elderly group.
  • Intramucosal gastric adenocarcinomas of poorly differentiated type in the young may be associated with H. pylori infection with antral chronic inflammation with lymphoid-follicle hyperplasia, regardless of the existence of intestinal metaplasia within the background gastric mucosa.
  • [MeSH-major] Adenocarcinoma / pathology. Gastric Mucosa / pathology. Helicobacter Infections / pathology. Helicobacter pylori / isolation & purification. Lymphoid Tissue / pathology. Pyloric Antrum / pathology. Stomach Neoplasms / pathology

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  • (PMID = 17041565.001).
  • [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
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89. Fukasawa T, Suzuki S, Fujii H: [A case report of early gastric cancer with Paneth-like tumor cells]. Nihon Shokakibyo Gakkai Zasshi; 2006 Nov;103(11):1251-6
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  • [Title] [A case report of early gastric cancer with Paneth-like tumor cells].
  • A 55-year-old man was given a diagnosis of grade 0IIc type gastric cancer of the midgastric posterior wall following endoscopy of the upper digestive tract, and subsequently underwent distal gastrectomy.
  • Tumor cells resembling Paneth cells were occasionally observed in differentiated adenocarcinoma that had invaded the submucosal layer, the tumor was CD10-positive, and showed differentiation to complete intestinal metaplasia.
  • Although complete intestinal metaplasia is associated with a low incidence of malignant transformation, this case was considered to be different from complete intestinal metaplasia, on which a mutation of the gene of p53 is involved in the early period of carcinogenesis.
  • [MeSH-major] Adenocarcinoma / pathology. Paneth Cells / pathology. Stomach Neoplasms / pathology

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  • (PMID = 17085906.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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90. Goto Y, Ando T, Nishio K, Kawai S, Ishida Y, Naito M, Goto H, Hamajima N: Grb2-associated binder 1 polymorphism was associated with the risk of Helicobactor pylori infection and gastric atrophy. Int J Med Sci; 2007;4(1):1-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Grb2-associated binder 1 polymorphism was associated with the risk of Helicobactor pylori infection and gastric atrophy.
  • BACKGROUND: Various single nucleotide polymorphisms (SNPs) have explained the association between Helicobacter pylori (H. pylori) and gastric atrophy and cancer.
  • This study investigated the associations of Grb2 associated binder 1 (Gab1) polymorphism and the combination of PTPN11 gene encoding src homology 2 domain-containing protein tyrosine phosphatase-2 (SHP2) and Gab1 gene with gastric cancer and gastric atrophy among H. pylori seropositive subjects.
  • METHODS: A single nucleotide polymorphism at intron 2 of Gab1 (JST164345) was examined for 454 Japanese health checkup examinees (126 males and 328 females) aged 35 to 85 without a history of gastric cancer and 202 gastric cancer patients (134 males and 68 females) aged 33 to 94 with pathologically confirmed diagnosis of gastric adenocarcinoma.
  • Among seropositive healthy controls, the OR of the Gab1 G/A+A/A for gastric atrophy was significant (OR=1.95, 95% CI: 1.12 -3.40).
  • Seropositive individuals with PTPN11 G/G and Gab1 G/A+A/A demonstrated the highest risk of gastric atrophy with significance (OR=3.49, 95% CI: 1.54-7.90) relative to PTPN11 G/A+A/A and Gab1 G/G, the lowest risk combination, as a reference.
  • Compared to gastric cancer case, the Gab1 did not influence the step of atrophy/metaplasia-gastric cancer sequence.
  • CONCLUSIONS: This study represents that the Gab1 polymorphism was associated with the low risk of H. pylori infection and the high risk of gastric atrophy among seropositive healthy controls, and that seropositive individuals with PTPN11 G/G and Gab1 G/A+G/G were associated with the greatest risk of gastric atrophy.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Gastric Mucosa / pathology. Helicobacter Infections / etiology. Helicobacter pylori. Polymorphism, Single Nucleotide
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Atrophy. Female. Humans. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Male. Metaplasia. Middle Aged. Odds Ratio. Protein Phosphatase 2. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Protein Tyrosine Phosphatases / genetics. Protein Tyrosine Phosphatases / metabolism. Risk Factors. SH2 Domain-Containing Protein Tyrosine Phosphatases. Stomach Neoplasms / etiology. src Homology Domains

