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Spotlight: Gastric Intestinal Metaplasia.
Shah SC, Gupta S, Li D, Morgan D, Mustafa RA, Gawron AJ
(2020) Gastroenterology 158: 704
MeSH Terms: Algorithms, Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Population Surveillance, Practice Guidelines as Topic, Precancerous Conditions, Risk Factors, Stomach Neoplasms
Added March 3, 2020
0 Communities
1 Members
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13 MeSH Terms
Histologic Subtyping of Gastric Intestinal Metaplasia: Overview and Considerations for Clinical Practice.
Shah SC, Gawron AJ, Mustafa RA, Piazuelo MB
(2020) Gastroenterology 158: 745-750
MeSH Terms: Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Health Knowledge, Attitudes, Practice, Humans, Metaplasia, Population Surveillance, Precancerous Conditions, Stomach Neoplasms
Added March 3, 2020
0 Communities
1 Members
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9 MeSH Terms
Advancing the Science in Gastric Pre-Neoplasia: Study Design Considerations.
Davitkov P, Altayar O, Shah SC, Gawron AJ, Mustafa RA, Sultan S, Morgan DR
(2020) Gastroenterology 158: 751-759
MeSH Terms: Biomedical Research, Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Humans, Incidence, Metaplasia, Population Surveillance, Precancerous Conditions, Prevalence, Research Design, Risk Factors, Stomach Neoplasms
Added March 3, 2020
0 Communities
1 Members
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13 MeSH Terms
AGA Technical Review on Gastric Intestinal Metaplasia-Epidemiology and Risk Factors.
Altayar O, Davitkov P, Shah SC, Gawron AJ, Morgan DR, Turner K, Mustafa RA
(2020) Gastroenterology 158: 732-744.e16
MeSH Terms: Ethnic Groups, European Continental Ancestry Group, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Precancerous Conditions, Risk Factors, Stomach Neoplasms, United States
Added March 3, 2020
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11 MeSH Terms
AGA Technical Review on Gastric Intestinal Metaplasia-Natural History and Clinical Outcomes.
Gawron AJ, Shah SC, Altayar O, Davitkov P, Morgan D, Turner K, Mustafa RA
(2020) Gastroenterology 158: 705-731.e5
MeSH Terms: Biopsy, Disease Progression, Endoscopy, Gastrointestinal, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Population Surveillance, Precancerous Conditions, Prevalence, Risk Factors, Stomach Neoplasms, United States
Added March 3, 2020
0 Communities
1 Members
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14 MeSH Terms
Differential Cell Susceptibilities to Kras in the Setting of Obstructive Chronic Pancreatitis.
Shi C, Pan FC, Kim JN, Washington MK, Padmanabhan C, Meyer CT, Kopp JL, Sander M, Gannon M, Beauchamp RD, Wright CV, Means AL
(2019) Cell Mol Gastroenterol Hepatol 8: 579-594
MeSH Terms: Acinar Cells, Animals, Carcinogenesis, Carcinoma, Pancreatic Ductal, Cell Transformation, Neoplastic, Disease Models, Animal, Genes, ras, Metaplasia, Mice, Mutation, Pancreatic Neoplasms, Pancreatitis, Chronic, Precancerous Conditions, Proto-Oncogene Proteins p21(ras), Signal Transduction
Show Abstract · Added August 6, 2019
BACKGROUND & AIMS - Activating mutation of the KRAS gene is common in some cancers, such as pancreatic cancer, but rare in other cancers. Chronic pancreatitis is a predisposing condition for pancreatic ductal adenocarcinoma (PDAC), but how it synergizes with KRAS mutation is not known.
METHODS - We used a mouse model to express an activating mutation of Kras in conjunction with obstruction of the main pancreatic duct to recapitulate a common etiology of human chronic pancreatitis. Because the cell of origin of PDAC is not clear, Kras mutation was introduced into either duct cells or acinar cells.
RESULTS - Although Kras expression in both cell types was protective against damage-associated cell death, chronic pancreatitis induced p53, p21, and growth arrest only in acinar-derived cells. Mutant duct cells did not elevate p53 or p21 expression and exhibited increased proliferation driving the appearance of PDAC over time.
CONCLUSIONS - One mechanism by which tissues may be susceptible or resistant to KRAS-initiated tumorigenesis is whether they undergo a p53-mediated damage response. In summary, we have uncovered a mechanism by which inflammation and intrinsic cellular programming synergize for the development of PDAC.
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.
2 Communities
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15 MeSH Terms
Active Kras Expression in Gastric Isthmal Progenitor Cells Induces Foveolar Hyperplasia but Not Metaplasia.
Choi E, Means AL, Coffey RJ, Goldenring JR
(2019) Cell Mol Gastroenterol Hepatol 7: 251-253.e1
MeSH Terms: Animals, Biomarkers, Humans, Hyperplasia, Metaplasia, Mice, Proto-Oncogene Proteins p21(ras), Stem Cells, Stomach
Added February 7, 2019
1 Communities
1 Members
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9 MeSH Terms
MEK Inhibitor Reverses Metaplasia and Allows Re-Emergence of Normal Lineages in Helicobacter pylori-Infected Gerbils.
