Key Documents
Lucy Tompkins
Academic Appointments
- Professor, Medicine - Infectious Diseases
- Professor, Microbiology & Immunology
Contact Information
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Clinical Offices
300 Pasteur Dr S101F; MC 5107 Stanford, CA 94305 Tel Work (650) 725-6542 Fax (650) 723-3474
Professional Snapshot
Clinical Focus
- Infectious Diseases
- Internal Medicine
- hospital epidemiology
Administrative Appointments
- Medical Director, Hospital Epidemiolgy and Infection Control Dept, Stanford Hospital and Clinics (1989 - present)
- Associate Dean for Academic Affairs, School of Medicine (2001 - present)
- Chief, Division of Infectious Diseases and Geographic Medicine; Associate Dean for Academic Affairs, Department of Medicine/Stanford U. Medical School (2001 - 2008)
Honors and Awards
- Fellow, Infectious Dis Soc of America (1987)
- Member, Western Assoc. Physicians (1990)
- Member, Am. Assoc Physicians (1995)
- Fellow, Am.Academy Microbiology (1997)
- Fellow, AAAS (2001)
Professional Education
| Fellowship: | University of Washington School of Medicine-GME, WA (1979) |
| Board Certification: | Internal Medicine, American Board of Internal Medicine (1976) |
| Residency: | University of Washington School of Medicine-GME, WA (1976) |
| Residency: | Dartmouth Hitchcock Medical Center, NH (1975) |
| Internship: | Dartmouth Hitchcock Medical Center, NH (1974) |
Graduate & Fellowship Program Affiliations
Scientific Focus
Research Interests
Molecular and cellular basis of pathogenicity of Helicobacter pylori infection and the relationship to gastric malignancy. We are studying the interaction between Helicobacter pylori, the causative agent of peptic ulcers and gastric cancer, and gastric epithelial cells. Genes encoded by a pathogenicity island in H. pylori comprise a secretory apparatus that secretes bacterial CagA protein into target gastric epithelial cells. CagA is phosphorylated on tyrosine residues by host cell kinases and is associated with signal transduction and changes in the cytoskeleton and motility. Cells that have received CagA develop an elongated phenotype and become motile. Further studies suggest that the full-length protein localizes to junctional adhesion sites and acts as an oncoprotein to stimulate the cMET receptor, leading to changes in cell polarity, motility and differentiation, changes which may be related to the development of gastric cancer. We have used an animal model of infection to study gastric lymphoma (MALT lymphoma), including the cellular response.
Publications
- Investigation of mediastinitis due to coagulase-negative staphylococci after cardiothoracic surgery. Infect Control Hosp Epidemiol. 2006; (3): 305-7
- Microarray detection of human parainfluenzavirus 4 infection associated with respiratory failure in an immunocompetent adult. Clin Infect Dis. 2006; (8): e71-6
- Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells. Proc Natl Acad Sci U S A. 2005; (45): 16339-44
- Prolonged incubation and extensive subculturing do not increase recovery of clinically significant microorganisms from standard automated blood cultures. Clin Infect Dis. 2005; (11): 1677-80
- Use of an open-reading frame-specific Campylobacter jejuni DNA microarray as a new genotyping tool for studying epidemiologically related isolates. J Infect Dis. 2003; (4): 691-4
