The overall goal of this award is to provide a mentored research environment so that the candidate can develop into an independent investigator in the field of gastric cancer induced by Helicobacter pylori infection. The candidate is currently receiving postdoctoral training support under an NIH Research Supplement for Underrepresented Minorities, working on the inflammatory response to H. pylori infection of the gastric mucosa. This award will allow the candidate to develop a related but independent project on the role of the immune response to H. pylori in the development of gastric cancer. The candidate has received extensive training in animal models of infection and the molecular analysis of inflammatory mediators. The immediate career goal is to initiate the proposed work that builds on previous training and expertise but that moves in a new direction relevant to gastric cancer. The long-term career goal is to obtain independent funding for this project and to secure a faculty-level academic appointment. These goals will be achieved by mentoring from two senior investigators with extensive experience in research training and in the proposed area of study. Career development will be enhanced by a close but progressively independent scientific relationship with the mentors. The full resources of the UCSD Cancer Center will be used by the candidate. Increasing independence will be achieved by presentations at scientific meetings, critical reviews, publication of work, and grant submissions in later years. The research project is formulated to develop an independent line of investigation that is based on the previous and current work of the candidate. H. pylori infects the gastric mucosa, leading to peptic ulcers and a high risk of gastric cancer. The central hypothesis of this proposal is that H. pylori-induced immune response dysregulates gastric epithelial cell turnover, resulting in carcinogenesis. The candidate has developed mouse and cell culture models of H. pylori infection and will use these to determine the roles of inflammatory mediators in gastric epithelial cell apoptosis and in the regulation of cell proliferation. Under this award, the candidate will be able to develop this work into a productive project that will gain independent funding.
|Obonyo, Marygorret; Sabet, Mojgan; Cole, Sheri P et al. (2007) Deficiencies of myeloid differentiation factor 88, Toll-like receptor 2 (TLR2), or TLR4 produce specific defects in macrophage cytokine secretion induced by Helicobacter pylori. Infect Immun 75:2408-14|
|Obonyo, Marygorret; Cole, Sheri P; Datta, Sandip K et al. (2006) Evidence for interleukin-1-independent stimulation of interleukin-12 and down-regulation by interleukin-10 in Helicobacter pylori-infected murine dendritic cells deficient in the interleukin-1 receptor. FEMS Immunol Med Microbiol 47:414-9|
|Obonyo, Marygorret; Guiney, Donald G; Fierer, Joshua et al. (2003) Interactions between inducible nitric oxide and other inflammatory mediators during Helicobacter pylori infection. Helicobacter 8:495-502|