||Education: MS |
Universtiy of Arizona, Tucson, Arizona, 2001
After receiving his M.S. in Pathobiology from the University of Arizona, Mr. Pitts joined the University of Colorado Health Sciences Center in 2001, as a Professional Research Assistant in the University of Colorado Cancer Center where he worked in the DNA Sequencing Core lab. He joined the Developmental Therapeutics/GI laboratory under the directorship of S. Gail Eckhardt, M.D. in 2005, and was promoted to Research Instructor in the Department of Medicine in 2008.
As part of the Developmental Therapeutics/GI Laboratory, Todd Pitts’ research is focused on pre-clinical studies of novel, targeted therapies for the treatment of advanced colorectal cancer, utilizing both in vitro cell culture models and in vivo mouse model systems. These studies serve as a rational basis for therapeutic treatment choices for patients with advanced GI cancers in the Cancer Center’s Phase I Clinical Trials Program.
Pitts TM, Tan AC, Kulikowski GN, Tentler JJ, Brown AM, Flanigan SA, Leong S, Coldren CD, Hirsch FR, Varella-Garcia M, Korch C, Eckhardt SG. Development of an integrated genomic classifier for a novel agent in colorectal cancer: approach to individualized therapy in early development. Clin Cancer Res. 2010 Jun 15;16(12):3193-204.
Tentler JJ, Tan AC, Weekes CD, Jimeno A, Leong S, Pitts TM, Arcaroli JJ, Messersmith WA, Eckhardt SG. Patient-derived tumour xenografts as models for oncology drug development. Nat Rev Clin Oncol. 2012 Apr 17;9(6):338-50.
Bradshaw-Pierce EL, Pitts TM, Kulikowski G, Selby H, Merz AL, Gustafson DL, Serkova NJ, Eckhardt SG and Weekes C. Utilization of Quantitative In Vivo Pharmacology Approaches to Assess Combination Effects of Everolimus and Irinotecan in Mouse Xenograft Models of Colorectal Cancer. (Accepted in PLoS ONE: In Production).
Pitts TM, Kulikowski GN, Tan AC, Murray BW, Arcaroli JJ, Tentler JJ, Spreafico A, Selby HM, Kachaeva MI, McPhillips KL, Britt BC, Bradshaw-Pierce EL, Messersmith WA, Varella-Garcia M, and Eckhardt SG. Association of the Epithelial-to-Mesenchymal Transition (EMT) Phenotype with Responsiveness to the p21-Activated Kinase Inhibitor, PF-3758309, in Colon Cancer Models. (Accepted in Frontiers in Pharmacology of Anti-Cancer Drugs)