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  • (PMID = 17211494.001).
  • [ISSN] 1449-1907
  • [Journal-full-title] International journal of medical sciences
  • [ISO-abbreviation] Int J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / GAB1 protein, human; 0 / Intracellular Signaling Peptides and Proteins; EC 3.1.3.16 / Protein Phosphatase 2; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / SH2 Domain-Containing Protein Tyrosine Phosphatases
  • [Other-IDs] NLM/ PMC1752235
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91. Chandrasoma P, Wijetunge S, Demeester SR, Hagen J, Demeester TR: The histologic squamo-oxyntic gap: an accurate and reproducible diagnostic marker of gastroesophageal reflux disease. Am J Surg Pathol; 2010 Nov;34(11):1574-81
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  • Biopsies were obtained from the esophagus, around the gastroesophageal junction and the stomach: proximal, body, and antrum.
  • Patients who had oxyntocardiac±cardiac±intestinal epithelia between the squamous epithelium proximally and the proximal limit of gastric oxyntic mucosa distally were defined as having a squamo-oxyntic gap.
  • Only oxyntocardiac epithelium was seen in 190 (11.5%) of the patients, oxyntocardiac and cardiac epithelia in 898 (54.3%), and intestinal metaplasia in addition to the other 2 epithelial types in 567 (34.2%).
  • The prevalence of intestinal metaplasia was directly proportional to length of the squamo-oxyntic gap, being 24.3% (340/1399) when the length was <1 cm, and 83.5% (147/176) with length 1 to 5 cm.
  • All patients with a length more than 5 cm had intestinal metaplasia.
  • The distribution of the 3 epithelia was constant irrespective of the length of the squamocolumnar gap; intestinal metaplasia, when present, was seen maximally in the proximal region of the gap, cardiac epithelium intermediate and oxyntocardiac epithelium in the most distal segment of the gap.
  • Distal gastric biopsies showed no evidence of significant inflammation, intestinal metaplasia or Helicobacter pylori infection in 1543 (93.2%) of the patients, indicating that the squamo-oxyntic gap was largely independent of gastric pathology.
  • The distal limit of the squamo-oxyntic gap, which is the junction between oxyntocardiac and gastric oxyntic epithelium is the true gastroesophageal junction.
  • The presence of intestinal metaplasia within the squamo-oxyntic gap is the most accurate risk indicator for esophageal adenocarcinoma and defines Barrett esophagus.
  • [MeSH-major] Adenocarcinoma / diagnosis. Barrett Esophagus / diagnosis. Epithelial Cells / pathology. Esophageal Neoplasms / diagnosis. Esophagus / pathology. Gastroesophageal Reflux / diagnosis. Parietal Cells, Gastric / pathology. Precancerous Conditions / diagnosis
  • [MeSH-minor] Biopsy. California. Endoscopy, Gastrointestinal. Humans. Metaplasia. Predictive Value of Tests. Reproducibility of Results. Retrospective Studies. Risk Assessment. Risk Factors. Severity of Illness Index

