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Research

SUMO, Ubiquitin and UBL Proteins

Dr. Yeh discovered two ubiquitin-like protein modifiers, SUMO and NEDD8, in the mid 1990’s. His laboratory continued to explore the biology of SUMO and NEDD8 modification using mouse models and and extended his findings to human diseases. He has organized five international meetings on this important topic. The Sixth International Conference on SUMO, Ubiquitin, UBL Proteins: Implications for Human Diseases will be held February 8-10, 2012.

Stem Cell Transplant to Repair Damaged Heart

We are exploring the use of adult stem cells, such as CD34+ cells or mesenchymal stem cells, to repair hearts damaged by acute myocardial infarction. Using molecular imaging in animal models, we have successfully demonstrated the mechanisms whereby adult stem cells helped to heal damaged heart. We are currently studying the use of induced pluripotent stem cells (iPS cells) to heal the heart damaged by chemotherapy.

Mechanism of Chemotherapy-induced Heart Failure

We have developed animal models to explain how chemotherapies can cause damage to heart muscles.   These mechanistic insights will allow us to design safer chemotherapy agents and to identify specific genes that pre-disposed patients to the development of heart failure.

Inflammation and Cardiovascular Disease

We have shown that C-reactive protein, a marker of inflammation, can directly activate human endothelial cells and that anti-atherosclerotic drugs down regulate inflammatory markers. We have also discovered that C-reactive protein can be produced by vascular smooth muscle cells in response to inflammatory stimuli. These findings have significant implications for inflammation and vascular biology.

Clinical Research

The mission of the Department of Cardiology clinical research team is to eliminate cardiac complications arising from cancer treatment and to provide optimal management of pre-existing heart disease to ensure proper delivery of the most effective cancer treatment available through patient care, research, prevention, and education. We are funded by the Cancer Prevention Research Institute of Texas (CPRIT) to carry out a clinical study to determine whether genetic markers can be used to predict patients’ predisposition to develop doxorubicin-induced cardiotoxicity.


© 2014 The University of Texas MD Anderson Cancer Center