Three types of metaplasia model through Kras activation, Pten deletion, or Cdh1 deletion in the gastric epithelium.
Animals
Cadherins
/ deficiency
Cell Lineage
Cell Proliferation
Cell Transformation, Neoplastic
/ genetics
Chromosomes, Artificial, Bacterial
Gastric Mucins
/ genetics
Gastric Mucosa
/ enzymology
Gastritis
/ enzymology
Gene Deletion
Gene Expression Regulation, Neoplastic
Integrases
/ genetics
Metaplasia
Mice, Transgenic
PTEN Phosphohydrolase
/ deficiency
Phenotype
Proto-Oncogene Proteins p21(ras)
/ genetics
Stomach Neoplasms
/ enzymology
Tissue Culture Techniques
Trefoil Factor-1
/ genetics
E-cadherin
Kras
Pten
gastric pit cell
metaplasia
mouse model
Journal
The Journal of pathology
ISSN: 1096-9896
Titre abrégé: J Pathol
Pays: England
ID NLM: 0204634
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
24
12
2017
revised:
22
08
2018
accepted:
24
08
2018
pubmed:
1
9
2018
medline:
20
12
2019
entrez:
1
9
2018
Statut:
ppublish
Résumé
Chronic inflammation and intestinal metaplasia are strongly associated with gastric carcinogenesis. Kras activation and Pten deletion are observed in intestinal-type gastric cancer, and Cdh1 mutation is associated with diffuse-type gastric cancer. Although various mouse models of gastric carcinogenesis have been reported, few mouse lines enable gene manipulation selectively in the stomach. Here we established a Tff1-Cre bacterial artificial chromosome transgenic mouse line in an attempt to induce gene modification specifically in the gastric pit lineage. In the stomach, Tff1-Cre-mediated recombination was most evident in the pit lineage in the corpus and in entire antral glands; recombination was also observed in a few gastric chief and parietal cells. Outside the stomach, recombination was patchy throughout the intestines, and particularly frequently in the duodenum (Brunner glands), cecum, and proximal colon. In the stomachs of Tff1-Cre;LSL-Kras
Substances chimiques
Cadherins
0
Cdh1 protein, mouse
0
Gastric Mucins
0
Tff1 protein, mouse
0
Trefoil Factor-1
0
Cre recombinase
EC 2.7.7.-
Integrases
EC 2.7.7.-
PTEN Phosphohydrolase
EC 3.1.3.67
Pten protein, mouse
EC 3.1.3.67
Hras protein, mouse
EC 3.6.5.2
Proto-Oncogene Proteins p21(ras)
EC 3.6.5.2
Types de publication
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
35-47Informations de copyright
Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.