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  • [CommentIn] Am J Surg Pathol. 2011 May;35(5):773; author reply 773-4 [21502913.001]
  • (PMID = 20871393.001).
  • [ISSN] 1532-0979
  • [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
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92. Schmitz JM, Durham CG, Ho SB, Lorenz RG: Gastric mucus alterations associated with murine Helicobacter infection. J Histochem Cytochem; 2009 May;57(5):457-67
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  • [Title] Gastric mucus alterations associated with murine Helicobacter infection.
  • The C57BL/6 mouse has been shown to develop gastric adenocarcinoma after Helicobacter felis infection.
  • This model was used to determine whether mucin and trefoil factor (TFF) expression after infection was altered in a similar fashion to the changes seen in the protective gastric mucus layer of the human stomach after H. pylori infection.
  • These alterations in mucin expression occurred as early as 4 weeks postinfection, before the development of significant mucous metaplasia or gastric dysplasia.
  • The decrease in muc5ac expression occurred only in the body of the stomach and was not secondary to the adaptive immune response to infection, because a similar decrease in expression was seen after infection of B6.Rag-1(-/-) mice, which lack B and T cells.
  • Because B6.Rag-1(-/-) mice do not develop gastric pathology after H. felis infection, these findings point to the potential role of Muc4 and Muc5b in disease progression.

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  • (PMID = 19153195.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / T32 AI-07041; United States / NIAID NIH HHS / AI / T32 AI007041; United States / NIDDK NIH HHS / DK / R24 DK064400; United States / NIDDK NIH HHS / DK / P01 DK-071176; United States / NIDDK NIH HHS / DK / P30 DK064400; United States / NIDDK NIH HHS / DK / P01 DK071176; United States / NIDDK NIH HHS / DK / R01 DK059911; United States / NIDDK NIH HHS / DK / R01 DK-059911
  • [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 / Gastric Mucins; 0 / Peptides; 0 / RNA, Messenger; 146046-78-8 / trefoil factor
  • [Other-IDs] NLM/ PMC2675072
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93. Cho YE, Kim JY, Kim YW, Park JH, Lee S: Expression and prognostic significance of human growth and transformation-dependent protein in gastric carcinoma and gastric adenoma. Hum Pathol; 2009 Jul;40(7):975-81
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  • [Title] Expression and prognostic significance of human growth and transformation-dependent protein in gastric carcinoma and gastric adenoma.
  • We investigated the expression profile of human growth and transformation-dependent protein using immunohistochemistry in gastric tissues including cancer (n = 138), adenoma (n = 37), intestinal metaplasia (n = 20), and normal gastric epithelium (n = 20), then correlated human growth and transformation-dependent protein expression in tumors with clinicopathologic features.
  • Human growth and transformation-dependent protein showed strong staining in the cytoplasm of intestinal-type adenocarcinoma and gastric adenoma, whereas normal gastric antral mucosa showed no staining.
  • Human growth and transformation-dependent protein expression in gastric cancer showed a close association with the Lauren classification, tumor stage, and Ki-67 proliferation index.
  • These findings suggest that human growth and transformation-dependent protein expression is a common occurrence during the progression from a normal gastric mucosa to an intestinal-type carcinoma and may be associated with tumor cell proliferation activity.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma / metabolism. Membrane Proteins / biosynthesis. Mitochondrial Proteins / biosynthesis. Stomach Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Immunohistochemistry. Intestinal Mucosa / metabolism. Kaplan-Meier Estimate. Ki-67 Antigen / biosynthesis. Male. Metaplasia / metabolism. Metaplasia / pathology. Middle Aged. Prognosis

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  • (PMID = 19269009.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FAM162A protein, human; 0 / Ki-67 Antigen; 0 / Membrane Proteins; 0 / Mitochondrial Proteins
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94. Ichinoe M, Mikami T, Hara A, Tsuruta T, Okayasu I: Background submucosal cysts in early gastric cancer cases have unique clinicopathologic features suggestive of postgastritis and significant smoking association. Am J Clin Pathol; 2007 Nov;128(5):746-52
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  • [Title] Background submucosal cysts in early gastric cancer cases have unique clinicopathologic features suggestive of postgastritis and significant smoking association.
  • Submucosal cysts (SMCs) might result from severe gastritis and be related to gastric carcinogenesis, although direct evidence is limited.
  • We studied clinicopathologic findings for gastric cancers arising in mucosa with SMC and the relation to gastritis.
  • In the stomach with SMCs, cancers were predominantly differentiated-type adenocarcinomas in men and showed a significant tendency for location in the upper gastric region.
  • Intestinal metaplasia was significantly more severe and the muscularis mucosae were thicker in cancer cases with SMC in comparison with cases without SMC and control cases of gastrointestinal stromal tumor (GIST).
  • Cases of gastric cancer with SMC show characteristic clinicopathologic features, and SMC formation may be caused by gastritis and influenced by smoking.
  • [MeSH-major] Adenocarcinoma / pathology. Cysts / pathology. Gastritis / pathology. Precancerous Conditions / pathology. Smoking / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Gastric Mucosa / microbiology. Gastric Mucosa / pathology. Helicobacter Infections / complications. Helicobacter Infections / pathology. Helicobacter pylori / immunology. Helicobacter pylori / isolation & purification. Humans. Intestines / pathology. Japan / epidemiology. Male. Metaplasia. Middle Aged. Risk Factors

