Thomas C Doetschman

Thomas C Doetschman

Specialist, Embryonic Stem Cell Culture
Primary Department
Contact
(520) 626-4901

Work Summary

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

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
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.
Bommireddy, R., Bueno, O., Martin, J., Ormsby, I., Chen, H., Gard, C., Molkentin, J., Boivin, G., Babcock, G., & Doetschman, T. (2009). Calcineurin deficiency decreases inflammatory lesions in transforming growth factor beta1-deficient mice. Clinical and Experimental Immunology, 158(3), 317-324.
Donovan, M. G., Selmin, O. I., Doetschman, T. C., & Romagnolo, D. F. (2017). Mediterranean Diet: Prevention of Colorectal Cancer. Frontiers in Nutrition, 4, 59-83.

Colorectal cancer (CRC) is the third most common cancer diagnosis and the second and third leading cause of cancer mortality in men and women, respectively. However, the majority of CRC cases are the result of sporadic tumorigenesis via the adenoma-carcinoma sequence. This process can take up to 20 years, suggesting an important window of opportunity exists for prevention such as switching toward healthier dietary patterns. The Mediterranean diet (MD) is a dietary pattern associated with various health benefits including protection against cardiovascular disease, diabetes, obesity, and various cancers. In this article, we review publications available in the PubMed database within the last 10 years that report on the impact of a MD eating pattern on prevention of CRC. To assist the reader with interpretation of the results and discussion, we first introduce indexes and scoring systems commonly used to experimentally determine adherence to a MD, followed by a brief introduction of the influence of the MD pattern on inflammatory bowel disease, which predisposes to CRC. Finally, we discuss key biological mechanisms through which specific bioactive food components commonly present in the MD are proposed to prevent or delay the development of CRC. We close with a discussion of future research frontiers in CRC prevention with particular reference to the role of epigenetic mechanisms and microbiome related to the MD eating pattern.

Doetschman, T., Havaranis, A., & Herrmann, H. (1975). Insulin binding to cells of several tissues of the early chick embryo. Developmental Biology, 47(1), 228-232.