The human pathogen Helicobacter pylori causes inflammation in the stomach of infected hosts, leading in some cases to the development of gastric cancer. Several mouse models have been developed to study Helicobacter-induced carcinogenesis with similarities to gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma (MALToma) in humans. These models require chronic infection of animals with mouse-colonizing isolates of H. pylori or with related gastric Helicobacter spp., such as the canine/feline species Helicobacter felis. Furthermore, consistent with the known influence of host and environmental factors in human gastric cancer, it is possible to manipulate the type and severity of gastric lesions in mouse Helicobacter infection models through the use of different mouse genetic backgrounds and/or by the administration of known cocarcinogens, such as alkylating agents (e.g., N-nitroso-N-methylurea), or even elevated quantities of dietary salt. Here, we describe protocols for the inoculation of mice with gastric Helicobacter spp. and the administration of these cocarcinogens. Furthermore, we will describe the various methodologies used to study gastric inflammation and carcinogenesis in Helicobacter-infected animals.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/978-1-62703-005-2_20 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Expression Patterns of DLL3 Across Neuroendocrine and Non-Neuroendocrine Neoplasms Reveal Broad Opportunities for Therapeutic Targeting.
Cancer Res Commun
January 2025
University of Minnesota, Minnesota, MN, United States.
Neuroendocrine neoplasms (NENs) encompass a diverse set of malignancies with limited precision therapy options. Recently, therapies targeting DLL3 have shown clinical efficacy in aggressive NENs, including small cell lung cancers and neuroendocrine prostate cancers. Given the continued development and expansion of DLL3-targeted therapies, we sought to characterize the expression of DLL3 and identify its clinical and molecular correlates across diverse neuroendocrine and non-neuroendocrine cancers.
View Article and Find Full Text PDFPreoperative Nutritional Status Influences Enteral Nutrition Weaning 6 Months Post-Surgery in Patients with Esophageal Cancer.
Asian Pac J Cancer Prev
January 2025
Department of Anesthesiology and Resuscitology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Objective: This study aimed to clarify whether nutritional status at admission affects enteral nutrition weaning 6 months after surgery in patients with esophageal cancer.
Methods: This was a retrospective study of 81 patients who underwent subtotal esophageal cancer resection between April 2014 and February 2016. The survey items were as follows: 1) sex, 2) age, 3) presence or absence of family members living together, 4) clinical stage, 5) surgical procedure, 6) reconstructed organs, 7) nutritional status at admission, 8) presence or absence of postoperative complications (anastomotic leakage, chylothorax, and recurrent laryngeal nerve paralysis), and 9) presence or absence of treatment other than surgery (chemo- or radiotherapy).
Detection of H-Pylori in the Explanted Liver Tissue and the Enlarged Perihepatic Lymph Nodes of Cirrhotic Patients with Decompensated End-Stage Liver Disease Recruited for Liver Transplantation.
Asian Pac J Cancer Prev
January 2025
Department of Anatomic Pathology, Faculty of Medicine, Kasralainy, Cairo University, Cairo, Egypt.
Background: Helicobacter pylori bacteria colonize the gastric mucosa and contribute to the occurrence and development of gastrointestinal diseases. According to the WHO, H. pylori bacteria are considered class I carcinogen.
View Article and Find Full Text PDFLINC01224 promotes the Warburg effect in gastric cancer by activating the miR-486-5p/PI3K axis.
In Vitro Cell Dev Biol Anim
January 2025
Gastroenterology Section, Medical Center of Digestive Disease, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou, China.
The Warburg effect, a common feature of solid tumors, rewires the metabolism and promotes growth, survival, proliferation, and long-term maintenance in gastric cancer (GC). We performed in vitro and in vivo studies of the pathogenesis of GC to investigate the effects and mechanism of LINC01224 in this cancer. qRT-PCR was used to measure the expression of LINC01224 or miR-486-5p in GC cells, and the expression of LINC01224 in GC tissues by FISH (Fluorescence in situ hybridization) analysis was evaluated.
View Article and Find Full Text PDFEnhanced ZBTB10 expression induced by betulinic acid inhibits gastric cancer progression by inactivating the ARRDC3/ITGB4/PI3K/AKT pathway.
Cell Oncol (Dordr)
January 2025
Division of Gastrointestinal Surgery Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Background: Gastric cancer (GC) ranks as the fourth leading cause of cancer-related deaths worldwide, with most patients diagnosed at advanced stages due to the absence of reliable early detection biomarkers.
Methods: RNA-sequencing was conducted to identify the differentially expressed genes between GC tissues and adjacent normal tissues. CCK8, EdU, colony formation, transwell, flow cytometry and xenograft assays were adopted to explore the biological function of ZBTB10 and betulinic acid (BA) in GC progression.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!