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  • (PMID = 17951195.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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95. Yamamichi N, Inada K, Ichinose M, Yamamichi-Nishina M, Mizutani T, Watanabe H, Shiogama K, Fujishiro M, Okazaki T, Yahagi N, Haraguchi T, Fujita S, Tsutsumi Y, Omata M, Iba H: Frequent loss of Brm expression in gastric cancer correlates with histologic features and differentiation state. Cancer Res; 2007 Nov 15;67(22):10727-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent loss of Brm expression in gastric cancer correlates with histologic features and differentiation state.
  • We observed frequent loss of Brm expression but not of BRG1 in human gastric cancer cell lines.
  • Brm immunostaining of 89 primary gastric cancers showed an obvious reduction in 60 cases (67%) and a severe decrease in 37 cases (42%).
  • Loss of Brm is frequent in the major gastric cancer types (well- or moderately-differentiated tubular adenocarcinoma and poorly-differentiated adenocarcinoma) and positively correlates with the undifferentiated state.
  • Among the minor gastric cancer types, Brm expression persists in signet-ring cell carcinoma and mucinous adenocarcinoma, but a marked decrease is observed in papillary adenocarcinoma.
  • Intestinal metaplasia never shows decreased expression, indicating that Brm is a valid marker of gastric oncogenesis.
  • In contrast, BRG1 is retained in most cases; a concomitant loss of BRG1 and Brm is rare in gastric cancer, contrary to other malignancies.
  • We further show that Brm is required for villin expression, a definitive marker of intestinal metaplasia and differentiation.
  • Via regulating such genes important for gut differentiation, Brm should play significant roles in determining the histologic features of gastric malignancy.
  • [MeSH-major] Adenocarcinoma / metabolism. Gene Expression Regulation, Neoplastic. Microfilament Proteins / biosynthesis. Stomach Neoplasms / metabolism. Transcription Factors / biosynthesis. Transcription Factors / genetics
  • [MeSH-minor] Cell Differentiation. Cell Line, Tumor. Colorectal Neoplasms / metabolism. Enzyme Inhibitors / pharmacology. Epigenesis, Genetic. Gastric Mucosa / metabolism. Gene Expression Profiling. Histone Deacetylase Inhibitors. Humans. Models, Biological

