Thomas C Doetschman

Thomas C Doetschman

Specialist, Embryonic Stem Cell Culture
Member of the General Faculty
Primary Department
Contact
(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

Selmin, O. I., Fang, C., Lyon, A. M., Doetschman, T. C., Thompson, P. A., Martinez, J. D., Smith, J. W., Lance, P. M., & Romagnolo, D. F. (2016). Inactivation of Adenomatous Polyposis Coli Reduces Bile Acid/Farnesoid X Receptor Expression through Fxr gene CpG Methylation in Mouse Colon Tumors and Human Colon Cancer Cells. The Journal of Nutrition, 146, 236-242.

The farnesoid X receptor (FXR) regulates bile acid (BA) metabolism and possesses tumor suppressor functions. FXR expression is reduced in colorectal tumors of subjects carrying inactivated adenomatous polyposis coli (APC). Identifying the mechanisms responsible for this reduction may offer new molecular targets for colon cancer prevention.

Kaiser, S., Park, Y., Franklin, J., Halberg, R., Yu, M., Jessen, W., Freudenberg, J., Chen, X., Haigis, K., Jegga, A., Kong, S., Sakthivel, B., Xu, H., Reichling, T., Azhar, M., Boivin, G., Roberts, R., Bissahoyo, A., Gonzales, F., , Bloom, G., et al. (2007). Transcriptional recapitulation and subversion of embryonic colon development by mouse colon tumor models and human colon cancer. Genome Biology, 8(7), R131.
Boivin, G., Washington, K., Yang, K., Ward, J., Pretlow, T., Russell, R., Besselsen, D., Godfrey, V., Doetschman, T., Dove, W., Pitot, H., Halberg, R., Itzkowitz, S., Groden, J., & Coffey, R. (2003). Pathology of mouse models of intestinal cancer: Consensus report and recommendations. Gastroenterology, 124(3), 762-777. PMID12612914.
Xiao, L., Sobue, T., Esliger, A., Kronenberg, M., Coffin, J., Doetschman, T., & Hurley, M. (2010). Disruption of the Fgf2 gene activates the adipogenic and suppresses the osteogenic program in mesenchymal marrow stromal stem cells. Bone, 47(2), 360-370.
Conway, S., Doetschman, T., & Azhar, M. (2011). The inter-relationship of periostin, TGF beta, and BMP in heart valve development and valvular heart diseases. Scientific World Journal, 11, 1509-1524.