Chris Cartwright, MD
Academic Appointments
- Professor, Medicine - Gastroenterology & Hepatology
- Member, Stanford Cancer Institute
Key Documents
Contact Information
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Clinical Offices
Gastroenterology Clinic 900 Blake Wilbur Dr Garden Level MC 5355 Palo Alto, CA 94304 Tel Work (650) 736-5555 Fax (650) 498-6323
- Academic Offices
Personal Information Email Tel (650) 725-8464Alternate Contact Susan Lydick GI Administrator Email Tel Work 650-723-6914Not for medical emergencies or patient use
Professional Overview
Clinical Focus
- Gastroenterology
- Inflammatory Bowel Diseases
Administrative Appointments
- Director, Program for Inflammatory Bowel Diseases, Stanford University School of Medicine (1989 - present)
Honors and Awards
- Outstanding AGA Women in Science, American Gastroenterological Association (2008)
- Premier Physician Award, Crohn's & Colitis Foundation of America - Greater Bay Area Chapter (2000)
- Member, American Society for Clinical Investigation (1995)
Professional Education
| BS: | Stanford University, Biology (1973) |
| MD: | University of Utah, Medicine (1978) |
| Internship: | UCSD Medical Center CA (1979) |
| Residency: | UCSD Medical Center CA (1981) |
| Fellowship: | UCSD Medical Center CA (1984) |
| Research Associate: | The Salk Institute, Cancer Biology (1989) |
Graduate & Fellowship Program Affiliations
Community and International Work
- Inflammatory Bowel Diseases, Bay Area
Scientific Focus
Current Research Interests
Research in my laboratory focuses on molecular mechanisms of intestinal cell growth control. A primary focus is on function and regulation of the Src family of tyrosine kinases in normal cells, and their deregulation in cancer cells. Molecular, cellular and physiologic approaches are used to explore basic questions about growth regulation. Areas of active investigation include studies of Src function in cell cycle progression, proliferation, differentiation, adhesion, survival and malignant transformation; discovery of endogenous inhibitors of Src kinases; analysis of inhibitor function in cell growth control and apoptosis; and exploration of new drug therapy for colon cancer. Our recent discovery of a Src inhibitor, RACK1, which works both to inhibit growth (by suppressing Src activity at G1 and mitotic checkpoints) and to induce death of colon cells, could be exploited for development of new and more powerful and selective strategies for treatment of human colon cancer.
Publications
- Rack1 promotes epithelial cell-cell adhesion by regulating E-cadherin endocytosis. Oncogene. 2012; (3): 376-89
- A novel pro-apoptotic function of RACK1: suppression of Src activity in the intrinsic and Akt pathways. Oncogene. 2009; (50): 4421-33
- Crohn's colitis complicated by cytomegalovirus infection. Dig Dis Sci. 2009; (9): 1864-7
- Peptide modulators of Src activity in G1 regulate entry into S phase and proliferation of NIH 3T3 cells. Biochem Biophys Res Commun. 2007; (2): 423-30
- RACK1 inhibits colonic cell growth by regulating Src activity at cell cycle checkpoints. Oncogene. 2007; (20): 2914-24
- Cytomegalovirus infection in steroid-refractory ulcerative colitis: a case-control study. Am J Surg Pathol. 2004; (3): 365-73
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