Thomas Griffith,  PhD

Associate Professor, Department of Urology

Thomas Griffith

Contact Info

tgriffit@umn.edu

Office Phone 612-624-8269

Administrative Assistant Name
Liz Mayock

Administrative Phone
612-626-7099

Additional Locations

Masonic Cancer Center

Center for Immunology Microbiology, Immunology, and Cancer Biology Graduate Program

Washington University School of Medicine Ph.D, 1996, Biology & Biomedical Science

Illinois State University M.S., 1992, Biological Sciences

Summary

Thomas S. Griffith earned his Ph.D. from Washington University (St. Louis, MO) in 1996 examining the cellular and molecular mechanisms of ocular immune privilege. From 1997-1999, Dr. Griffith was a postdoctoral scientist at Immunex Corporation (Seattle, WA). While at Immunex, Dr. Griffith contributed to the initial characterization of TRAIL (TNF-related apoptosis-inducing ligand). Dr. Griffith moved to the Department of Urology at the University of Iowa in 1999, where he continued his evaluation of TRAIL as an antitumor therapeutic. Since August 2011, Dr. Griffith has been an Associate Professor in the Department of Urology at the University of Minnesota. Dr. Griffith is also a member of the Masonic Cancer Center, the Center for Immunology, and the Microbiology, Immunology, and Cancer Biology Graduate Program at the University of Minnesota.

Research

Research Summary/Interests

Tumor immunology, apoptosis
The research in my laboratory studies the therapeutic potential of apoptotic cell death in the treatment of cancer. The tumor necrosis family member, TRAIL/Apo-2 ligand, is a potent inducer of tumor cell apoptosis, but is non-toxic against normal cell and tissues, suggesting that TRAIL might be administered as an antitumor therapeutic without the side effects seen with other TNF family members, namely TNF and Fas ligand, and traditional chemotherapeutics.

Employment of various gene delivery systems, such as non-replicative viral vectors, is making it possible to administer genes directly into tumors sites in situ. Using this technology, a recombinant, replication-deficient adenoviral vector encoding the full-length TRAIL cDNA (Ad-TRAIL) was developed in the laboratory as a way to induce tumor cell death. Current experiments are investigating the ability of Ad-TRAIL to activate systemic antitumor immunity.

Additional studies are investigating the ability of apoptotic cells to influence the immune response. For these studies, we use a number of experimental model of tolerance as well as an experimental model of sepsis.

Publications

  • EL Brincks, P Gurung, RA Langlois, EA Hemann, KL Legge, TS Griffith. 2011. The magnitude of the T cell response to a clinically-significant dose of influenza virus is regulated by TRAIL. Journal of Immunology. In press.
  • P Gurung, D Rai, SA Condotta, JC Babcock, VP Badovinac, TS Griffith. 2011. Immune unresponsiveness to secondary heterologous bacterial infection after sepsis induction is TRAIL-dependent. Journal of Immunology 187: 2148.
  • LA Norian, BR James, and TS Griffith. 2011. Advances in viral vector-based TRAIL gene therapy for cancer. Cancers 3: 603.
  • P Gurung, TA Kucaba, SP Schoenberger, TA Ferguson, TS Griffith. 2010. TRAIL-expressing CD8+ T cells mediate tolerance following soluble peptide-induced peripheral T cell deletion. Journal of Leukocyte Biology 88: 1217.
  • P Gurung, TA Kucaba, TA Ferguson, TS Griffith. 2009. Activation-induced CD154 expression abrogates tolerance induced by apoptotic cells. Journal of Immunology 183: 6114.
  • EL Brincks, A Katewa, TA Kucaba, TS Griffith, KL Legge. 2008. CD8 T cells utilize TNF-related apoptosis-inducing ligand (TRAIL) to control influenza virus infection. Journal of Immunology 181: 4918.
  • RL VanOosten and TS Griffith. 2007. Activation of tumor-specific CD8+ T cells after intratumoral Ad5-TRAIL/CpG ODN combination therapy. Cancer Research67: 11980.