Murine Models of Helicobacter (pylori or felis)-associated Gastric Cancer.
Gastric adenocarcinoma is the fifth most common cancer and third most common cause of cancer-related death in the world. The majority of these cancers develop in genetically susceptible individuals who are chronically infected with the Gram-negative bacterium Helicobacter pylori. Often these individuals have also been exposed to certain environmental factors that increase susceptibility, such as dietary components. Murine models of Helicobacter-induced gastric cancer are valuable tools for investigating the mechanisms responsible for the stepwise pathological changes of chronic atrophic gastritis, intestinal metaplasia, dysplasia and gastric adenocarcinoma. Helicobacter felis colonization greatly accelerates the development of gastric neoplasia in mice, and causes pathologies similar to those observed with Helicobacter pylori-associated gastric carcinogenesis in humans. These mouse models are therefore useful for investigating genetic and environmental factors that may be involved in the pathogenesis and treatment of gastric cancer. Detailed in these protocols are procedures for inducing Helicobacter-associated carcinogenesis in mice as well as the histological analysis and interpretation of gastric pathology in these animals.
Department of Cellular and Molecular Physiology, Gastroenterology Research Unit, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.|Authors share first authorship.
Carrie A
CA
Duckworth
Department of Cellular and Molecular Physiology, Gastroenterology Research Unit, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.|Authors share first authorship.
Michael D
MD
Burkitt
Department of Cellular and Molecular Physiology, Gastroenterology Research Unit, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.
Jonathan M
JM
Williams
Department of Cellular and Molecular Physiology, Gastroenterology Research Unit, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.
Bryony N
BN
Parsons
Department of Cellular and Molecular Physiology, Gastroenterology Research Unit, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.
Joseph M F
JMF
Tang
Department of Cellular and Molecular Physiology, Gastroenterology Research Unit, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.|Correspondence: Prof D. Mark Pritchard, Department of Cellular and Molecular Physiology, Gastroenterology Research Unit, Institute of Translational Medicine, University of Liverpool, Ashton St, Liverpool, L69 3GE. Tel: 0151 794 5772; e-mail: dmpritch@liv.ac.uk.
D Mark
DM
Pritchard
D000230:Adenocarcinoma / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use; D063646:Carcinogenesis / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000187:drug effects / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D044922:Helicobacter felis / Q000187:drug effects / Q000276:immunology / Q000472:pathogenicity*; D016480:Helicobacter pylori / Q000187:drug effects / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D051379:Mice; D010257:Paraneoplastic Syndromes / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D013274:Stomach Neoplasms / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology* / Q000473:pathology
D000900:Anti-Bacterial Agents; D000970:Antineoplastic Agents
felis; gastric atrophy; gastric cancer; gastric inflammation; helicobacter; parietal cells; pylori