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  • (PMID = 18006815.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Microfilament Proteins; 0 / SMARCA2 protein, human; 0 / Transcription Factors; 0 / villin
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96. Ndububa DA, Agbakwuru EA, Olasode BJ, Aladegbaiye AO, Adekanle O, Arigbabu AO: Correlation between endoscopic suspicion of gastric cancer and histology in Nigerian patients with dyspepsia. Trop Gastroenterol; 2007 Apr-Jun;28(2):69-71
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  • [Title] Correlation between endoscopic suspicion of gastric cancer and histology in Nigerian patients with dyspepsia.
  • Gastric mucosal biopsies of 77 dyspeptic patients whose endoscopic features were suggestive of cancer and 56 patients with uncomplicated duodenal ulcer (DU) were subjected to histopathological analysis.
  • Gastric cancer was confirmed in 18 (23.4%) of the 77 patients but not in 59 (76.6%).
  • 4 (5.2%) of the 18 patients had early gastric cancer (EGC).
  • Histopathological findings in the stomach biopsy of the 59 patients in whom cancer could not be confirmed were compared with those of the 56 patients with DU.
  • Intestinal metaplasia (IM) was present in 32.2% of the 59 cases with endoscopic suspicion of gastric cancer and in 16.1% of the 56 DU controls (P < 0.05).
  • The difference in the prevalence of gastric mucosal atrophy and Helicobacter pylori infection between the two groups (83% vs. 71.4%) did not reach statistical significance (P > 0.10).
  • All 18 patients with gastric cancer were positive for Helicobacter pylori and the prevalence of the infection approached 95% in those with IM and MALT.
  • This study shows that IM and MALT present with endoscopic appearances that resemble that of gastric cancer and that along with the latter, their main aetiological agent is Helicobacter pylori.
  • [MeSH-major] Gastric Mucosa / pathology. Gastroscopy. Lymphoma, B-Cell, Marginal Zone / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adult. Aged. Aged, 80 and over. Case-Control Studies. Dyspepsia / etiology. Female. Helicobacter Infections / epidemiology. Helicobacter pylori / isolation & purification. Humans. Male. Middle Aged. Nigeria. Prospective Studies. Stomach Neoplasms

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  • (PMID = 18050843.001).
  • [ISSN] 0250-636X
  • [Journal-full-title] Tropical gastroenterology : official journal of the Digestive Diseases Foundation
  • [ISO-abbreviation] Trop Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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97. 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-major] Deoxyguanosine / analogs & derivatives. Gastric Mucosa / pathology. Gastritis / urine. Intestinal Mucosa / pathology
  • [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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98. Tiwari SK, Manoj G, Sharma V, Sivaram G, Saikant R, Bardia A, Sharma VK, Abid Z, Khan AA, Habeeb MA, Habibullah CM, Kumar BS, Nandan A: Relevance of Helicobacter pylori genotypes in gastric pathology and its association with plasma malondialdehyde and nitric oxide levels. Inflammopharmacology; 2010 Apr;18(2):59-64
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  • [Title] Relevance of Helicobacter pylori genotypes in gastric pathology and its association with plasma malondialdehyde and nitric oxide levels.
  • Persistent infection with Helicobacter pylori confers an increased risk of peptic ulceration and gastric adenocarcinoma.
  • Reactive oxygen and nitrogen species play a crucial role in the progression from normal gastric mucosa to cancer.
  • The aim of the present study was to investigate the plasma malondialdehyde and nitric oxide levels in H. pylori related gastroduodenal diseases and associate their levels with gastric pathology and genotypes of H. pylori.
  • Subsequently, genotypic and histopathological assessment was performed in gastric biopsies obtained during endoscopy.
  • In conclusion, the study demonstrates close relationship between the plasma malondialdehyde and nitric oxide levels, gastric histopathology and genotypes of H. pylori.
  • [MeSH-minor] Adult. Female. Gastritis / blood. Gastritis / microbiology. Gastritis / pathology. Gastritis, Atrophic / blood. Gastritis, Atrophic / microbiology. Gastritis, Atrophic / pathology. Genotype. Humans. Intestines / microbiology. Intestines / pathology. Male. Metaplasia / blood. Metaplasia / microbiology. Metaplasia / pathology. Middle Aged. Stomach Neoplasms / blood. Stomach Neoplasms / microbiology. Stomach Neoplasms / pathology