Yang Q, Yasuda T, Choi E, Toyoda T, Roland JT, Uchida E, Yoshida H, Seto Y, Goldenring JR, Nomura S
(2019) Gastroenterology 156: 577-581.e4
MeSH Terms: Acrylonitrile, Aniline Compounds, Animals, Benzimidazoles, Biopsy, Needle, Disease Models, Animal, Gastric Mucosa, Gerbillinae, Helicobacter Infections, Helicobacter pylori, Immunohistochemistry, Male, Metaplasia, Random Allocation, Reference Values, Treatment Outcome
Added November 14, 2018
0 Communities
1 Members
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16 MeSH Terms
Dynamics of infection as a determinant of progression of gastric precancerous lesions: 16-year follow-up of an eradication trial.
Mera RM, Bravo LE, Camargo MC, Bravo JC, Delgado AG, Romero-Gallo J, Yepez MC, Realpe JL, Schneider BG, Morgan DR, Peek RM, Correa P, Wilson KT, Piazuelo MB
(2018) Gut 67: 1239-1246
MeSH Terms: Adult, Aged, Anti-Bacterial Agents, Disease Progression, Drug Administration Schedule, Female, Follow-Up Studies, Helicobacter Infections, Helicobacter pylori, Humans, Male, Metaplasia, Middle Aged, Precancerous Conditions, Risk Factors, Stomach Neoplasms
Show Abstract · Added June 29, 2017
OBJECTIVE - To evaluate the long-term effect of cumulative time exposed to infection on the progression of gastric lesions.
DESIGN - 795 adults with precancerous gastric lesions were randomised to receive anti- treatment at baseline. Gastric biopsies were obtained at baseline and at 3, 6, 12 and 16 years. A total of 456 individuals attended the 16-year visit. Cumulative time of exposure was calculated as the number of years infected during follow-up. Multivariable logistic regression models were used to estimate the risk of progression to a more advanced diagnosis (versus no change/regression) as well as gastric cancer risk by intestinal metaplasia (IM) subtype. For a more detailed analysis of progression, we also used a histopathology score assessing both severity and extension of the gastric lesions (range 1-6). The score difference between baseline and 16 years was modelled by generalised linear models.
RESULTS - Individuals who were continuously infected with for 16 years had a higher probability of progression to a more advanced diagnosis than those who cleared the infection and remained negative after baseline (p=0.001). Incomplete-type IM was associated with higher risk of progression to cancer than complete-type (OR, 11.3; 95% CI 1.4 to 91.4). The average histopathology score increased by 0.20 units/year (95% CI 0.12 to 0.28) among individuals continuously infected with . The effect of cumulative time of infection on progression in the histopathology score was significantly higher for individuals with atrophy (without IM) than for individuals with IM (p<0.001).
CONCLUSIONS - Long-term exposure to infection was associated with progression of precancerous lesions. Individuals infected with with these lesions may benefit from eradication, particularly those with atrophic gastritis without IM. Incomplete-type IM may be a useful marker for the identification of individuals at higher risk for cancer.
© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.
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16 MeSH Terms
A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach.
Petersen CP, Meyer AR, De Salvo C, Choi E, Schlegel C, Petersen A, Engevik AC, Prasad N, Levy SE, Peebles RS, Pizarro TT, Goldenring JR
(2018) Gut 67: 805-817
MeSH Terms: Animals, Flow Cytometry, Gastric Mucosa, Immunohistochemistry, Intercellular Signaling Peptides and Proteins, Interleukin-1 Receptor-Like 1 Protein, Interleukin-13, Interleukin-33, Macrophages, Metaplasia, Mice, Mice, Inbred C57BL, Mice, Knockout, Parietal Cells, Gastric, Peptides, Real-Time Polymerase Chain Reaction, Receptors, Interleukin, Signal Transduction, Stomach
Show Abstract · Added April 18, 2017
OBJECTIVE - Alternatively activated macrophages (M2) are associated with the progression of spasmolytic polypeptide-expressing metaplasia (SPEM) in the stomach. However, the precise mechanism(s) and critical mediators that induce SPEM are unknown.
DESIGN - To determine candidate genes important in these processes, macrophages from the stomach corpus of mice with SPEM (DMP-777-treated) or advanced SPEM (L635-treated) were isolated and RNA sequenced. Effects on metaplasia development after acute parietal cell loss induced by L635 were evaluated in interleukin (IL)-33, IL-33 receptor (ST2) and IL-13 knockout (KO) mice.
RESULTS - Profiling of metaplasia-associated macrophages in the stomach identified an M2a-polarised macrophage population. Expression of IL-33 was significantly upregulated in macrophages associated with advanced SPEM. L635 induced metaplasia in the stomachs of wild-type mice, but not in the stomachs of IL-33 and ST2 KO mice. While IL-5 and IL-9 were not required for metaplasia induction, IL-13 KO mice did not develop metaplasia in response to L635. Administration of IL-13 to ST2 KO mice re-established the induction of metaplasia following acute parietal cell loss.
CONCLUSIONS - Metaplasia induction and macrophage polarisation after parietal cell loss is coordinated through a cytokine signalling network of IL-33 and IL-13, linking a combined response to injury by both intrinsic mucosal mechanisms and infiltrating M2 macrophages.
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.
0 Communities
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19 MeSH Terms