Chris Cartwright, MD

Clinical Focus

• Ulcerative Colitis
• Crohn's Disease
• Cancer in Inflammatory Bowel Diseases
• Gastroenterology

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

• Board Certification: Gastroenterology, American Board of Internal Medicine (1987)
• UCSD Medical Center (1984) CA
• Board Certification: Internal Medicine, American Board of Internal Medicine (1981)
• UCSD Medical Center (1981) CA
• UCSD Medical Center (1979) CA
• University of Utah School of Medicine (1978) UT
• BS, Stanford University Biology (1973)
• MD, University of Utah Medicine (1978)

Postdoctoral Advisees

• Gayathri Swaminathan

Graduate & Fellowship Program Affiliations

• Cancer Biology
• Medicine

Community & International Work

• Inflammatory Bowel Diseases More »

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

• Crohn's colitis complicated by cytomegalovirus infection. Levesque BG,  Pai R, Cartwright CA.  Dig Dis Sci.  2009; 54 (9): 1864-7
• A novel pro-apoptotic function of RACK1: suppression of Src activity in the intrinsic and Akt pathways. Mamidipudi V,  Cartwright CA.  Oncogene.  2009;
• RACK1 inhibits colonic cell growth by regulating Src activity at cell cycle checkpoints. Mamidipudi V,  Dhillon NK, Parman T, Miller LD, Lee KC, Cartwright CA.  Oncogene.  2007; 26 (20): 2914-24
• Peptide modulators of Src activity in G1 regulate entry into S phase and proliferation of NIH 3T3 cells. Mamidipudi V,  Miller LD, Mochly-Rosen D, Cartwright CA.  Biochem Biophys Res Commun.  2007; 352 (2): 423-30
• Cytomegalovirus infection in steroid-refractory ulcerative colitis: a case-control study. Kambham N,  Vij R, Cartwright CA, Longacre T.  Am J Surg Pathol.  2004; 28 (3): 365-73
• RACK1 inhibits the serum- and anchorage-independent growth of v-Src transformed cells. Mamidipudi V,  Chang BY, Harte RA, Lee KC, Cartwright CA.  FEBS Lett.  2004; 567 (2-3): 321-6
• RACK1 regulates G1/S progression by suppressing Src kinase activity. Mamidipudi V,  Zhang J, Lee KC, Cartwright CA.  Mol Cell Biol.  2004; 24 (15): 6788-98
• RACK1 regulates Src-mediated Sam68 and p190RhoGAP signaling. Miller LD,  Lee KC, Mochly-Rosen D, Cartwright CA.  Oncogene.  2004; 23 (33): 5682-6
• Detection of protein kinase-binding partners by the yeast two-hybrid analysis. Chang BY,  Cartwright CA.  Methods Mol Biol.  2003; 233 327-43
• RACK1: a novel substrate for the Src protein-tyrosine kinase. Chang BY,  Harte RA, Cartwright CA.  Oncogene.  2002; 21 (50): 7619-29
• The interaction of Src and RACK1 is enhanced by activation of protein kinase C and tyrosine phosphorylation of RACK1. Chang BY,  Chiang M, Cartwright CA.  J Biol Chem.  2001; 276 (23): 20346-56
• The Shp-2 tyrosine phosphatase activates the Src tyrosine kinase by a non-enzymatic mechanism. Walter AO,  Peng ZY, Cartwright CA.  Oncogene.  1999; 18 (11): 1911-20
• RACK1, a receptor for activated C kinase and a homolog of the beta subunit of G proteins, inhibits activity of src tyrosine kinases and growth of NIH 3T3 cells. Chang BY,  Conroy KB, Machleder EM, Cartwright CA.  Mol Cell Biol.  1998; 18 (6): 3245-56
• Regulation of the Src tyrosine kinase and Syp tyrosine phosphatase by their cellular association. Peng ZY,  Cartwright CA.  Oncogene.  1995; 11 (10): 1955-62
• Src activity increases and Yes activity decreases during mitosis of human colon carcinoma cells. Park J,  Cartwright CA.  Mol Cell Biol.  1995; 15 (5): 2374-82
• Elevated c-yes tyrosine kinase activity in premalignant lesions of the colon. Peña SV,  Melhem MF, Meisler AI, Cartwright CA.  Gastroenterology.  1995; 108 (1): 117-24
• Elevated c-Src tyrosine kinase activity in premalignant epithelia of ulcerative colitis. Cartwright CA,  Coad CA, Egbert BM.  J Clin Invest.  1994; 93 (2): 509-15
• Intestinal crypt cells contain higher levels of cytoskeletal-associated pp60c-src protein tyrosine kinase activity than do differentiated enterocytes. Cartwright CA,  Mamajiwalla S, Skolnick SA, Eckhart W, Burgess DR.  Oncogene.  1993; 8 (4): 1033-9
• c-Yes tyrosine kinase activity in human colon carcinoma. Park J,  Meisler AI, Cartwright CA.  Oncogene.  1993; 8 (10): 2627-35
• The hepatitis B virus-encoded transcriptional trans-activator hbx appears to be a novel protein serine/threonine kinase. Wu JY,  Zhou ZY, Judd A, Cartwright CA, Robinson WS.  Cell.  1990; 63 (4): 687-95