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  • (PMID = 20143166.001).
  • [ISSN] 1568-5608
  • [Journal-full-title] Inflammopharmacology
  • [ISO-abbreviation] Inflammopharmacology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 31C4KY9ESH / Nitric Oxide; 4Y8F71G49Q / Malondialdehyde
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99. Kojima K, Kishimoto T, Nagai Y, Tanizawa T, Nakatani Y, Miyazaki M, Ishikura H: The expression of hepatocyte nuclear factor-4alpha, a developmental regulator of visceral endoderm, correlates with the intestinal phenotype of gastric adenocarcinomas. Pathology; 2006 Dec;38(6):548-54
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  • [Title] The expression of hepatocyte nuclear factor-4alpha, a developmental regulator of visceral endoderm, correlates with the intestinal phenotype of gastric adenocarcinomas.
  • However, adult gastric mucosa does not express HNF-4alpha.
  • We investigated the possible involvement of HNF-4alpha in intestinal metaplasia and the intestinalisation of gastric adenocarcinomas.
  • METHODS: Thirty-five cases of adenocarcinomas and 46 cases of adjacent non-neoplastic mucosa with (22 lesions) or without (24 lesions) intestinal metaplasia were immunostained for HNF-4alpha.
  • The gastric or the intestinal phenotype was also examined using immunohistochemistry for MUC5AC, MUC2, CD10, and gastric-type mucin (GTM).
  • Adenocarcinomas were classified into the gastric type (G-type, 42.9%), the mixed gastric and intestinal type (GI-type, 31.4%), and the intestinal type (I-type, 25.7%).
  • RESULTS: The HNF-4alpha expression was exclusively seen in glandular cells with intestinal metaplasia, which was correlated with MUC2 expression (p<0.05) and inversely correlated with MUC5AC expression (p<0.05).
  • CONCLUSIONS: HNF-4alpha expression is associated with the intestinal phenotype of non-neoplastic and neoplastic gastric glandular cells, suggesting a possible involvement in the establishment and/or maintenance of the intestinal phenotype of the gastric mucosa and adenocarcinomas.
  • [MeSH-major] Adenocarcinoma / pathology. Endoderm / physiology. Hepatocyte Nuclear Factor 4 / metabolism. Intestines / pathology. Stomach Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Gastric Mucosa / embryology. Gastric Mucosa / pathology. Gene Expression Regulation, Neoplastic. Humans. Phenotype

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  • (PMID = 17393984.001).
  • [ISSN] 0031-3025
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HNF4A protein, human; 0 / Hepatocyte Nuclear Factor 4
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100. Miao XP, Li JS, Li HY, Zeng SP, Zhao Y, Zeng JZ: Expression of ornithine decarboxylase in precancerous and cancerous gastric lesions. World J Gastroenterol; 2007 May 28;13(20):2867-71
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  • [Title] Expression of ornithine decarboxylase in precancerous and cancerous gastric lesions.
  • AIM: To investigate the expression of ornithine decarboxylase (ODC) in precancerous and cancerous gastric lesions.
  • METHODS: We studied the expression of ODC in gastric mucosa from patients with chronic superficial gastritis (CSG, n=32), chronic atrophic gastritis [CAG, n=43; 15 with and 28 without intestinal metaplasia (IM)], gastric dysplasia (DYS, n=11) and gastric cancer (GC, n=48) tissues using immunohistochemical staining.
  • All 134 biopsy specimens of gastric mucosa were collected by gastroscopy.
  • CONCLUSION: The expression of ODC is positively correlated with the degree of malignity of gastric mucosa and development of gastric lesions.
  • This finding indicates that ODC may be used as a good biomarker in the screening and diagnosis of precancerous lesions.
  • [MeSH-major] Adenocarcinoma / enzymology. Ornithine Decarboxylase / metabolism. Precancerous Conditions / enzymology. Stomach Neoplasms / enzymology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Gastric Mucosa / enzymology. Gastric Mucosa / pathology. Gastritis / enzymology. Gastritis / pathology. Gastritis, Atrophic / enzymology. Gastritis, Atrophic / pathology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Metaplasia / enzymology. Metaplasia / pathology

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  • (PMID = 17569126.001).
  • [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 / Biomarkers, Tumor; EC 4.1.1.17 / Ornithine Decarboxylase
  • [Other-IDs] NLM/ PMC4395642
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