Thomas C Doetschman
Professor, BIO5 Institute
Professor, Cancer Biology - GIDP
Professor, Cellular and Molecular Medicine
Professor, Genetics - GIDP
Primary Department
Department Affiliations
(520) 626-4901
Work Summary
I am investigating a human connective tissue disorder in mice. I am also investigating the role of gut bacteria in colon cancer risk in both a mouse model of colon cancer and in humans with colon cancer.
Research Interest
Dr. Thomas Doetschman, PhD, Biochemistry & Biophysics, University of Connecticut, has been involved in cardiovascular research for over a decade through investigations into the cardiovascular roles of the three TGFβ ligands and FGF2 ligand isoforms in genetically engineered mice. These mice have determined that TGFβ2 plays major roles in heart and vascular development and for maintenance of valvular and large vessel integrity in the adult and that both the TGFβ1 and FGF2 are involved in adult heart disease.His work has also demonstrated roles of TGFβ in cancer and immunology. He found that a major function of TGFβ1 is to inhibit autoimmunity and to establish homeostatic balance between immune regulatory and inflammatory cells. He has shown that an imbalance in the latter is critical in the tumor suppressor function of TGFβ in the colon.Dr. Doetschman has also played an important role in the development of the mouse genetic engineering field. He has been responsible for the establishment of 3 mouse genetic engineering facilities, in Cincinnati OH, Singapore and the University of Arizona’s BIO5 Institute. Keywords: "Cancer", "Microbiome", "Mouse Genetic Engineering", "Connective Tissue Disorder"

Publications

Ball, C. L., Daniel, S. G., Besselsen, D. G., Hurwitz, B. L., & Doetschman, T. C. (2017). Functional changes in the gut microbiome contribute to Transforming Growth Factor β-deficient colon cancer. mSystems, 2(5), 1-17.
BIO5 Collaborators
David G Besselsen, Thomas C Doetschman, Bonnie L Hurwitz
Shao, C., Yin, M., Deng, L., Stambrook, P., Doetschman, T., & Tischfield, J. (2002). Loss of heterozygosity and point mutation at Aprt locus in T cells and fibroblasts of Pms2-/- mice.. Oncogene, 21, 2840-2845.
Luo, W., Wolska, B., Grupp, I., Harrer, J., Haghighi, K., Ferguson, D., Slack, J., Grupp, G., Doetschman, T., Solaro, R., & Kranias, E. (1996). Phospholamban gene dosage effects in the mammalian heart. Circulation Research, 78(5), 839-847.
Luo, W., Grupp, I., Harrer, J., Ponniah, S., Grupp, G., Duffy, J., Doetschman, T., & Kranias, E. (1994). Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of beta- agonist stimulation. Circ Res, 75(3), 401-409.
Xiao, L., Liu, P., Li, X., Doetschman, T., Coffin, J., Drissi, H., & Hurley, M. (2009). Exported 18-kDa isoform of fibroblast growth factor-2 is a critical determinant of bone mass in mice. Journal of Biological Chemistry, 284(5), 3170-3182.