Wednesday, October 9, 2024
10/9/2024
ABSTRACT The knowledge gaps this application addresses are how precancerous lesions (i.e. metaplasia) arise and subsequently fuel adenocarcinoma of the stomach. Infection with Helicobacter pylori (H. pylori) and autoimmune gastritis both cause chronic inflammation and increase the risk of gastric cancer. This application includes numerous mouse models and human tissue samples to investigate the importance of immune cells (mast cells and Th2 T cells) and cytokines (IL4 and IL13) in inducing gastric metaplasia and promoting the development of gastric metaplasia and tumorigenesis. Identifying inflammatory cells and signals that initiate metaplasia and drive tumor development could improve the ability to identify individuals at an increased risk of disease progression, and new immune based strategies to prevent and treat preneoplastic lesions associated with gastric diseases, including gastric cancer.
HHS’ Tracking Accountability in Government Grants System (TAGGS) website provides access to detailed descriptions of grants, loans, aggregated direct payments and other types of financial assistance awarded by the HHS Operating Divisions (OPDIVs) and the Office of the Secretary Staff Divisions (STAFFDIVs).
